human nutrition - a health perspective, 2nd edition

H U M A N N U T R I T I O N

A health perspective

second Edition

Mary E. Barasi

Illustrations by Megan Morris

LONDON

BA, BSc, MSc, R. Nutr.Principal Lecturer in Nutrition, University of Wales Institute, Cardiff, UK

Hodder ArnoldA MEMBER OF THE HODDER HEADLINE GROUP

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CONTENTS

Preface v

List of tables vii

List of figures ix

PART ONE THE STUDY OF NUTRITION AND FOOD HABITS 1

Chapter 1 What is nutrition? 3

Chapter 2 What are the influences on eating habits? 18

Chapter 3 Basics of a healthy diet 36

PART TWO THE NUTRIENTS IN FOOD AND THEIR ROLE IN HEALTH 55

Chapter 4 Proteins 57

Chapter 5 Fats 75

Chapter 6 Carbohydrates 99

Chapter 7 Energy needs 123

Chapter 8 Energy balance 137

Chapter 9 Vitamins 161

Chapter 10 Minerals, electrolytes and fluid 194

PART THREE THE APPLICATION OF NUTRITIONAL KNOWLEDGE 229

Chapter 11 Pregnancy and lactation 231

Chapter 12 Infants, children and adolescents 251

iii

❚ CONTENTS

iv

Chapter 13 Adults and the elderly population 279

Chapter 14 Diet and coronary heart disease 304

Chapter 15 Diet and cancer 324

Chapter 16 Challenges to nutritional status 338

Chapter 17 Optimizing nutrition 364

Chapter 18 Public health nutrition and health promotion 380

Index 397

v

PREFACE

The need for a second edition of this book stemsfrom the continuing rapid changes occurring in our understanding of nutrition. A number of these developments can be identified here.Advances have taken place in the way thatinformation is collected and reviewed and theconcept of an evidence base informing practicehas become established. Research findings frommany studies can be subjected to reviews, usingan approach that should be both systematic andclear in its methodology. In this way, it is increas-ingly possible to provide some answers to impor-tant questions, on the basis of a body of researchevidence that has been thoroughly analysed andcombined with data from similar studies to pro-duce quantitative outcomes. This approach ofsystematic review strengthens the conclusionsthat are made, and provides a sound basis forpolicy or practice to be developed. The CochraneDatabase contains information relating to clini-cal systematic reviews and is a prime example ofthe application of this methodology. In thefuture, all practice should be evidence based, andpatients and consumers should expect this.

A technological advance that has sometimesworked counter to the concept of an evidencebase has been the widespread use of the Internet,with the proliferation of web-based resources.These can provide almost instant access to goodquality information through online databasesand access to scientific publications and rep-utable web sites, often with extensive links torelated information. However, there is also theopportunity for much unscientific and uncon-trolled information to be presented, and thismay be confusing, inaccurate, misleading andpotentially dangerous. For users of such infor-mation, there is a real need to have some basicnutrition knowledge to enable them to discerntruth from fiction.

One of the most exciting developments atthe beginning of the new millennium has beenthe human genome project, with mapping of human DNA. This reflects the enormousadvances that have occurred in molecular biol-ogy in recent years. These are already having

their impact in nutrition, with research out-comes identifying genetic variants that explainsome of the recognized differences in the wayindividuals respond to nutrients or exhibitincreased susceptibility to nutritional disorders.There is a great deal to be discovered in thisfield. At some point in the future, we willunderstand much more about the way thatgenes and nutrients interact.

The moves towards healthy eating in the lasttwo decades of the twentieth century led to recog-nition that food and nutrition can have positivehealth benefits. From this has developed a con-cept of optimal nutrition, wherein food or nutri-ents can be actively used to promote health, inways that are additional to their nutritional role.This has generated new developments withinthe food industry to produce functional or smartfoods that aim to address these demands. Atpresent, there is a lack of sound evidence aboutthe mechanisms of action or the benefits inhumans for some of these components. Conse-quently, the amounts required to be consumedfor optimal benefit are also unknown, and moreresearch in this area is needed.

The importance of nutrition as part of publichealth is now recognized at Government level.The Food Standards Agency (FSA) has beenestablished since 2001 to take the lead in theUK. The Nutrition Strategy Framework* identi-fies a number of objectives to improve bothknowledge and practical aspects of nutritionthroughout society. In order to achieve these,practical guidance on nutritional issues will beneeded at various levels in society and willrequire informed educators. Traditionally, healthprofessionals have been responsible for health-related issues, including nutrition. Those with thegreatest responsibility are dietitians and nutri-tionists, yet doctors and nurses may be the peoplewho are most readily accessible to the generalpopulation. It has been recognized that all healthprofessionals need nutritional knowledge at some

*Food Standards Agency 2000: Your food – farm to fork.London: FSA.

❚ PREFACE

vi

level. This, in turn, needs to be disseminated toothers working within communities who can helpto further disseminate the messages about dietaryimprovements.

This new edition of the book retains thestructure of the first edition, but has been sub-stantially updated and extended. A new chapterhas been added to include optimal nutrition andsmart or functional foods.

The book takes a practical approach, involv-ing the reader in thinking about their own nutri-tion, in order to understand better why people eatas they do, and the difficulties that others mayhave in changing their food intake. There areactivities and study questions within each chapterthat are intended to stimulate further thought andpractise problem-solving. References for furtherreading are provided at the end of each chapterfor those who wish to pursue further study.

Sections in the book include an introductionto the study of nutrition and the foundations ofhealthy eating. This is followed by a section onthe macronutrients and micronutrients, andincludes a consideration of energy balance and

a new section on the need for fluids. The finalsection of the book considers more appliedaspects of nutrition during the normal stages ofthe life cycle, in situations that challenge nutri-tional status as well as the relationship betweennutrition and major diseases. Optimal nutrition,and nutrition policy and health promotion areconsidered in this section.

The author is grateful to all those who havehelped in the development of the book, includ-ing colleagues and students who offer endlesschallenges with interesting and stimulatingquestions. I would also like to thank MeganMorris for her imaginative contribution in theillustrations throughout the text. The produc-tion of the book has been efficiently managedby Georgina Bentliff and Heather Smith fromthe publishers.

Thank you also to my family for their sup-port throughout the work on this edition.

Mary BarasiCardiff

2003

vii

LIST OF TABLES

1.1 Different levels of studying nutrition 52.1 Factors influencing the availability of foods 282.2 Factors influencing the acceptability of foods 282.3 Core, secondary and peripheral foods 313.1 Dietary reference values for fat and carbohydrate for adults, as a percentage of daily

total food energy intake (excluding alcohol) 443.2 Nutritional details of the five groups in the UK National Food Guide (the Balance of

Good Health) 494.1 The amino acids classified according to the nature of their side-chains 604.2 Sources of protein 614.3 Amino acids that may become indispensable under certain circumstances 634.4 The use of complementary foods to make up for limiting amino acids in some

plant foods 694.5 Dietary reference values for protein for adults 705.1 Classification of fatty acids by saturation, chain length and family 785.2 Fat contents of selected foods per 100 g, per average serving portion and as per cent

energy from fat 825.3 Trends in total fat and energy intakes, per person per day, showing mean population

figures and intakes in the highest and lowest income groups studied by the National Food Survey 83

5.4 Percentage of energy from the main groups of fatty acids 835.5 Sources of fat and fatty acids in the British diet 845.6 Summary of fate of fat digestion products 885.7 Typical compositions of lipoprotein particles 886.1 Non-starch polysaccharide content of some common foods, showing soluble and

insoluble fractions 1066.2 Classification of starch according to digestibility 1086.3 Food groups contributing to total and non-milk extrinsic sugars intakes 1187.1 The energy conversion factors used in the current UK food composition tables 1257.2 Percentage of energy from carbohydrate, protein and fat in selected foods 1267.3 Energy yields obtained from the oxidation of different substrates 1297.4 The effect on energy yield of different metabolic mixtures and respiratory quotient 1297.5 Physical activity ratios for calculation of energy expenditure 1347.6 Estimated average requirements for energy for adults in megajoules per day

(Calories/ day) 1358.1 Action levels for weight management based on waist circumference 1468.2 Medical and other consequences of obesity 153

10.1 Average amounts of minerals found in the adult human body 19410.2 Average values for daily turnover of body water in a temperate climate 22210.3 Average caffeine (in milligrams per average serving) for some beverages 22310.4 The water content of some foods (as a percentage) 22411.1 Guidelines on weight gain in pregnancy 23611.2 Summary of dietary reference values for pregnancy 23811.3 Possible indicators of nutritional vulnerability in pregnancy 24111.4 Dietary reference values for lactation 24712.1 Reference nutrient intakes for selected nutrients for infants 254

❚ LIST OF TABLES

viii

12.2 The estimated average requirement for energy for children up to the age of 12 months 255

12.3 Suggested food groups to be included in the diet at 6–9 months and 12 months 26112.4 Sources of iron, vitamin C and vitamin D suitable for weaning 26212.5 Dietary reference values for children from 4 to 18 years 26712.6 General recommendations on fat and carbohydrates 26812.7 Contributions of the main macronutrient groups to total energy intake for young

people aged 4 to 18 26912.8 Minimum nutritional standards for school meals 27112.9 Summary of Caroline Walker Trust Nutritional Guidelines for School Meals 27213.1 Types of foods eaten by the highest and lowest income groups studied by the

National Food Survey 2000 29013.2 ‘Value for money’ of foods bought by high-income and low-income groups 29013.3 Cost of common snack foods, in pence, to supply 420 kJ (100 Calories) 29113.4 Factors contributing to poor food intake in the elderly 29713.5 Percentages of elderly subjects with nutrient intakes from food sources below the LRNI 29913.6 Prevalence of suboptimal indices for nutrients in elderly subjects 30015.1 Summary of stages in cancer development 32615.2 Some proposed links between dietary components and cancers 33115.3 Summary of diet and health recommendations 33516.1 Grouping of some commonly eaten foods according to glycaemic index 35517.1 Functional foods in sports nutrition 37418.1 Summary of chronic diseases and other health problems with possible dietary links 38318.2 Population goals for nutrients, foods and lifestyle factors, consistent with the

prevention of major public health problems in Europe 38418.3 Model for stages of change 389

ix

1.1 A pyramid represents the contents of the diet and can be used as the basis of a food guide 7

1.2 Measurement of skinfold for assessment of body fat content 121.3 Summary of the main methods of anthropometry 132.1 Physiological factors controlling hunger and food intake 192.2 Habit influences eating behaviour 222.3 Psychological need as a trigger to eating 232.4 Sensory appeal as a trigger for eating 242.5 Why do we eat? 252.6 Some of the main components of a person’s food habits 263.1 The stages of development of a clinical deficiency 413.2 The normal distribution curve of nutrient requirements in a population and levels

used for setting dietary recommendations 423.3 Distribution of riboflavin intakes in a population of 12-year-old boys 453.4 The USA Food Guide pyramid: a guide to daily food choices 473.5 The UK National Food Guide: the Balance of Good Health 483.6 Example of a day’s food intake and the numbers of servings from the National

Food Guide 504.1 Origin of human dietary protein 584.2 Digestion of proteins 624.3 Summary of amino acid metabolism 644.4 Summary of uses of protein 664.5 Components of nitrogen balance 684.6 Example of cases of protein deficiency 715.1 Spatial configuration of saturated, cis and trans unsaturated fatty acids 785.2 Chemical structure of cholesterol 815.3 Sources of visible and invisible fats 815.4 Why do we eat fat? 855.5 Digestion and absorption of fats 875.6 Exogenous lipid transport 895.7 Endogenous lipid transport and metabolism 905.8 The role of adipose tissue in metabolism 925.9 Aspects of insulin resistance 946.1 Structural formulae for three simple sugars 1006.2 The condensation of two molecules of glucose to form maltose 1016.3 Structures of starch and cellulose 1036.4 The relationship of non-starch polysaccharides to other sources of carbohydrate 1056.5 Digestion of carbohydrates 1096.6 Rise in blood glucose after eating, and the calculation of glycaemic index 1106.7 Metabolism of carbohydrates 1116.8 Why do we need carbohydrates in the diet? 1126.9 Development of dental caries and the role of diet 1156.10 Summary of the effects of non-starch polysaccharides in the digestive tract 1197.1 The bomb calorimeter 1247.2 The components of energy output 1287.3 Factors affecting basal metabolic rate 131

LIST OF FIGURES

❚ LIST OF FIGURES

x

7.4 Summary record of daily activity 1348.1 Components of energy balance 1388.2 Using energy in everyday life 1418.3 Exercise on prescription 1418.4 Actions of leptin 1438.5 Weight assessment chart for adults 1458.6 Central (apple) and peripheral (pear) fat deposition 1468.7 The relationships between fat and sugar intakes and body weight 1498.8 A summary of factors contributing to positive energy balance 1528.9 Some possible interventions for weight loss: slimming group, surgical

intervention and exercise 1558.10 The relationship between changes in lean body mass and in fat 1589.1 Conversion of beta-carotene to retinol 1639.2 Role of vitamin A in vision 1659.3 Summary of the signs of vitamin A deficiency 1669.4 The formation of biologically active vitamin D occurs in two stages 1689.5 Vitamin D deficiency in children – rickets 1699.6 Structures of tocopherols and tocotrienols 1719.7 Phylloquinone (vitamin K1) is derived from plants and is lipid soluble 1739.8 Structure of thiamin 1759.9 Structure of riboflavin 1779.10 Structures of nicotinic acid and nicotinamide, collectively known as niacin 1789.11 Structures of the three closely related compounds known as vitamin B6:

pyridoxine, pyridoxal and pyridoxamine 1809.12 Structure of folic acid 1819.13 The metabolic role of folate in homocysteine metabolism 1839.14 Structure of ascorbic acid 1889.15 Some dietary sources of vitamin C 1889.16 Summary of factors influencing vitamin C status 19010.1 A summary of factors involved in calcium balance 19710.2 The regulation of plasma calcium 19810.3 Changes in bone mass with age 19910.4 Factors influencing bone health 20110.5 Influences on iron absorption 20510.6 Signs of zinc deficiency 20910.7 The role of copper in the body 21110.8 Sources of selenium in the diet 21210.9 Causes and effects of iodine deficiency 21510.10 Sources of sodium 21810.11 Roles of sodium and potassium in blood pressure 22111.1 Sources of dietary folate 23311.2 Adaptive mechanisms in pregnancy to conserve energy 23511.3 Some general diet tips for pregnancy 23711.4 Summary of fetal influences on later health 24411.5 The process of lactation 24611.6 Arguments for and against breastfeeding 24812.1 Example of a standard growth curve used to monitor child development 25312.2 Summary of how to wean a baby 26312.3 Example of a healthy packed lunch 273

LIST OF FIGURES ❚

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12.4 A summary of potential nutritional problems encountered by children and teenagers 274

13.1 The possible advantages and disadvantages of a vegetarian diet 28413.2 Factors resulting in increased risk in older adults 29414.1 The development of coronary heart disease 30614.2 The increase in risk with increases in serum cholesterol levels 30914.3 Additive effects of risk factors on damage to coronary arteries 31014.4 Main risk factors in the development of coronary heart disease 31014.5 Social class and gender differences in heart disease mortality 31114.6 A summary of dietary risk factors for coronary heart disease 31414.7 Interactions between glutathione, vitamin C and vitamin E during antioxidant activity 32015.1 Possible promoting and protective factors in the diet in relation to cancer development 33416.1 Symptoms of food intolerance 34016.2 IgE-mediated food allergy 34116.3 Diagnosis of food intolerance 34516.4 The relationship between infection and nutrition 34616.5 The provision of energy in sport 35216.6 Effects of different amounts of carbohydrate in the diet on the refuelling of

muscle glycogen in the 24–48 hours after exercise 35416.7 Effects of different amounts of carbohydrate in the diet on muscle glycogen

levels during three consecutive periods of exercise over 72 hours 35416.8 Nutritional implications of alcohol abuse 36017.1 Examples of fortified foods 36917.2 How microflora are used in the bowel 37517.3 Probiotics and prebiotics 37718.1 The health gain rhomboid 38818.2 The folic acid campaign 39318.3 Economics of health promotion 394

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THE STUDY OF NUTRITIONAND FOOD HABITS

PA R TONE

3

what is nutrition?

The aims of this chapter are to:

❏ define nutrition as a discipline for study and reflect on its importance;❏ look at ways in which dietary information is collected;❏ encourage the reader to think about their own food intake, their own and others’ perceptions of nutrition;❏ consider why nutrition is important and how it is included in nutrition policies.

On completing the study of this chapter, you should be able to:

❏ think about nutrition and food in relation to yourself;❏ understand what is meant by nutrition, and why it is an important science, involving many different disciplines;❏ explain and discuss the various ways in which nutrition is studied, together with their advantages and

disadvantages;❏ understand and evaluate the information about nutrition that is disseminated in the scientific as well as the

non-specialist literature;❏ explain how nutritional status can be assessed;❏ understand the basis on which nutrition policy may be made at government level.

Definitions of nutrition

Everybody has their own experience of food andeating, so it is likely that people will have differ-ent ideas about what is meant by nutrition. Somemay see eating as a means of meeting our basicphysiological needs and warding off hunger, and others as a pleasurable experience in its ownright and something to anticipate and plan.These represent the two extremes implied by thesayings ‘eat to live’ and ‘live to eat’.

In reality, eating is far more complicatedthan this, involving aspects of our psychologicalmake-up and current state of mind, our geneticblueprint, the social environment of which weare a part, our economic situation and externalfactors relating to the availability of the food.These will be explored in more detail in Chapter 2.Eating also does more than just keep us alive.When insufficient food or specific nutrients are supplied, some physiological adaptation may

occur to minimize the consequences. Eventually,however, a deficiency state will arise.

At the beginning of the twentieth century,most of the science of nutrition was directed atdiscovering the essential nutrients, studying theeffects of insufficient intakes and determiningthe quantities needed to prevent deficiency states.Since then it has gradually been recognized thatgood nutrition is not simply a matter of provid-ing enough of all the nutrients. We now realizethat diets in the affluent Western countries,although apparently containing all the necessarynutrients, are probably contributing to many ofthe diseases afflicting these populations. Muchresearch has been focused on finding whichnutrients are linked to which diseases, in aneffort to promote a change in the dietary intakeand hence an improvement in health. Since the1970s a great deal of advice has been aimed atencouraging people to eat a healthier balance of

C H A P T E R

1

❚ WHAT IS NUTRITION?

4

foods, thereby reducing disease. The emphasis in the twenty-first century has started to movetowards promoting positive health through diet,know as optimum nutrition. However, nutrition-ists recognize that altering people’s food intakeis complicated because diets are influenced bymany factors other than the need to eat and thedesire for well-being.

It can be seen that arriving at a definition of nutrition is far from straightforward. Tworather different definitions have been suggested,describing nutrition as:

‘the study of foods and nutrients vital to healthand how the body uses these to promote andsupport growth, maintenance and reproductionof cells’ or

‘the study of the relationship between peopleand their food’.

The first definition deals only with the nutri-ents, what happens to them within the humanbody and what the results are if insufficientamounts are provided. However, people do not eatnutrients, they eat food. This definition ignoresall the external factors that play a role in ourapproach to food and that are crucial in anystudy of what people are eating. These factorsare different for each individual, depending oncultural background and the circumstances of aperson’s life.

The second definition takes a much broaderperspective, from the supply of food and all the influences thereon, to the individual’s foodselection and, finally, to the physiological andbiochemical effects of the nutrients in thehuman body, and the consequences for healthand survival. It also recognizes that nutritionistsdo not only study the effects of nutrients on biochemical and physiological functioning,they have an additional responsibility to trans-late their knowledge for those who produce,process and market the foods. Furthermore,nutritionists must be involved in the formula-tion of policy that determines the access byconsumers to food. Finally, consumers need thehelp of nutritionists to enable them to make thebest of the food available. Only by broadeningour definition of the subject across the full

range of human relationships with food cannutrition have its justified place in human well-being.

Why is nutrition important?

To answer this question, it is perhaps useful toconsider the various levels at which nutritioncan be studied. Table 1.1 illustrates some exam-ples of the application of nutritional science inother fields of study. In each case, nutritionplays a specific role, and the emphasis requiredmay differ from its application in all other roles.Thus, nutrition is a science with many differentapplications and meanings to different special-ists. Nevertheless, each of these specialists,working in their own particular field of expert-ise, needs to have knowledge of nutrition inorder to apply the findings of their work to thenutritional context.

There has been an upsurge of general inter-est in nutrition in the last 20–30 years; this hasnot just been among the scientific community,but also among the general population. Whyhas this happened?

First, it is notable that dietary intakes havebeen and are changing rapidly. In the Westernworld, we have an ever-increasing selection of foods available to us. People can now eatevery day the foods our ancestors had only onspecial occasions. New foods are appearing thathave been conceived and developed by food

Why are you studying nutrition?At what level will you be applying your nutritional knowledge?At what level might the following be using nutrition:

nurse pharmacistdietitian journalistobstetrician parent?home economist

Try to think of some other examples of peopleworking with nutrition, at each of the differentlevels in Table 1.1.

Activity 1.1

WHY IS NUTRITION IMPORTANT? ❚

5

technologists; sometimes these contain unusualingredients, which provide nutrients in unex-pected amounts (this can be a problem for thenutritionist in giving advice). New processingtechniques, such as irradiation, may affect thenutrients in food. New products, speciallydesigned to promote health are now available;these are discussed in Chapter 17.

In modern society, meal patterns have becomeless rigid and many people no longer eat meals atregular mealtimes. The members of a family mayeach have an independent meal at different timesof the day and the traditional family meal is a rare event.

Concerns about food safety and environ-mental issues have resulted in changes in dietaryhabits, the most notable amongst these being the rise in vegetarianism in the UK and thegrowth of demand for organically grown food.Nevertheless, the great majority of food boughtcomes from large retail supermarkets that exert agreat deal of influence over customer choice.

Health issues have been given a great deal of prominence in the media. Statistics show thatpopulations in Western countries have excessmortality (i.e. death rates) and morbidity (i.e. ratesof illness) from many diseases related to diet,such as cardiovascular disorders, bowel diseases

and cancers, as well as a high prevalence of obe-sity and diabetes. At the same time, we are oftenshocked by images of starvation in other parts ofthe world where conflict, drought and other dis-asters have resulted in millions of people suffer-ing acute malnutrition and starvation.

As greater numbers of nutritionists are trainedand the discipline becomes more widely studied,knowledge accumulates based on sound evidence.Public health nutrition is now a discipline in itsown right, with a specific remit of promotinghealth through good nutrition. However, as with allscientific research, more questions follow everyfinding. Consensus is being reached on some of theways in which diet is involved in Western diseases,and advice can now be based on much firmer evi-dence. However, new research may cause currentadvice to be modified. New angles on nutritionresearch, particularly from the field of molecularbiology, are explaining observations made earlierat the whole-body level. Improved methodologiesallow more sensitive and appropriate measure-ments to be made. For example, in the study ofenergy balance, the use of radioactively labelledwater has provided a means of measuring energyexpenditure in subjects during their normal lives.This has provided a wealth of information aboutthis important area of nutrition.

Different levels of studying nutritionTABLE 1.1Level of study Examples of applicationMacro/population studies Government statistics (for formulation of policy, e.g. about agriculture,

or health)Epidemiology (to study relationship between diet and disease)Food producers (to respond to changes in consumer demand and to

lead demand)Individual/whole person studies Sociology (to study patterns of behaviour related to food)

Food science/technology (to identify changes in individual preferences for food; sensory qualities)

Sports science (to identify links between diet and performance)Medicine (to study influences of diet on the health of the individual

and recovery from illness)Micro/laboratory studies Physiology (to understand the role of nutrients in functioning of

body systems)Biochemistry (to investigate the biochemical role of nutrients in

normal and abnormal functioning)Molecular biology (to study gene–nutrient interactions)


6

The media are very sensitive to public con-cern, so that news about nutritional findingsreceives a great deal of publicity. Unfortunately,the style of reporting may distort the scientificdetail, so that what is eventually presented by the media may not accurately represent the findings. Moreover, excessive prominence maybe given to very minor and insignificant find-ings, especially if they appear to contradict earlier results. Consequently, rather than beingbetter informed, the public may become con-fused. It is essential, therefore, that thosetrained in nutrition have a clear understandingof nutritional issues, and are able to disentanglesome of the inaccuracies presented by themedia.

What do people eat?

Different peoples around the world have differ-ent dietary patterns, determined by a number offactors. The major factors influencing what iseaten in different cultures are the foods avail-able in that particular culture, traditional prac-tices and beliefs, and any religious prescriptions.The relative importance of these foods is thestarting point for many of the published pyra-mid-shape food guides (Figure 1.1).

The basis of the diet for most people is a corefood, referred to as the ‘staple’, around whichthe majority of meals are constructed. Withoutthe staple, a meal would not be perceived as ameal. There are usually only a very few core

Activity 1.2

■ What effect would you expect this article to haveif it were published in the national newspapers?

■ What alternative explanations for the findingsmight there be?

■ Why might an article like this be nutritionallydangerous?

Try to find some articles in newspapers or magazinesthat you feel are misleading and potentially harmful.■ Attempt to identify what it is about the articles

that concerns you.■ Try to think of an explanation for the way the

article has been written.

Doctors at the University of Nirvana have made arevolutionary new discovery, which will changethe life of literally millions of people. Volunteers in their laboratories have been eating only threedifferent foods a day and have lost an astonish-ing 30 lbs in a month!

The secret of their success is eating just onefood at each meal. It doesn’t matter what foodyou eat, but it must never be eaten with any-thing else. So, if you feel like ice cream for break-fast, chocolate for lunch and a steak for dinner –go ahead, the weight will still fall off and youwill emerge a slimmer, fitter person.

Doctors claim that anyone can get the sameresults, as long as they stick to the diet regime of

only one food at each meal. They explain that thebody needs other foods to help the digestionprocess. When we eat only one food at a time, foodbreakdown stops, and so the calories can’t pile on!

Results like this have never been obtainedbefore, and it is likely that the whole country willbecome ‘One Food a Meal’ crazy.

The scientists do offer a word of caution, how-ever. The weight loss is so astonishing that youshould not need to stay on the diet for more than 4 weeks at a time. It may be dangerous if you con-tinue on it for longer than this.

You read the following article in your local paper:

Amazing Weight Loss Breakthrough!!

HOW IS INFORMATION ABOUT PEOPLE’S DIETS COLLECTED? ❚

7

Figure 1.1 A pyramid represents the contents of the diet and can be used as the basis of a food guide.

foods in any one culture, sometimes only one.They are generally cereals, or roots and tubers.

Secondary foods are also eaten; theseenhance the meal, but are not an essential part ofit. They may be endowed with specific propertiesof their own; for example they may promotestrength (protein-rich foods, such as meat) orgood health (fruit and vegetables), or they maymaintain bodily forces in balance (‘hot’ and ‘cold’foods as in some Eastern cultures). In addition,some secondary foods may be important at par-ticular life stages.

The third category of foods are peripheralfoods. These are non-essential, but pleasant to eat.Examples include biscuits, cakes, confectionery,preserves, sauces, puddings and alcoholic bever-ages. They may also include flavourings andseasonings.

Thus, despite the huge diversity of foodseaten around the world, it is possible to identifycommon patterns in the foods that people eat.In general, a greater part of the diet comes from

the staple in the poorer parts of the world, andthe peripheral foods make an excessively largecontribution in richer countries. Clearly, thecore and secondary foods in any national orcultural diet must supply the essential nutrientsin appropriate amounts to sustain life and pro-mote health. Some diets appear to achieve thisbetter than others, as is shown by the fact thatmortality rates from diseases that can be attrib-uted to diet are lower in some countries of theworld than in others.

How is information about people’s dietscollected?

To permit any exploration of the role of food inthe health and welfare of the whole individual,rather than its biochemical effect at the systemor cellular level, it is necessary to investigatewhat people eat. It is relatively straightforwardfor individuals to think about their own food


8

intake, and to keep some sort of diary of whatthey have eaten. Most people can identify foodsthat they like or dislike, that they eat often orrarely. However, not everyone possesses enoughinterest in or knowledge about their own foodintake to keep a detailed record over a period oftime and, for most people, keeping a food recordwill be quite difficult.

Many of us would also be able to make somestatements about the food intake of members ofour family, or close friends. However, this infor-mation would inevitably be less detailed than ourown, as we can rarely know about absolutelyeverything someone else has eaten. For a nutritionist, trying to find out what people eatposes a number of problems and requires variedapproaches.

Population and household information

Information about the diet of a population canbe obtained either in a very general way or withprogressively more detailed techniques. In manycountries, data are collected together in ‘foodbalance sheets’, which estimate the amount offood moving into and leaving a country, inmuch the same way as monetary transactions ona financial balance sheet. This can provide anoverview of the theoretical availability of foodin a country. Such statistics are collated andpublished by the United Nations’ Food andAgriculture Organization (FAO) for most coun-tries of the world, and are used to provide anoverview of food availability.

In Europe, several Household Budget Surveysexist, each providing valuable data about dietaryintakes in the specific country. The DAFNE (DataFood Networking) initiative is a collaborativeeffort across Europe to develop a bank of regu-larly updated and comparable data in order toassess and monitor trends in dietary patterns.

In the UK, data have been collected by theHousehold Food Consumption and ExpenditureSurvey, in particular, the National Food Survey(produced annually by the Ministry of Agri-culture, Fisheries and Food) since 1940. This has provided a continuous surveillance of thefood coming into households for consumption,together with money spent on food according to

household composition, economic status andgeographical location. In 1994, the Survey startedto collect data about food eaten outside thehome, a reflection of the growing importance ofeating out. The National Food Survey in this formended in March 2001, and has been replaced by a new Expenditure and Food Survey (EFS),which will be published by DEFRA (Departmentfor Environment, Food and Rural Affairs).Information about food consumption, nutrientintakes and food expenditure will, therefore, con-tinue to be collected and published.

A study of this nature, however, cannot tellus the intake of an individual, as all of the dataare collected with the household as the unit,without any indication of food distributionwithin. More information is required on fooddistribution patterns within households. The EFSwill continue to publish information at the levelof the household, although individual memberswill keep their own diaries. It is hoped that thiswill reduce the incidence of underreporting andincrease accuracy.

The use of supermarket till receipts collectedover 4 weeks, together with 4-day individualdiaries has been used to assess patterns of fatand energy intake and has been shown useful.The involvement of supermarket checkout datato obtain information about population dietarypatterns has potential in dietary surveys. Novelways to collect data continue to be developed.

Individual information

Information on dietary intake of individuals isusually obtained by asking subjects to keep arecord of everything they have eaten over aperiod of time. The level of precision with whichthis is carried out and the duration of the studyhave been subject to debate. In general, the moreexact the method of measurement tries to be, theless it is likely to reflect the normal, freely cho-sen diet of the subject.

The exact method used will be determined bythe aims of the study. Decisions have to be takenby the researcher to determine the reliability andvalidity of the methods used. In other words, ifthe method chosen provides results that can bereproduced on a subsequent occasion, it has a

HOW IS INFORMATION ABOUT PEOPLE’S DIETS COLLECTED? ❚

9

reasonable degree of reliability. A second moredifficult question to answer relates to the valid-ity of the information, i.e. how well it measuresthe subject’s intake. Since food and, therefore,nutrient intakes are not constant from day today for the majority of people, an average intakeover a period of time would reflect ‘habitual’intakes. The duration over which food intake hasto be recorded to obtain a valid measure ofhabitual intake has been studied and shown tovary for different nutrients. Ultimately, the deci-sion on how long a recording period should bedepends on the nutrients to be analysed. Forexample, for energy and macronutrient intake,Black (2001) reports that a 7-day intake recordwill provide a result within 15–20 per cent of thetrue level of intake. For micronutrients, the vari-ability is up to 30–40 per cent for those that arewidely distributed in foods, and very large forvitamins, such as A and C, which occur in largeamounts in fewer foods. Some of the methodsused are discussed below.

The weighed inventoryThis is considered to be the ‘gold standard’ ofdietary intake studies. In this method, all the foodeaten by the subject during a period, usually 1 week, is weighed and recorded, together withany plate waste. Actual nutrient intakes are thencalculated, using data from food compositiontables applicable to the particular country (in theUK McCance and Widdowson’s tables, publishedby the Royal Society of Chemistry, are the mostwidely used – see Food Standards Agency,2002b). The major drawback of the method isthat it requires a considerable degree of motiva-tion and cooperation on the part of the subject. Itis quite an intrusive method, which takes time atmeals and may thus deter a busy person.

Most subjects tend to underrecord theirhabitual food intake, possibly because theyactually eat less during the study period, or forget/omit to record some of the foods eaten.This seems to be a particular problem in thosewho are trying to restrain their food intake insome way. Snack foods are often omitted, per-haps because of inconvenience or forgetfulness.Recent work has shown that the fat and carbo-hydrate intakes are underreported to a greater

extent than protein intakes. Food choice mayalso be altered to facilitate weighing.

Food diariesIn this technique, the food eaten is simplyrecorded in a notebook, without being weighed.Comprehensive instructions are provided to thesubject to explain the procedure. Cooking meth-ods, brand names and recipes are requested. The respondent is asked to provide an estimate ofthe portion size using household measures, e.g.spoons, cups, units, slices or recording packetweights. The researcher then has the task ofquantifying portions eaten. Food models or pic-tures may help in the quantification of portionsizes. A number of photographic atlases of foodportions have been developed and validated inrecent years. Other visual images, including thosegenerated by computer may be used in the future,but would also need to be validated. Tables ofaverage portion sizes are available in the UK,based on measurements of typical portions (FoodStandards Agency (FSA), 2002a). Database infor-mation is available for a large number of typicalservings of foods, although they remain only anestimate for each particular subject. A large data-base, known as DINER (Data Into Nutrients forEpidemiological Research) has been developed aspart of the EPIC study, which contains informa-tion on over 7000 foods and portion sizes. The food diary method requires that the subject isliterate and physically able to write. Alternativeways of recording the size of portion eaten includephotographing the meal, and the use of comput-erized scales with an associated tape-recorder, forexample, the PETRA (Portable Electronic TapeRecording Automated) Scales system, which canboth weigh and store a description of the meal. Inboth cases, however, the data still require inter-pretation and collation by the researcher.

The diary method remains subject to possi-ble changes in the diet by the respondent andfailure to record all foods eaten. However, ifrespondents are adequately instructed, reason-ably comprehensive records can be obtained.Generally, women produce more reliable recordsby this method than men.

A record of foods eaten with no attempt toassess the quantity (a menu record) is a further


10

modification of this approach. Average servingscan be used by the researcher and, although theaccuracy of individual intake calculation isreduced, this method can provide an overviewof dietary patterns.

A simpler and more straightforward approachused increasingly is to compile a food intakerecord based on food groups, such as those in theBalance of Good Health (FSA, 2001a). This allowsan overall profile of the diet to be obtained andthe balance to be assessed against a standarddesirable pattern.

Food frequency questionnairesThese provide a means of studying intake retro-spectively. The use of questionnaires is an inex-pensive technique: it can be self-administered bylarge numbers of people and requires only a shortperiod of time. This tool is often used in epidemi-ological research. It has the advantage that cur-rent diets are not altered. Analysis of the data canbe done rapidly using a computerized scoringsystem. Disadvantages are that the results areculture-specific and a different group may requirea new questionnaire. Additionally, individualswith unusual diets within the study group maynot fit the predetermined criteria for coding.Even for people with a relatively consistentdietary pattern, it can be quite a complicated taskto convert information about a habitual foodintake into a frequency over a week, for specificfoods. This is complicated further by trying toassess portion sizes of these foods. This type ofquestionnaire often looks at a subset of foodsproviding specific nutrients, rather than at thewhole diet, and is generally tailored to the aimsof a particular study.

In general, questionnaires can give usefulinformation, which may be used to rank indi-viduals within groups into subsets according tointake, rather than to provide precise data onactual intakes.

The diet interviewThis technique is widely used by dietitians toobtain a general picture of a person’s food intake.It requires a skilled interviewer to elicit an accu-rate picture of a person’s diet history. The timeframe is usually 7 days. This can be sufficient topinpoint potential excesses or deficiencies. The

interview may be more or less detailed, depend-ing on the type of information required and itspurpose. It usually consists of questions aboutthe daily eating pattern, along the lines of ‘Whatdo you usually have for breakfast, mid-morning,lunch, etc.?’ It then aims to draw a more precisepicture by focusing on the current (or previous)day’s intake, by asking ‘What did you have forbreakfast, mid-morning, lunch, etc. today, oryesterday?’ Many people have little awareness ofwhat they eat, so that it may be quite difficult for them to remember even the previous day’sfood intake. An estimation of portion sizes mayalso be made, often with the help of food models.A checklist of foods may be used to remind subjects about foods that they do eat, but forgotto mention.

Some of the limitations of a diet history arethat it requires both a skilled interviewer and asubject with a reasonable memory. For the latterreason, it is unlikely to be suitable for childrenand for anyone with a failing memory. It alsodepends on the subject having a recognizeddietary pattern, and a ‘usual intake’. In addition,it is time consuming both to complete the inter-view and to carry out any subsequent analysisof the data collected. Hand-held computers withdietary analysis packages can simplify theprocess, allowing information from the subjectto be entered directly.

A dietary recall interview can be simplified tofocus just on the previous 24 hours and obtain a‘snapshot’ of a typical intake. This can be doneby telephone and need not take more than 15–20minutes. However, bias is introduced as the daychosen may be atypical. It is also likely that foodportion sizes are inaccurate, and the complete-ness of the record is memory dependent.

Practical issues in dietary survey methodsThe way in which food is perceived by the sub-ject may affect what is recorded. This mightinclude perceptions of what their culture groupbelieves they ‘should’ be eating as well as whatthe interviewer might expect.

Interaction at a subtle level between aninterviewer and subject in the diet history interview may produce varying results whendifferent people carry out the interview with thesame subject.

STUDIES OF NUTRITIONAL STATUS ❚

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Obtaining dietary intake information fromchildren and adolescents poses particular chal-lenges. With young children, below the age of 8 years, the limiting factors are likely to beknowledge of the names of foods as well as lim-ited attention span and memory. The use of asurrogate reporter may introduce bias. As chil-dren become older, the ability to record the foodintake increases, but at the same time there maybe a greater desire to ‘please’ the interviewer andaccuracy of records may be low. There are noeasy solutions to collecting dietary intake datain these age groups, and new or refined surveymethods are needed. Some of the problemsfound in this group include underreporting andnon-response, which are also discussed below.

In the last few years, there has been recogni-tion among nutritionists that much of thedietary intake data that are collected contain anelement of underreporting. This is confirmed bycomparison of energy intake with calculated ormeasured energy expenditure in many differentgroups. Measurements of energy expenditureusing the doubly labelled water technique areavailable in some research settings. Biomarkerssuch as urinary nitrogen levels can also be usedto confirm the accuracy of food intake records,although these increase the intrusion of themethod, and could reduce compliance.

General findings, for example, based on stud-ies of 77 groups (reported by Black, 2001) show aratio of energy intake to energy expenditure of0.83 (when a ratio of 1.0 would be expected). Inaddition, there is variability between subjects inthe extent of misreporting. For 29 per cent of thegroups studied, results for energy were within 10 per cent of those for expenditure. In 69 percent of the groups, energy intake figures weremore than 10 per cent below energy expenditure.Only in 2 per cent of the groups were the intakeresults more than 10 per cent greater than theexpenditure results.

In summary, food intakes are usually under-reported. This has implications for the calcula-tion of energy intakes, but also nutrient intakes.If nutrient intakes are expressed in relation tothe total energy intake, a measure of the nutrientdensity of the diet can be obtained, expressed as the weight of nutrient/MJ or 1000 Calories.This can then be used for comparison between

individuals, even if underreporting has occurred.These findings raise concerns about the accuracyof dietary intake studies, and underline the need for new methods to be developed that canmore accurately capture information about indi-vidual intakes. Alternatively, more precise tech-niques for validating the intake records areneeded.

Studies of nutritionalstatus

These include measurements of:■ anthropometric indicators■ biochemical indicators■ clinical indicators.

Anthropometric indicators

Anthropometric (literally ‘measuring man’) indi-cators are basic measurements of the humanbody. By relating these to standards typical of the test population, any deviations indicate

1 With a partner, try out a diet history interviewon one another.a Go through all of the times in the previous

day when your partner might have eatensomething, and ask him/her questionsabout it.

b Try to find out how much of everythingthey ate, how it was prepared, what brandname they had.

c Did they eat all of it, or were there any left-overs?

2 Reflect on how easily you managed to com-plete this activity.a Did you and your partner have a pattern of

eating?b How easy was it to assess amounts of food

eaten?c Did you have the same ideas about what was

a small/medium/large serving of a food?d Could you remember everything you had

to eat 2 days ago, 3 days ago, etc.? How farback would your memory of your diet bereliable?

Activity 1.3


12

abnormal nutritional status. Measurements com-monly used are height and weight; these can beused to calculate the body mass index (BMI):

BMI (or�

Weight (in kilograms)Quetelet’s index) [height (in metres)]2

The desirable range for BMI is given as 20–25,with values above 30 being associated withobesity. Similarly, values below 18 are indica-tive of undernutrition.

In children, height and weight results can becompared with standard growth curves (seeChapter 12), which indicate the rate of physicaldevelopment of a child, particularly when asequence of measurements is made. In addition,head and chest circumference measures can alsobe useful in children to indicate rates of growthof the brain and body.

Skinfold thickness measurements at mid-triceps, mid-biceps, subscapular and supra-iliacsites using Harpenden or similar callipers give asurprisingly accurate value for body fat, whenused by a skilled person. Figure 1.2 shows thesites for skinfold measurements.

Arm muscle circumference can be calculatedby subtracting the thickness of the fatfold froma mid-arm circumference measurement. Thiscan indicate muscle development or wasting,and can be a useful indicator in clinical situations

of change in muscle mass, for example, duringillness and rehabilitation.

Waist: hip ratio is increasingly used as anindicator of body fat distribution: the circumfer-ence of the waist at the umbilicus and of the hipsaround the fattest part of the buttocks are usedto calculate this ratio. A nomogram may beused, or a simple calculation performed to obtainthe ratio. Values above 0.8 in women and 0.9 inmen are indicative of a tendency for central fatdeposition, and a possible increased health risk.Waist measurements alone have been shown tocorrelate well with body fatness, and may beused in future as a quick indicator of risk fromoverweight. Other ratios, such as waist to height,have also been suggested to be equally useful, asthey tend to be ‘unisex’ and, therefore, a singlefigure can be used as a cut-off point.

Demispan is a measurement of skeletal size,which can be used as an alternative to heightmeasurement, where it is difficult to obtain anupright posture in a subject. Demispan is thedistance between the sternal notch and the rootsof the middle and third fingers with the armstretched out at shoulder height to the side ofthe body. It is particularly useful in elderly peo-ple, in whom height might have been lost due tovertebral collapse. The demispan value can thenbe used to produce two alternative indices

Figure 1.2 Measurement of skinfold for assessment of body fat content. (a) The four commonest sites used aresubscapular, supra-iliac, mid-biceps and mid-triceps. Measurements from all four sites are added together for usein formulae to obtain fat mass. (b) For mid-triceps measurement the mid-point of the upper arm is found. (c) Thecallipers in use. The skinfold is taken lengthways along the arm, grasped firmly between thumb and forefinger,avoiding underlying muscle. The callipers are applied about 1 cm below the operator’s fingers and the fold is heldthroughout the measurement. Three measurements are made and the results averaged.

STUDIES OF NUTRITIONAL STATUS ❚

13

Figure 1.3 Summary of the mainmethods of anthropometry.

which show good agreement with BMI. These are demiquet, which uses weight/demispan2 andmindex which is weight/demispan. The methodsof anthropometry are summarized in Figure 1.3.

Biochemical indicators

Biochemical indicators can include assessmentof blood and urine samples for levels of a vari-ety of nutrients and/or their byproducts or forlevels of nutrient-linked enzyme activities. Inaddition, analysis may be performed on samplesof hair or bone marrow.

Blood (plasma, cells or serum) can provide agreat deal of information. Analysis can be usedto determine:■ actual levels of a nutrient in relation to

expected levels (e.g. vitamin B12, folate,carotenes, vitamin C in white blood cells);

■ the activity of a nutrient-dependent enzyme(e.g. transketolase for thiamine);

■ the activity of a nutrient-related enzyme(e.g. alkaline phosphatase for vitamin D);

■ the rate of a nutrient-dependent reaction(e.g. clotting time for vitamin K);

■ the presence of a nutrient carrier or its satu-ration level (e.g. retinol-binding protein,transferrin (iron)); or

■ levels of nutrient-related products (e.g.lipoprotein levels).Urine samples may be used to monitor the

baseline excretion of a water-soluble nutrient orto follow its excretion after a loading dose.Metabolites of nutrients also appear in the urineand their levels can be monitored. Twenty-four-hour urine collections can be assayed for creati-nine to indicate muscle turnover rates or fornitrogen content to check protein intakes.

Analyses of bone include bone marrowbiopsies, which will show the blood-formingcells, and radiographic examination, which candetect stages of bone development or rare-faction in ageing. Bone densitometry can pro-vide an essential measure of the density of theskeleton.

It is also possible to measure the levels of some trace elements in the hair, although the scientific accuracy of these assays is not proven and, therefore, they should not be reliedupon.


14

A large amount of research is currentlydirected at finding new and sensitive biomarkersfor the activity of nutrients in the body.Developments in molecular biology have openedup possibilities of assessments at gene level toprovide much more precise indicators of whatrole the nutrient is fulfilling and at what levels itneeds to be present. A major challenge is totranslate in vitro findings from laboratory stud-ies to meaningful measures of nutritional statusin humans.

Clinical indicators

Clinical indicators are used to detect changes inthe external appearance of the body. A numberof nutritional deficiencies may cause alterationsin superficial structures, although many arenon-specific. In addition, changes in appearancemay also be unrelated to nutritional state. Signsoccur most rapidly in those parts of the bodywhere cell turnover is frequent, such as hair, skin and digestive tract (including mouth andtongue). Therefore, a clinical examination mayinclude the hair, face, eyes, mouth, tongue, teeth,gums, glands (such as the thyroid), skin andnails, subcutaneous tissues (to detect fat thick-ness, oedema), and the musculoskeletal system(to note bone deformities, ability to walk, musclewasting). Some internal organs, like the liver,may be felt to note any enlargement. Reflex testsmay be performed to test nerve pathways andmuscle function. A trained observer will be ableto detect many changes in appearance; gener-ally, these are followed up with more specifictests of nutritional status.

What can we learn fromnutritional assessment?

The techniques described above can be combinedto obtain a more detailed picture of the dietaryintake and nutritional status of a population.Food intake at the household level has beenmonitored in the UK for over 50 years in theNational Food Survey produced by the Ministryof Agriculture, Fisheries and Food (MAFF).However, this does not collect information abouthealth. In the mid-1980s a new approach was

adopted in the UK, with the introduction of aseries of studies organized by the Department ofHealth and MAFF. The first of these was theDietary and Nutritional Survey of British Adults(commissioned in 1986-87, published as Gregoryet al., 1990). This collected information aboutfood intake using 7-day records, together withblood and urine analyses, anthropometry andlifestyle features. The Health Survey for Englandwas set up in 1991 to monitor trends in thenation’s health, using a health and socio-economic questionnaire, physical measurementsand blood analysis. This is now running continu-ously and provides an ongoing picture thatincludes key nutrition-related health indicators.

The National Diet and Nutrition Survey(NDNS) is a cyclical programme, which collectsdietary information from surveys of the differentage groups in the UK. In this way each subsec-tion of the population should be re-studied every 8 years. Surveys have been published of pre-school children, older people over 65 years, the4–18 age group; a new survey of adults is due for publication. Other groups, such as vegetarians, people living on a low income and pregnant women are likely to be studied.Monitoring of people’s diet is an essential part ofthe work of the Food Standards Agency, set upin 2000 in the UK. This now has responsibilityfor commissioning surveys of nutritional intake,as part of its Nutrition Strategy Framework(FSA, 2001b).

Diet is dynamic and, for this reason, ongo-ing programmes of study and surveillance arenecessary, to monitor both what people are eat-ing and the effects of any dietary changes onthe patterns of disease.

The NDNS programme aims to:■ provide detailed quantitative information

about intakes and sources of nutrients, andthe nutritional status of the population;

■ measure blood and other indices that give evi-dence of nutritional status, and relate these todietary, physiological and social data;

■ monitor the diet for its nutritional adequacy;■ monitor the extent to which dietary targets

are being met.In Scotland, both the Scottish Heart Study,

which included over 10 000 subjects aged 40–59,

HOW IS THE INFORMATION GOING TO BE USED? ❚

15

and one part of the European MONICA projecthave provided more specific information aboutthe Scottish diet.

Other countries approach the monitoring of nutrition in similar ways. In the USA, theNational Health and Nutritional ExaminationSurvey (NHANES) collects data about foodintakes, anthropometric indices, blood pressureand blood levels of minerals and vitamins.Surveillance of the diets of populations occursin Australia, Canada and several Europeancountries. Cross-population studies are also per-formed; the SENECA (Survey in Europe onNutrition and the Elderly, a Concerted Action)study is one such example.

How is the informationgoing to be used?

The declared purpose of any nutritional surveil-lance programme is to identify links betweendiet and disease, and thereby to formulate pol-icy and advice aimed at minimizing the risk ofdisease, by altering the diet.

All countries have food policies that relate tothe provision of a safe food supply, and thatincorporate a wide range of measures relating toproduction, taxation, trade, politics and socialand consumer issues. In some cases these mayrun counter to health policies, for example, bythe promotion of fats, dairy produce and meat.These policies may also concentrate on legisla-tion about pesticide residues, additives or foodprocessing. Incorporating a nutrition policy into a food policy is, however, more problematicas there may be conflicting interests betweenfood producers and the health professionals.Where nutrition is supported at governmentlevel, it is necessary for the government to facili-tate the nutrition policy by changes to legisla-tion, taxation, food labelling or other measures.Without such changes, a nutrition policy mightnot be workable. It is, therefore, important thatgovernment policy-making is informed bygood-quality nutrition surveillance information,and that appropriate policy decisions are made.

The UK Food Standards Agency works withthe Department of Health to improve the healthof the UK population through encouraging and

facilitating the adoption of a healthy balanceddiet. The FSA has put forward its plans in theNutrition Strategic Framework to enable it toachieve the following objectives.■ Secure a sound evidence base for action to

promote a healthy diet.■ Develop appropriate means of informing the

general public.■ Identify and address barriers to changing

dietary behaviour.■ Evaluate and monitor the effectiveness of

the action taken.In order to achieve these objectives, the

FSA is working with many other key players,including the Scientific Advisory Committee onNutrition (SACN), which has replaced Committeeon Medical Aspects of Food Policy (COMA), gov-ernment departments including Health andEducation, the food industry and the scientificcommunity. Their work will build on many ofthe goals already achieved since the publicationof ‘The health of the nation’ white paper, whichset out specific health goals for England to beachieved within a decade (DoH, 1992). Theserelated to heart disease and stroke, accidents,mental health, sexual health and cancer. ANutrition Task Force (NTF) was set up to discussways in which the targets relating to nutritioncould be achieved, using all the parties involvedin the food chain to form ‘healthy alliances’.

One of the major aims of the NTF was to pro-duce a simple and easy to understand NationalFood Guide to provide a basic tool for teachingthe elements of a balanced healthy diet. This wasto be available to all educators, at whatever level,so that a consistent message was given from allsides. The National Food Guide (the Balance ofGood Health) was developed, tested and eventu-ally launched in 1994 (HEA, 1994). This is stillused in the UK and has recently been reissued bythe FSA as the Balance of Good Health; it is discussed more fully in Chapter 3. The NTF set in train a great number of initiatives and, as aconsequence, nutritional issues are now muchmore to the fore in the national health agenda.The FSA now has the responsibility for takingthese forward into the first decade of the twenty-first century. There is more information aboutfood policy in Chapter 18.


16

References and further reading

Bassey, E.J. 1986: Short report: demispan as a measure of skeletal size. Annals of Human Biology13(5), 499–502.

Beaglehole, R., Bonita, R., Kjellstrom, T. 1993: Basic epidemiology. Geneva: WHO.Beghin, I., Cap, M., Dujardin, B. 1988: A guide to nutritional assessment. Geneva: WHO.Bingham, S.A., Gill, C., Welch, A. et al. 1994: Comparison of dietary assessment methods in nutritional

epidemiology: weighed records v. 24hr. recalls, food-frequency questionnaires and estimated-dietrecords. British Journal of Nutrition 72, 619–43.

Bingham, S.A., Welch, A.A. McTaggart, A. et al. 2001: Nutritional methods in the European ProspectiveInvestigation of Cancer in Norfolk. Public Health Nutrition 4(3), 847–58.

Black, A.E. 2001: Dietary assessment for sports dietetics. British Nutrition Foundation NutritionBulletin 26, 29–42.

Cade, J., Thompson, R., Burley, V. et al. 2002: Development, validation and utilisation of food-frequency questionnaires – a review. Public Health Nutrition 5(4), 567–87.

Colhoun, H., Prescott-Clarke, P. (eds) 1996: Health survey for England 1994. London: HMSO.DoH (UK Department of Health) 1992: The health of the nation. A strategy for health in England.

London: HMSO.

1 Nutrition is a very broad discipline. It may be of interest to people from a variety of backgrounds, whocan also make useful contributions to its knowledge base.

2 There has been a huge increase in interest in nutrition in the last decade and people want to be betterinformed.

3 To be informed about nutrition, it is necessary to know what people eat and how his can be measured.The advantages and disadvantages of these methods are important to consider.

4 The dietary information must be supplemented by information about health. Both of these needcontinual updating, as neither remains static.

5 This information is used in making policy decisions about dietary advice to improve health.

SUMMARY

1 Which methods of obtaining information aboutfood intakes would you use in each of thefollowing examples, and for what reason:a A study to identify groups in a population

who have a high, or low, intake of dietaryfibre (non-starch polysaccharide; NSP).

b An investigation into iron intakes in a groupof children who do not eat meat.

c A comparison of food intakes between twopopulations who have different diseasepatterns.

d A pregnant woman who needs advice abouther diet.

2 Discuss with a colleague the benefits anddisadvantages of adding specific nutrients to

manufactured foods. Do you think this practice would help or hinder the work of anutritionist?

3 What factors, apart from nutrition, might play arole in the health of a population? How couldthese be taken into account in results ofnutritional assessment?

4 Perform a small survey among youracquaintances and friends to discover:a what they understand by the term nutrition;b how relevant to their health and well-being

they consider their food intake to be;c if they would consider changing their diet to

improve their health.Draw some conclusions from your findings.

STUDY QUESTIONS

REFERENCES AND FURTHER READING ❚

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Food Standards Agency 2001a: The balance of good health. London: FSA.Food Standards Agency 2001b: Your food – farm to fork. London: FSA.Food Standards Agency 2002a: Food portion sizes, 3rd edn. London: The Stationery Office.Food Standards Agency 2002b: McCance and Widdowson’s the composition of foods, 6th summary

edn. Cambridge: The Royal Society of Chemistry.Gregory, J., Foster, K., Tyler, H. et al. 1990: The dietary and nutritional survey of British adults.

London: HMSO.HEA (Health Education Authority) 1994: Introducing the National Food Guide: The balance of good

health. Information for educators and communicators. London: Health Education Authority.Livingstone, M.B.E., Prentice, A.M., Strain, J.J. et al. 1990: Accuracy of weighed dietary records in

studies of diet and health. British Medical Journal 300, 708–12.Livingstone, M.B.E., Robson, P.J. 2000: Measurement of dietary intake in children. Proceedings of

the Nutrition Society 59, 279–93.Margetts, B.M. Nelson, M. 1997: Design concepts in nutritional epidemiology, 2nd edn. Oxford:

Oxford University Press.Nelson, M., Haraldsdottir, J. 1998: Food photographs: practical guidelines II. Development and use

of photographic atlases for assessing food portion size. Public Health Nutrition 1(4), 231–8.Ransley, J.K., Donnelly, J.K., Khara, T.N. et al. 2001: The use of supermarket till receipts to determine

the fat and energy intake in a UK population. Public Health Nutrition 4(6), 1279–86.Trichopoulou, A., Naska, A. (eds) 2001: The DAFNE initiative. Assessment of dietary patterns across

Europe using household budget survey data. Public Health Nutrition 4 (5B).Welch, A.A., McTaggart, A., Mulligan, A.A. et al. 2001: DINER (Data Into Nutrients for Epidemiological

Research) – a new data-entry program for nutritional analysis in the EPIC-Norfolk cohort and the7-day diary method. Public Health Nutrition 4(6), 1253–65.

Basics of a healthy diet

18

what are the influenceson eating habits?


❏ discuss the reasons for eating and possible mechanisms controlling eating;❏ describe food habits;❏ explore the factors influencing food choice, the interactions between them and how they change;❏ help the reader understand how their own food habits are determined.


❏ describe the physiological and metabolic signals that determine food intake;❏ discuss how social and cultural influences play a part in modifying basic physiological mechanisms;❏ analyse your own food habits, and show how these have developed and are influenced currently;❏ recognize the importance of individuals’ particular food habits and appreciate how these may be resistant

to change.

Most people, if asked why they eat, would respondwith ‘to stay alive’ or ‘because of hunger’. Bothof these are appropriate answers: the body has aphysiological need for food and, when deprivedfor even a short period of time, a sensation of

hunger is experienced. This is a normal physio-logical response, which is designed to balancethe output and storage of nutrients with theirinput from food.

In addition, however, people eat for a num-ber of other reasons. In the West, eating is amatter of habit because food is usually widelyavailable, often at all hours of day or night.There are also socially accepted ‘mealtimes’,when there is an expectation of eating, regard-less of hunger, and there are social norms asso-ciated with eating, which define what behaviouris and is not acceptable.

Food provides us with sensory satisfaction,it is (usually) pleasant to eat, and this aspect ofcertain foods can induce people to eat whenthey have no physiological need to do so.

We have a very personal relationship withfood. It is something we deliberately take intoour body and which becomes part of us. Thiscan have very profound meanings for somepeople, but for everyone it implies that there arepsychological influences on eating.

Before studying this chapter, spend a little timethinking about:■ why you eat;■ what you eat;■ what are some of the reasons for choosing the

particular foods.You may find that this is a surprisingly difficulttask. We are generally quite unconscious of ourreasons for eating and choosing particular foods.Only when we have a basic framework withwhich to study these influences can we begin to gain insight into our own behaviour related to food.

Activity 2.1

2C H A P T E R

REASONS FOR EATING ❚

19

Each of these influences on eating will bediscussed in turn, to demonstrate that evensomething as basic as supplying the body withthe energy for its survival can involve morethan an understanding of physiology.

Reasons for eating

Physiological need

Signals relating to all of the processes involved inthe initiation and cessation of eating are inte-grated and organized by the brain. These control-ling mechanisms have been studied mainly in

experimental animals. This is because humansare more complicated, with many cultural andsocial conventions, which influence food intake,and which can override the physiological mech-anisms. A schematic diagram of the various com-ponents of the control mechanism integrated bythe brain is given in Figure 2.1.

In an individual whose weight remains con-stant, there is evidently a balance between theinput of food and its metabolism and energy output. Consideration of the various stages of theprocess helps to identify where control mech-anisms could be operating.

Figure 2.1 Physiological factors controlling hunger and food intake.

❚ WHAT ARE THE INFLUENCES ON EATING HABITS?

20

Sensory signalsThe sight, smell or even thought of food triggersthe cephalic phase of appetite, which stimulateshunger and prepares the digestive tract for theingestion of food by secretion of saliva and gas-tric juices. When eating starts, the food stimu-lates the senses of taste and touch (via the textureand consistency of the food). Variety in the sens-ory properties of foods offered in a meal can further stimulate eating, whereas a meal thatcontains only one item rapidly leads to satiation.This is the sensation that stops food intake at ameal and is associated with a feeling of fullness.

Pre-absorptive informationIngested food causes gastric distension. This isdetected by stretch receptors, which send sig-nals to the brain. The presence of food and earlydigestion products in the duodenum causes therelease of a large number of gut hormones,some of which have been shown to inhibit foodintake. The most extensively studied of these ischolecystokinin (CCK), which has been shownto produce satiety in many animal species,including humans. CCK is stimulated particu-larly by the presence of protein and fat diges-tion products in the duodenum. The presence ofresidual protein in the stomach at the start of ameal has a restraining effect on food intake, andparticularly on the intake of protein. Newly dis-covered peptides, such as PYY and ghrelin signalto the brain that the stomach is full (Wilding,2002). Satiety is described as the sensation thatdelays the next food intake, thus affecting theinterval between meals.

Ingestion of liquids, even those containingmacronutrients, is less well regulated by thesemechanisms than ingestion of solids.

Post-absorptive signalsAll of the digestion products have been proposedas regulators of food intake. Fluctuations inblood glucose level and, therefore, its availabil-ity to the cells of the nervous system and brain,were originally believed to be the cornerstone offeeding behaviour regulation. Carbohydrate-richmeals suppress further intake for between 1 and3 hours after eating. This may be associated withthe period during which insulin levels are raised

after a meal. This is the glucostatic theory offood intake. However, it cannot satisfactorilyexplain control of eating in all situations.

A further theory, the lipostatic theory, pro-poses a relationship between body fat reservesand eating behaviour, such that an increase instored fat would reduce intake. It is onlyrecently, however, that a mechanism to supportthis has been identified.

Leptin is a relatively recently discovered (in1994) protein, released principally from adiposetissue as well as other tissues. Because it isreleased at one site and acts at a distant site, itfulfils the criteria of a hormone. Amounts pro-duced reflect the size of the fat store in bothhumans and animals. Leptin release from adi-pose tissue is also influenced by levels of feed-ing, such that fasting results in a rapid fall inleptin secretion and levels rise again on refeed-ing. In addition, exposure to cold inhibits leptinrelease. Leptin secretion from adipose tissue isalso influenced by several other hormones.Release is stimulated by insulin, glucocorti-coids, oestrogens and cytokines (released as partof immune reactions). The major inhibitors ofleptin release are adrenaline and noradrenaline,mediated by the sympathetic nervous system.One of the functions of leptin is to act in thehypothalamus, where it causes the release of anumber of neuropeptides, including neuropep-tide Y. This has a potent action to inhibit foodintake. In obese humans and animals, leptinreceptors have a low sensitivity, resulting inpoor recognition of the size of fat stores and,therefore, dysregulation of food intake.

Further regulation of food intake may occurvia the activity of lipoprotein lipase, an enzymefound in adipose tissue.

Amino acid levels also have an effect onfeeding behaviour, with shifts in plasma andbrain concentrations of particular amino acidscausing changes in intake. There is competitionbetween different amino acids for uptake acrossthe blood–brain barrier; consequently, an eleva-tion of one amino acid may inhibit the uptakeof others. The importance of some amino acidslies in their role as precursors for brain neuro-transmitter substances; these may be the effect-ors of changes in feeding behaviour.


21

MetabolismThe blood levels of metabolites are regulated by the liver and peripheral tissues, which removethem from the circulation and may also have aneffect on feeding behaviour.

It is becoming clear that metabolism of theenergy-providing nutrients is regulated with dif-ferent levels of precision. Alcohol, as a potentialtoxin, must be oxidized completely and removedas quickly as possible. Its metabolic regulation isperfect and all alcohol is completely metabolized.

The capacity of the body to store carbo-hydrate and protein is limited, and blood levelsof glucose and amino acids are carefully con-trolled. It is now believed that under normal cir-cumstances very little carbohydrate is actuallyconverted to fat. The conversion of carbohydrateto fat is very inefficient, with approximately 25per cent of the potential energy wasted as heat.Metabolism of both glucose and amino acids isthought to ‘autoregulate’ to match the intakelevel.

Fat metabolism, however, exhibits no such‘autoregulation’, probably because of the largecapacity for fat storage in the body. Therefore, fatmetabolism does not correlate well with fatintake and there is no evidence that fat oxidationadjusts when intake increases. Consequently, onecan conclude that fat intake plays a smaller rolein the control of food intake than do either carbohydrates or proteins. This may provide anexplanation for the ‘fattening’ effects of high-fatdiets, which can be consumed without any con-sequent change to fat oxidation. Also evidencefrom feeding studies of diets where fat contenthas been covertly increased shows that a changein fat levels has no effect on satiety and sub-sequent food intakes. This means that such dietsare easy to consume leading to ‘passive overcon-sumption’, and may be a significant contributoryfactor in obesity.

Integration by the brainEarly research identified hunger and satiety centres in the hypothalamus; these could be artificially stimulated or destroyed, resulting in starvation or overeating. The function of thesecentres was thought to be the maintenance ofadequate levels of energy-providing nutrients in

the blood. The dietary macronutrients, carbo-hydrates, fats and proteins, were the primarycandidates for these regulatory factors. It is nowclear that this is an oversimplified picture. Thebrain receives information from receptors andmetabolites about the whole feeding process,from the initial thought about food to the finalmetabolism of its breakdown products. Changesin plasma concentrations of nutrients resultingfrom metabolism in the liver and peripheral tis-sues are also monitored. A number of these havebeen mentioned in the earlier sections. In particu-lar, leptin levels are believed to be important,through their action on neuropeptide Y, causinginhibition of food intake. Low levels of leptin arethought to cause a number of adaptive changesto minimize weight loss, including increased foodintake. In addition, levels of serotonin, whichpromotes feelings of satiety, are influenced bythe amounts of tryptophan crossing the blood–brain barrier. By these means, food intake andmetabolic processes can be regulated to match thebody’s needs. This complex integration occurs in the brain, probably by appropriate changes inthe levels of neurotransmitters.

In addition, it has been proposed that uncon-scious reflex pathways are established, parti-cularly during childhood, whereby the body‘learns’ the metabolic consequences of particulareating patterns and responds accordingly. If suchreflexes are not established, perhaps due to erraticeating behaviour in childhood, then controlmechanisms remain less efficient. Much remainsto be learned about the complex control of eating.

Habit as an influence on eating behaviour

In parts of the world where food is readily avail-able, intake could occur at any time of day ornight. Most people do not eat continuously, butusually at fairly clearly defined ‘mealtimes’,with ‘snack times’ interspersed between them.This behaviour has become a habit, and manyWesterners believe that they should have threemeals a day together with two or three snacks,with the main meal either in the middle of theday or in the evening (see Figure 2.2). In othersocieties, especially among the poor, fewermeals are eaten, maybe only one or at most two


22

within a day. Therefore, it appears that there is nophysiological need to eat so frequently, althoughit will be necessary to eat to satiation when meal-times are infrequent. If eating is more continu-ous, the sensations of satiety or hunger maynever be experienced. The brain, therefore, lacksthe necessary input to recognize these, whichmay result in poor regulation of eating behaviourat some point in life.

What is the difference between mealsand snacks?

A snack is an eating occasion where just onetype of food is eaten, perhaps accompanied by adrink, and might include biscuits, chocolate orsandwiches, for example. Often this is eaten inan informal setting, or perhaps in the street, orwhile travelling. In the last 20 years, more infor-mal eating has been taking place, as lifestylesbecome more flexible. In some instances, all ofthe food taken during the course of a day may beclassified as ‘snacks’, with perhaps as many asten or more being consumed. This is particularlyprevalent among young people, and causes concern to nutritionists as some of the snackfoods eaten are low in micronutrients, but maycontain substantial amounts of fat and/or sugar.

However, not all snack foods are nutritionallypoor: sandwiches, fruit, nuts and drinks, such asmilk or fruit juice, can provide useful nutrients.

A meal generally contains a selection of dif-ferent separate items, usually eaten with utensils(although in some cultures this is not usual), and takes some time to prepare and to eat.Traditionally, this would be eaten in a designatedeating place, for example, at a table. More flex-ible lifestyles, however, mean that meals now maybe eaten in more informal settings, perhaps froma tray while watching the television, or in thestreet out of the packaging in the case of fish andchips or a burger. Because it includes more items,a meal is more likely to contain a greater numberof nutrients, although there are still meals whichcan be nutritionally very poor.

There needs to be a degree of organization ofmealtimes in a society that operates by the clock.Chaos would ensue if in every office, classroomand business organization people wandered offto eat whenever they felt like it. Some acceptedschedule is essential, both from the consumers’and from the cooks’ point of view. It could beargued that rigorous timing of meals is intro-duced too early in life. Some infants in the firstmonths of life are still fed ‘by the clock’, usually4-hourly. Feeding ‘on demand’ gives the infantthe opportunity to be fed when actually hungry,although it does introduce a level of unpre-dictability into the mother’s life.

Some people eat just because food is avail-able. They are unable to resist the desire to eat,and are apparently less sensitive to their owninternal cues about needing food than to exter-nal signals. Others may deliberately avoid foodor eat in very small amounts, disregarding theirinternal signals and gauging what they eat byexternal cues related to the size of the plate,what other people are having or what they thinkis an appropriate amount for them.

Both of the above types have developed par-ticular habits that control their eating, which areusually more powerful than the physiologicalneed. In the extreme, these can result in dis-ordered eating – both overeating, or bingeing,and compulsive dieting, or perhaps a cyclingbetween these two extremes. These are discussedfurther in Chapter 8.

Figure 2.2 Habit influences eating behaviour.


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Psychological need

Eating is a pleasurable activity, and can satisfysome of our internal needs. Boredom provides amajor incentive to eating and may fill manyempty hours for people. Depression or anxietycan also make people turn to food for comfort.This is believed to stem from the reassurancegiven by food provided by parents to children,linking positive feelings about parental care and love with the food. It is important that the‘food as comfort’ response is not made too fre-quently, as it is likely to result in overweight,often with associated emotional problems (seeFigure 2.3).

We may also offer food to people to comfortthem; for example, a child who has fallen andbeen hurt may be cuddled and then offeredsomething to eat (often a sweet or biscuit). Aftera funeral, people may come together to sharefood. This acts as a comforting gesture for boththose providing the food, as well as those eatingit. If we remember that provision of food is linkedwith loving and caring, it is easy to see howrejection of the food by the intended recipientcan be hurtful and painful. This happens withyoung children who are learning about food, butcan become manipulative and cause their carers

considerable hurt. They may use food rejection toexpress feelings of anger, jealousy or insecurity,or to gain attention. Children who have to followa special diet for health reasons may be particu-larly at risk of this type of behaviour. Using foodas a weapon can become a habit maintained intoadult life. Sometimes this weapon is turnedagainst the self, in situations where food intake ischaotic (see Chapter 8).

Sensory appeal

The way in which a food stimulates our sensesby its appearance and smell, taste and texturemay also increase our desire to eat it. Most people claim that the taste of the food is theprime consideration, although for adolescentsthe appearance also rates highly.

The visual appeal of the food, althoughimportant to attract the eye, can be quite deceptive, however, and gives no indication ofnutritional value. Most sighted people would be very wary of accepting and eating a foodthey could not see. Our expectations of the tasteof a food are prepared by its appearance – weexpect an orange-coloured drink to have asweet, citric taste; anything else might lead torejection. The food industry is well aware of theimportance of the ‘correct’ visual stimulus anduses a range of colorants to produce an accept-able finished appearance. However, the numbersof these are less than they were 10–20 years ago as consumers become more concerned aboutsafety aspects, and are increasingly prepared to buy foods with a more ‘natural’ colour (seeFigure 2.4).

The smell of the food must also meet ourexpectations. We use this to detect if food has‘gone off ’ and we are enticed to eat by pleasantaromas. We can recognize many foods purelyfrom their smell. Smell and taste interact to pro-duce the flavour of the food; if the sense ofsmell is lost; for example, when suffering froma cold, food may seem tasteless. The number oftaste buds is highest in children, who have themon the insides of the cheeks and throat, as wellas over the surface of the tongue. These begin todecrease from adolescence and are considerablyreduced by the age of 70.

Figure 2.3 Psychological need as a trigger to eating.


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Children’s food preferences and choices aredriven primarily by taste. Relative to adults, chil-dren have a preference for very sweet taste, andavoid bitter tastes. The liking for intense sweet-ness declines into adolescence, more so in girlsthan boys. There is also a link between energydensity and sweetness, and this is believed to bea means by which intake of high-energy foods isassured to support growth and development inchildren. Once adulthood is reached, the need forsuch energy-dense foods is reduced, and the lik-ing for intense sweetness tends to disappear. Thetaste acuity for the bitter taste also declines, andadults accept bitter tastes more readily. There isalso a move to less energy-dense foods, whichare often those associated with a healthier diet,with increasing age. Taste perception can changein certain circumstances: pregnant women, sur-gical patients and people with cancer all reportan altered ability to taste certain foods. It hasbeen suggested that zinc status plays a role inthis. Unusual appetites for particular foods mayalso develop. People can become accustomed to aparticular taste if this is perceived to be anadvantage. The bitter tastes found in beer, quin-ine (in tonic water) and coffee appear to be anacquired taste for many people, although somefind them unpleasant all their lives.

The texture and taste of the food in themouth provide us with the pleasurable aspects of

eating. The feel of the food in the mouth caninclude its texture, temperature and even anypain it produces. We expect particular foods to bepresented at a certain temperature (e.g. ice creamor hot tea). Extremes of temperature can causepain to the mouth and teeth. Chilli contains achemical substance (capsacin), which irritates thenerve endings, triggering pain. Some substancescan cause a local anaesthetic effect in the mouth –chewing coca leaves (widespread practice in partsof South America) has this effect; its purpose is todull the hunger sensation among peoples whohave little food.

Food technologists can measure optimal levels of various sensory characteristics (such assugar content, aroma, water content, tempera-ture), which are associated with the highest levelof pleasure. These are aptly named ‘bliss points’.These are not fixed forever and can becomemodified if the diet changes, although the initialalteration to the diet will be associated with areduction in pleasure. For example, an individ-ual who normally takes two spoonfuls of sugarin their tea probably will have that concentra-tion of sugar as their ‘bliss point’. Cutting outsugar will result in a reduction in ‘bliss’. In time,the subject is likely to adapt to the newer taste,the level of ‘bliss’ is restored at a lower sweet-ness, and drinking tea with the original level of sugar will no longer be acceptable. Thissequence will apply to other changes made tothe diet that have sensory implications, includ-ing cutting down fat or salt intakes.

Variety also encourages us to eat. Studies onboth animals and humans have shown clearlythat, when offered a variety of food, total intakeis greater than when just a single food is offered.Thus, it is possible to make rats overweight byoffering them a ‘cafeteria diet’, containing chips,burgers, crisps, chocolate, etc., rather than ordin-ary rat pellets; they eat more of the mixed diet.Humans will also overeat when offered some-thing new; for example, having apparently eatentheir fill of a main course, many people will stillmanage to have a dessert afterwards. It has also been noted that more food is eaten whenmeals are accompanied by wine and taken in asocial setting. These factors occurring togethercan promote an unconscious overconsumption.

Figure 2.4 Sensory appeal as a trigger for eating.

FOOD HABITS ❚

25

Overweight is much less common in commu-nities around the world where only a few foodsappear regularly in the diet – it seems thatmonotony imposes its own limits on eating. Onthe other hand, organizing food into differentcourses, with different flavours, seems toenhance the food intake.

Social influence

Food may also be used in a social context toplease or displease others. Offering food ordrink is recognized as a gesture of hospitality,and refusal may be interpreted as rejection. Thismay extend to the obligation to eat food that isnot wanted or even disliked, to avoid offendingthe giver. This may be a particular problem for visitors to other countries, who may be presented with unknown or even unacceptablefood, yet feel obliged to consume it.

In situations where food is scarce, or budgetsare very restricted, wasting food may be socially

unacceptable, and individuals may feel it neces-sary to eat everything provided. The opposite mayalso apply – waste may be quite acceptable wherefood supplies are plentiful, or where left-overfood can be put to other uses, such as feeding pigsor poultry.

All of these influences and some of theirinterrelationships are summarized in Figure 2.5.

Food habits

So far, we have learned that the primary reasonfor eating is to satisfy our hunger, but that whatand when we eat can also reflect who we are,the society we live in, our upbringing and howwe perceive ourselves. We can define foodhabits as the typical behaviour of a particulargroup of people in relation to food. They provide an important signal of the identity ofthe group. They will determine food choice, aswell as eating times and numbers of meals, sizeof portions, methods of food preparation and

Figure 2.5 Why do we eat?


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who takes part in the meal. Food habits are aproduct of the environmental influences on aculture and, in general, are resistant to change.

Some of the components of an individual’sfood habits are shown in Figure 2.6.

Acquisition of food habits

The acquisition of food habits is largely uncon-scious, since they are acquired at a young agefrom parents, which incidentally ensures trans-mission between generations. The strongestinfluence on a child in its acquisition of foodhabits is generally its mother, who is likely to bethe most closely involved with the provision offood. Children learn what is acceptable as food,and what is not. Foods that are associated withgood times are often preferred to those that donot have these connotations. We may rememberparticularly foods that we ate on holiday andseek these out to help relive happy memories.Children are dependent on the food practicesand beliefs of the adult caregivers; this may

restrict a child’s opportunities to try many foods,if they are not part of the adult’s food choice. Inaddition, some foods may be seen as inappropri-ate for children and, therefore, not offered.

After the initial socialization within thehome environment, children learn more foodpractices from other people, or institutions out-side the home. A major force may be the school,where behaviour is learned from other children,as well as through the food provided in schoolmeals and tuck shops, and more formal teachingabout food in lessons. All of these will broadenthe child’s view of food and will affect the foodpractices.

Later still, other people may influence foodhabits as different views are encountered with awidening social circle. Foreign travel also pro-vides experience of different food habits.

Changing food habits

Although food habits are resistant to change,they are not static. Change may come fromwithin the culture. For example, the increase infemale employment in the West has resulted in adramatic increase in the availability of conveni-ence food. Fewer households now eat meals prepared from basic ingredients on a regularbasis. Weekday meals in particular are composedto a great extent of convenience items, with perhaps the addition of a home-prepared vege-table or starchy staple (such as rice or potato).The prevalence of microwave ovens, togetherwith widespread ownership of freezers, has meantthat meals can be ready in minutes, and that even quite young children can prepare themselves

Using your experience, try to identify which of thefactors given in Figure 2.5 are likely to be mostimportant for the following people:a yourselfb a pre-school-age childc a mother with young childrend a teenage girl/boye an elderly woman, living on her own.Account for your answers.

Activity 2.2

Figure 2.6 Some of the maincomponents of a person’s foodhabits.

FOOD HABITS ❚

27

something hot to eat with little risk of accident.The consequence of this has been that, in manyfamilies, mealtimes are no longer taken together.Instead, individual members of the family mayeat at times convenient to themselves, oftenheating up different meals in the microwave. Inaddition, around 30 per cent of meals eaten arelikely to be consumed away from home, in workor school canteens, cafes, fast-food outlets, restau-rants or in the car. The National Food Survey(Department for Environment, Food and RuralAffairs (DEFRA), 2001) showed that on averagethree meals per week were eaten outside thehome (not from the home food supply), and thisrepresents 30 per cent of the expenditure on food.

Another source of change is the increase in the availability of information about worldcookery. Examples of the cuisine of differentcultures are found in restaurants, supermarketsand as cookery programmes on the television,and the wide availability of many exotic ingre-dients makes it possible for these ‘foreign’ dishesto be included into traditional food habits. Manybooks describe how to prepare these dishes.

The media are also responsible for chan-ging food habits. This may occur through the following.■ Advertising and the promotion of new food

products (although the information givenhere may be biased).

■ Programmes or articles that aim to increasepeople’s knowledge about food, perhaps inthe context of nutrition and health.

■ Providing role models in the form of charac-ters in programmes and advertising. Thesecontribute a subtle force towards change in food habits by the food they eat and theattitudes they express. Some of the messagesput forward are not necessarily conducive tohealth; for example, there is believed to be aprevailing message that only thin womenare healthy and attractive, which causes oftendisastrous changes to food habits among thefemale population.Food habits may have to change when an

individual suffers from an illness requiringdietary alteration for its management. The dif-ficulty of changing food habits is best seen insuch subjects, who often struggle to maintain

dietary changes, even when there are very goodhealth reasons for doing so.

Nutrition educators and health promotersaim to change food habits towards a healthierbalance. This is a very complex process becauseof the multi-faceted influences on food habits.Different influences may be at work in deter-mining what is eaten from day to day or evenfrom meal to meal. A further factor is thestrength of the attitude of the subject towardsfood and healthy eating. If they are ambivalentabout either of these, change may be difficult to bring about. Finally, the subjective recogni-tion that change is needed to the diet is a powerful influence in determining whether it is undertaken.

Therefore, an educator may need to considerthe strength of the subject’s belief:■ that food and healthy eating are important;■ that these can influence their individual

health in a beneficial way;■ that making changes to food and eating has

a high priority amongst factors that influ-ence food choice.Studies have identified many barriers to

making changes towards healthy eating that aremore prevalent amongst those subjects whomake fewer changes. In the study by Margetts et al. (1998), these included:■ a perception that there is a lack of clear

messages about healthy foods;■ a belief that the tastiest foods are the ones

that are ‘bad’;■ confusion about what to eat;■ difficulty of eating healthy food away from

home;■ costs of healthy eating;■ lack of concern about what is eaten.

In addition, changes towards healthier eat-ing are less likely to be found among younger,lower income groups and those who smoke. This emphasizes that dietary change is closelylinked to other lifestyle indicators in complexways.

Food choices

Within the context of a culture’s food habits,each individual makes their own, personal food


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choices, which are likely to be different fromthose of anyone else. There are many ways tostudy individual food choices, and much hasbeen written about them. There are still areas ofuncertainty, however, and research into determin-ants of food choice, especially within familygroups, is ongoing. Viewpoints may be anthro-pological, economic, physiological or adminis-trative, political, psychological or sociological,as well as nutritional. The following is a nutri-tional perspective on food choice.

In very broad terms, people can only choosefrom the range of food available to them; thus,factors that determine food availability areimportant. Given a range of foods, an individualwill not necessarily choose to eat all of them.The choice will depend on what is acceptable tothem, personally. Hence the two main determin-ants of food choice are availability and accept-ability. The main factors influencing these areshown in Tables 2.1 and 2.2.

AvailabilityPhysical/environmental factorsIn the West, this factor is less important now thanit was 20 or more years ago. Food preservation,storage and distribution around world marketsare so efficient that it rarely matters whether the

local area produces a food or not. It can generallybe imported from elsewhere. This creates a uni-formity of foods available, and there is concernthat many interesting varieties of locally pro-duced foods are being lost, or remain availableonly in a speciality market. Differences exist,however, in what food is available to buy in alocality. This will be dependent on factors such aspopulation density and, therefore, the number ofshops in the vicinity, and ease of access, whichwill determine the cost of transporting food intothe area. The perishability of a food will alsodetermine the range over which it can be trans-ported. For these reasons, rural areas in mostcountries generally have a smaller range of foodavailable than urban areas.

However, in places not reached by the worldmarket, where locally grown produce is eaten,physical factors such as type of soil, rainfall or transportation are important determinants ofwhat food is actually available. Perishability offood and the means of preservation availablewill also determine how long food can be kept.Thus, for a subsistence family in a developingcountry, physical factors are extremely import-ant determinants. Their access to the local mar-ket and the range of foods available there willhave a major impact on the food they eat.

Factors influencing the availability of foodsTABLE 2.1Physical/environmental Legislative Economic Food handlingLocality (soil/climate) National/international laws Money Access to shopsTransport/marketing Budget priorities Cooking skillsDistribution costs Health recommendations Cost of foods KnowledgePerishability Significance of foods Cooking facilities

Variety Time available

Factors influencing the acceptability of foodsTABLE 2.2Cultural Physiological Social/psychologicalNational identity Physiological need Status (of self/of foods)Culture group Hunger/satiety Group identityCore, secondary and peripheral foods Appetite/aversion CommunicationMeal patterns Sensory appeal RitualReligious ideology Personal preference/choice Emotional supportTaboos/prohibitions Therapeutic diets Reward/punishment

FOOD HABITS ❚

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Legislative factorsGovernment legislation aims to ensure that foodavailable for purchase is of a suitable quality andhas not been adulterated. There is also agricul-tural policy, which regulates the prices receivedby the producers of crops. Trade agreements and sanctions may operate at particular timesbetween different countries. In addition, the UK,as a member state of the European Union, is sub-ject to Europe-wide laws relating to food andagricultural production. All these factors willinfluence the type of food available for sale inshops and its exact composition, especially interms of additives and minimum standards ofcomposition.

In recent years, the labelling of foods hasbecome more explicit, with more informationabout the nutritional composition appearing onthe label. This is to be applauded as an import-ant means of educating people about nutrition,as well as providing useful information for any-one who wishes to understand more about thefood they eat. European laws on labelling affectproducts marketed in the UK.

Legislation has also been needed to controlthe introduction of some of the new foodsresulting from developments in food technol-ogy. Recent introductions in Britain haveincluded irradiated foods, items produced fromresearch in genetic engineering and foods con-taining synthetic substitutes (e.g. for fat). Inaddition, there is a growing market in ‘func-tional foods’. All have been the subject of safetytesting, and have needed to obtain governmentapproval before being marketed.

Economic factorsThe cost of food is a major determinant of whatpeople perceive as available to them; it ranksonly after taste in general surveys of influenceson choice. Within the range of foods available tothem, people can only eat what they can afford,or choose to afford. The second point is impor-tant, since it brings into consideration the priori-ties that exist in spending money. The annualNational Food Survey shows that in 2000(DEFRA, 2001) on average people in Britain spent9.5 per cent of their budget on food, althoughthis is less among the better off, and can be muchmore (up to 30 per cent or more) among lower

income groups. Even though the percentage ofincome spent is higher, the amount of moneyspent is actually less; in 2000, households in thelowest income group spent 15 per cent less thanthe UK average on food and drink. People seetheir food budget as one of the more flexibleitems in their expenditure; other expenses suchas fuel, rent, cigarettes and alcohol may take priority. When income is small and food budgetcuts are made, food distribution within the fam-ily may change, food treats may still be boughtand the children’s likes and dislikes attended to.The variety of foods eaten becomes smaller andthe diet becomes more monotonous. These issuesare discussed further in Chapter 13.

Food handlingIf food is available and there is money withwhich to buy it, bringing it home and preparingit for eating remain as possible areas of difficulty.Getting to the shops and bringing food homemay be a major problem, especially for familieswith no car, older people or those with disabil-ities. This will determine where the shopping isdone, how often and the sorts of foods that canbe bought and carried home. Many supermarketsin Britain have moved to peripheral locationsoutside towns, which makes shopping easier forthe car-owning customers who spend a lot ofmoney, but very difficult for those families livingfurther away, without transport. These then relyon the local shops, which inevitably keep lessstock, thereby restricting choice.

Once the food is in the kitchen, most of it hasto be prepared in some way for eating. This willdepend largely on the knowledge and skill of thecook, facilities and time available. Cooking skillsare variable; it has been suggested that fewer people now know how to cook. This has beenattributed to the escalating reliance on pre-prepared convenience foods, which eliminate the need for cooking skills. Often the only skillrequired is the ability to open a packet or can andheat the contents. Some foods can even be eatencold out of the packaging in which they werebought. In families where cooking does takeplace, the complexity of the preparation of thefood will reflect the cook’s personal experience of food and cooking, education, interest and timeavailable.


30

AcceptabilityCultural factorsEach cultural group possesses its own typicalfood selection patterns. These may be similar tothose of related cultural groups, but are unlikelyto be the same. Even within a relatively smallcountry such as the UK, there are differentregional foods, such as haggis in Scotland, laverbread in Wales and jellied eels in London.However, all these groups also share similar‘British’ food choices, such as fish and chips orroast beef. It is not just the choice of food thatmay vary between the cultures, but also the way in which it is cooked, the seasonings andflavourings used and the way it is served.

Traditional foods confer a sense of identityand belonging. This is very deeply held, since formost people it derives from the socializationprocess in childhood, discussed earlier. Thestrength and persistence of this cultural identitymay be illustrated by two examples. First, whenpeople holiday in another country, many willseek out foods with which they are familiar.Although they may be prepared to try the localdishes, it is often with a sense of curiosity and a preconceived idea that they will be strange.More importantly, when people emigrate toanother country for long-term settlement, theyoften suffer a sense of alienation or differencefrom the adopted environment. They may adoptthe host country’s style of dress and speak thelanguage, but the food that is eaten in the priv-acy of their home may remain very traditional.This provides a link with the homeland and sup-port in an alien environment.

If in addition to providing a cultural iden-tity, the food is also associated with religiousbeliefs, traditional food habits may persistlonger still. Studies on migrants to Britain showthat first-generation members adhere stronglyto traditional food practices. With the secondgeneration, these practices are less widespread,unless they are associated with religious pre-scription. Conflict may arise between the gener-ations as a result. Short-term migration doesnot, however, bring about changes to the diet,with evidence pointing to a reluctance to includehost-country foods and an adherence to tradi-tional foods, even if they are hard to find.

The types of foods that may be served toform a meal are culturally determined. Peoplemay classify foods in different ways: for example,into ‘sweet’ and ‘savoury’, or ‘healthy’ and ‘lesshealthy’, ‘snack food’ (or ‘junk food’) and ‘propermeal’. Nutritionists categorize foods more sys-tematically in terms of their main nutritionalrole in the diet. Currently, most Western countriesuse five food groups: cereal/grain (or starchy)foods, fruit and vegetables, meat and meat sub-stitutes, milk and dairy produce, fatty and sugary foods. An appropriate amount of eachgroup should be eaten to provide a nutritionally balanced diet.

Foods can also be described in terms of theirplace in the diet, as core, secondary or periph-eral foods (Table 2.3).

As well as providing the accepted norms forwhat can be eaten, cultural identity will alsodetermine what should not be eaten. Each cul-ture has clearly defined ideas about what is‘food’ and ‘non-food’. In many instances, thesedistinctions have arisen for sound reasons,including scarcity of a particular plant or ani-mal, or its potential harmfulness. In addition,there may be prohibitions on particular foods at certain times of life, particularly in infancyand during pregnancy. Many cultures have prohibitions associated with pregnancy, basedon beliefs about possible effects on the fetus.Although generally harmless, some may restrictintakes of foods, such as meat or other usefulsources of iron, for which needs are increased inpregnancy. It is also believed by some that eat-ing a particular mixture of foods around thetime of conception can influence the gender ofthe embryo.

A taboo that occurs in most world cultures isthat against cannibalism, but even this deep-rooted taboo is not universal. There are recordsthroughout history of people reverting to canni-balism in times of severe hardship, such aswartime siege, or following an air crash in aninaccessible region, as well as some cases ofmurder followed by cannibalism.

Many world religions also forbid the eatingof particular foods completely or at specialtimes. These include a prohibition on porkamong Muslims and Jews, and on all animals

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31

among the Hindus. These are considered furtherin Chapter 13.

Physiological factorsAppetite is associated with memories of particu-lar foods, and is the desire for a specific food orfoods. In animals, there is some evidence thatsuch desires for particular foods are linked to aspecific nutritional need. This is very difficult todemonstrate in humans and has, therefore, notbeen proven. The opposite is an aversion to aspecific food; this is often linked to an unpleas-ant memory of that food or an experience asso-ciated with it.

Personal preferences for foods are usuallylinked to a liking for the sensory attributes of thefood, which contribute to the pleasure of eating

it. Liking a food is frequently given as the mainreason for choosing it; however, people will eatfoods they feel neutral about, or even dislike in certain circumstances, for example, to pleaseothers. Most people select their food from arelatively small number of items that appear frequently in their diet. New foods may be triedon occasions, often as a result of advertising orpromotion of the product in the media. Thewealthier members of society include more var-iety in their choices than those on a low income.Compared with traditional hunter–gatherer soci-eties, who would eat a wide range of wild prod-ucts from the land at different seasons, ourWestern diet is quite limited.

Children are considered to be the age groupmost reluctant to diversify their diet, with someindividuals eating so few foods that they threatentheir nutritional status.

Because of the importance of personal pref-erence in making food choice, it is importantthat individuals are allowed to exercise somecontrol over what is eaten. Loss of control canlead to loss of appetite. This can be a reason forpoor intakes in hospitalized patients or residentsin other institutions, where menus are centrallydetermined, perhaps repetitive and little choiceis offered.

Core, secondary and peripheral foodsTABLE 2.3Core foods Secondary foods Peripheral foodsThe most important foods in Enhance the meal, but not Non-essential, but pleasant to eatthe diet – the staple of the essentialregion (normally a cereal or a root)

Usually one or two foods only May have specific perceived Special occasion foods, e.g. eaten (in Britain: bread/cereals and properties (e.g. protein-rich, at festivals, celebrations (e.g. potatoes) healthy, promoting balance, turkey at Christmas or

suitable for particular ages/ Thanksgiving, birthday cake)conditions in life)

Tend to appear in most meals May include meat/fish, Food with special properties, e.g. vegetables, pulses, fruit bedtime drinks

Nutritionally, a source of May include biscuits, cakescarbohydrate, some protein and confectionery, alcoholic drinks,a range of minerals and vitamins exotic fruit, sauces, drinks,

e.g. tea/coffee

Make a list of your food intake over the previousfew days. For each food, identify to which of thecategories in Table 2.3 it belongs.■ Which of the categories appears most

frequently?■ Are your meals made up of all three categories?■ What about your snacks?

Activity 2.3


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The need to follow a special diet for therapeu-tic reasons will affect personal food selection,and is a further area where loss of control andself-determination may cause problems withcompliance. This is a particular problem in ado-lescents, who may refuse to comply with dietaryrestrictions, as part of the maturing process. Foodselection may be deliberately restricted in thosewishing to control their weight: eating behaviourbecomes inhibited, and less food than is requiredto alleviate hunger may be eaten. Also, specificfood groups (the ‘fattening foods’) may beavoided, while others are eaten in their place (the‘slimming foods’). If the inhibition of intake isbroken, for a number of reasons, food intake maybecome excessive, resulting in binge eating, untilthe inhibitory influence is restored. This patternof restrained eating appears to exist, to a greateror lesser extent, in up to 80–90 per cent ofwomen in Western society. In some it results inclinically recognized conditions of anorexia orbulimia nervosa.

Special diets may be adopted for moral orideological perspectives, and these will imposeconstraints on individual food choice. Of these,the vegetarian diet has become the most preva-lent in Britain in recent years. The extent towhich people stop eating all animal producevaries, and some of those claiming to be vege-tarian may still actually consume some animalfoods, even white meat as well as fish, eggs,cheese and milk. Reasons for choosing this dietmay stem from abhorrence of the killing of ani-mals (and the methods used), and concern aboutthe exploitation of animals reared in crampedconditions for food. More recent publicity aboutaspects of food safety related to foods of animalorigin, such as beef, chicken, eggs and milk, has convinced others that avoiding these foodsmay be healthier (see Chapter 13 for further discussion).

Whatever the rationale for the special diet,the individual’s freedom of choice is restricted. Itmakes the person different from the rest of theirculture group (this may be one of the objec-tives!). Consequently, it may create barriers tothe sharing of food, causing alienation and possibly avoidance of social eating situations, orlack of compliance with therapeutic diets. Giving

as much freedom of choice as possible within the constraints of a special diet will help theindividual to regain their self-determination andenhance compliance.

Choosing to follow a ‘healthy’ diet is a posi-tive choice made by an increasing number ofpeople. This has arisen from the recognition thatmany of the diseases prevalent in Western soci-ety may have a dietary origin. The understandingof these links may not be very accurate and evenconfused, as may also the understanding of whatconstitutes a ‘healthy’ diet. A common belief isthat eating too much fat causes heart disease inmen, or that too much chocolate will makewomen fat. Thus, one or two aspects of currentdietary guidelines may be adopted, while othersare ignored. Only a tiny percentage of the popu-lation manage to achieve all of the dietary guide-lines, and the idea of a ‘whole-diet’ approach tohealthy eating has not been widely recognized.The concept of ‘healthiness’ also becomes blurredby food safety issues, including concerns aboutadditives in foods, genetically modified products,food that is not fresh, ready-made foods contain-ing unknown ingredients and possible contamin-ation by microorganisms, such as Listeria orSalmonella.

Social/psychological influencesAlthough our own physiological needs andwants are important determinants of what wefind acceptable to eat, we are nevertheless alsoinfluenced in our actions by the prevailing socialconditions, as well as our own psychologicalmake-up.

Food and the way it is presented can be usedto express status in society. The most obviousdistinction is that between having and not hav-ing food. The wealthy generally have access tomore and varied food, while the poor have lesschoice and are more likely to go hungry. Insome societies, it is a sign of wealth and statusto be obese.

Individual foods may also have differing status: those that are more expensive or difficultto get, such as grouse, venison or caviar, will be perceived as being high status. On the otherhand, foods such as tripe or pig’s trotters may beequally unusual, but because of their association

FOOD HABITS ❚

33

with low-income diets, have a low status. Every-day foods, such as potatoes, sausages and bakedbeans, will also have relatively low status. Thestatus of foods may change with time, depend-ing on how they are valued. For example, in thenineteenth century, brown bread was consideredcoarse and fit only for the lower classes; now itis seen as healthy and desirable in the diet, andits status has increased considerably.

What is eaten in particular circumstances islikely to reflect the assumed status of the food.When eating alone, it does not matter what weeat, and people may ‘treat’ themselves to com-binations of foods that they would not eat in company. As soon as food is eaten in company,value judgements are made on the basis of thefoods. The status of the foods served reflects theimplied status in which the diners are held. Thus,the type of food shared in a meal implies morethan satisfying a physiological need. Sharingfood with others is very symbolic: it confirms pre-viously established links, and a sense of mutualidentity. There is also powerful peer pressure infood selection.

Relationships within groups of people areconfirmed in the sharing of food: usually themost powerful or most important members ofthe group are served first. This not only confirmstheir superiority, but allows them to choose theprime parts of the meal.

The food preferences of men and womenoften differ; in most cultures men consume moremeat and women consume more fruit and vege-tables. Women tend to eat more of the foods that are regarded as ‘healthy’. It is suggested thatthese differences are associated with the trad-itional gender roles, which still exist in society.Women remain in charge of the food-relatedactivity; therefore, they tend to know moreabout food. Information about healthy dietstends to be seen more by women, as it featuresin women’s magazines, or in leaflets availablefrom supermarkets or in doctors’ surgeries.However, despite this greater knowledge, or levelof information, decisions about what is eaten areshown to be dictated in many families by themen and children, rather than the women.Studies of changes in food intake on marriageshow that both partners make some adjustments,

with husbands adopting more of the wives’habits initially, but reverting to their originalhabits in time. Nevertheless, married men tendto have healthier diets than single men.

Differences have also been reported in the wayfood is eaten, with men taking gulps and mouth-fuls, whereas women nibble and pick. As a conse-quence of this, it is suggested that some foods aremore appropriate for women (such as fish or fruit)and other foods for men (red meat, bread).

Food can be a powerful means of communi-cation. A box of chocolates given as a present isperhaps the most widely used example of foodacting as a token of affection. Some may find iteasier to give the chocolates than to put intowords what they are feeling. A cup of tea is atypically British answer to a difficult social situ-ation, when words are hard to find. A family eat-ing a meal together is sharing not only food, butthe affection they feel for each other. Rejectingthe meal in this situation can, therefore, be a verypotent dismissal of the love being offered.Reciprocal invitations to meals or parties by bothadults and children strengthen the social bonds.Children may exchange small items of food, suchas sweets, to communicate their friendship.

A special form of communication by meansof food exists in the ritual use of food. Manyreligions use foods as offerings to their deities.Christians use bread and wine. The end of thegrowing season and the harvest are marked inmany communities by a festival, with a sampleof the crops being offered in thanksgiving, oftento the poorest members of the community.

Certain life events are marked by specificritual meals – baptismal feasts, wedding break-fast, the funeral wake. Group membership mayalso be marked by rituals involving food ordrink; for example, the pre-wedding ritual ofstag night and hen party, where the men and thewomen separately undergo a ‘rite of passage’,usually involving large amounts of alcohol.

Food represents security from the earliestage, so that in times of stress it can form animportant support. Anxiety can provoke eatingas a means of coping with tension, although insome individuals stress can result in a loss ofappetite and an inability to eat. Anxiety mayalso lead to feeding others, for example, anxious


34

mothers may overfeed their children to relievetheir own anxiety about them. Abnormal eatingpatterns have also been linked with uncertaintyabout a person’s role or position in society. Ithas been suggested that both overweight andanorexia nervosa may originate from a dissoci-ation between the socially desirable body imageand that with which the individual feels psy-chologically at ease.

In the case of obesity, it is argued thatovereating occurs as a deliberate attempt to addsubstance to the body (generally female) in aneffort to cope with the demands of the world. Inanorexia nervosa, the body size is deliberatelyreduced to escape from the pressures of societyon the adult female, and return to the childshape.

1 Eating is regulated by the brain, which integrates many afferent signals coming from external andinternal sources. This allows food intake to be matched to metabolic needs. However, this regulation is more efficient for some components of the diet than for others.

2 Apart from the physiological need to eat, food intake is also regulated by psychological needs, socialinfluences, the sensory satisfaction obtained from eating, and by habit.

3 What is eaten is also influenced by many factors that determine both the availability of food and itsacceptability to the individual.

4 Despite many differences between cultures in actual foods eaten, influences on eating and food choiceare similar.

5 The interaction of influencing factors may be a key determinant in achieving dietary change.

SUMMARY

1 What information is available to the brain toallow food intake to be regulated? Consider themacronutrients in the diet and discuss howprecise this regulation is for each one.

2 The sensory appeal of food in very important.Give examples of some situations where:a sensory properties may not be detected by

the eater;b additional care needs to be taken to enhance

sensory appeal.3 Consider the food habits of members of your

family or your immediate friends.a Have they changed in the last 10 years?b If so, can you account for any changes?c If they have remained the same, what have

been the major factors maintaining thisconsistency?

4 Suggest ways in which government actioncould influence food habits. What barriers tochange might this encounter?

5 What might be the nutritional consequences of a diet composed entirely of:a core foodsb secondary foodsc peripheral foods?

6 In what ways can the following influence foodhabits:a travelb educationc multi-ethnic societies?

STUDY QUESTIONS


Blundell, J.E., Halford, J.C.G. 1994: Regulation of nutrient supply: the brain and appetite control.Proceedings of the Nutrition Society 53, 407–18.

Burnett, C. 1994: The use of sweets as rewards in schools. Journal of Human Nutrition and Dietetics7, 441–6.


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Charles, N., Kerr, M. 1988: Women, food and families. Manchester: Manchester University Press.Cotton, J.R., Burley, V.J., Weststrate, J.A. et al. 1994: Dietary fat and appetite: similarities and differ-

ences in the satiating effect of meals supplemented with either fat or carbohydrate. Journal ofHuman Nutrition and Dietetics 7, 11–24.

Craig, P.L., Truswell, A.S. 1994: Dynamics of food habits of newly married couples: who makeschanges in the foods consumed? Journal of Human Nutrition and Dietetics 7(5), 347–62.

DEFRA, 2001: National Food Survey 2000 Annual report on food expenditure, consumption andnutrient intakes. London: The Stationery Office.

Margetts, B.M., Thompson, R.L., Speller, V. et al. 1998: Factors which influence ‘healthy’ eating pat-terns: results from the 1993 Health Education Authority health and lifestyle survey in England.Public Health Nutrition 1(3), 193–8.

Mennell, S., Murcott, A., van Otterloo, A.H. 1992: The sociology of food: eating, diet and culture.London: SAGE Publications.

Stubbs, R.J., Harbron, C.G., Murgatroyd, P.R. et al. 1995: Covert manipulation of dietary fat andenergy density: effect on substrate flux and food intake in men eating ad libitum. AmericanJournal of Clinical Nutrition 62(2), 316–29.

Weststrate, J.A. 1996: Fat and obesity. British Nutrition Foundation Nutrition Bulletin 21, 18–25.Wilding, J.P. 2002: Neuropeptides and appetite control. Diabetic medicine 19, 519–27.Wood, R.C. 1995: The sociology of the meal. Edinburgh: University Press.


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❏ review the development of ideas about healthy eating;❏ describe the basis and application of dietary reference values;❏ discuss the dietary goals that have been put forward, and some of the dietary planning tools and mechanisms

that are available to assist with constructing a diet.


❏ explain the fundamental ideas about healthy eating and the goals that have been developed;❏ understand the significance of dietary reference values and be able to use them appropriately;❏ use a dietary planning guide to evaluate diets;❏ understand and show how to make use of information available on food labels in constructing a diet;❏ evaluate information given in pamphlets about healthy eating;❏ explain the health implications of alcohol consumption.

In Chapter 2 the factors affecting food habits andfood choice were discussed. The choice of foodsoffered to people in Western societies is enor-mously diverse, with novel foods being developedby food technologists. However, instead of mak-ing it easier for us to choose what to eat accord-ing to our particular desires at a specific time, theincreased variety makes it more difficult. Conse-quently, many people cope with the huge selec-tion, often over 6000–9000 different items in amajor supermarket, by consistently selecting onlya very narrow range of foods.

In addition, many people are increasinglyconcerned with improving their health, andconsumers wish to make food choices that willhelp in this. Various views are put forward tosupport particular dietary choices; the mostpolarized are those between plant-based ormeat-based diets. There is now a substantialbody of evidence to support the view that, wherefood is abundant, increasing the intake of plant-based foods, in particular fruit and vegetables,

can help to reduce the incidence (i.e. the numberof new cases in a given time period in a popula-tion) of chronic disease. However, the exact pro-portions of meat-based and plant-based foodsin the diet that might support optimal health areimpossible to determine. Epidemiological evi-dence does, however, support the view that dietsbased largely on plant foods are most associatedwith health and longevity, where food suppliesare adequate. It is thus particularly important to provide some guidance for people to be ableto select foods that will help to maintain theirhealth.

A healthy diet – which foods to choose?

If we are interested in and committed to takingcare of ourselves and others, the ‘healthiness’ ofour selection of food needs to be considered.However, ‘healthiness’ is not the only feature welook for in our food. Most of us would be very

C H A P T E R

3

A HEALTHY DIET – HOW MUCH TO EAT? ❚

37

reluctant to eat an unfamiliar food just becausewe were told it was healthy; the property ofhealthiness would be included in the generalconsideration of the food in deciding whether ornot to include it in the diet.

However, food that constitutes a ‘healthydiet’ is in the main not very different from thatwhich makes up a less healthy diet – it is thebalance of the parts making up the total meal ordiet that is important. As has been said else-where in this book, there are no ‘bad’ foods; it istheir place in the general picture of the diet thatis important. Some foods provide only a verynarrow range of nutrients, perhaps even justone. If such foods comprise a substantial part ofthe daily intake, the consumer will run the riskof not meeting nutritional requirements for arange of nutrients. The greater the range offoods, the less likely are there to be ‘gaps’ in thenutrient intake, and the more likely it is that theconsumer will meet the nutritional needs.

We are attracted by variety in foods, andwould find a diet containing just one or twofoods very monotonous. This might result in asmaller intake of the foods. The converse is also true: when presented with a variety offoods, we move from one to another and arelikely to eat more. The appearance of a tempting

dessert after a filling meal can readily overridefeelings of satiety, simply because of the nov-elty aspect!

Selecting several foods is, therefore, benefi-cial for our nutrient intake. Traditional mealpatterns can help us to decide on combinationsof foods to make up meals, as well as whatfoods to have at specific points of our day. Thepattern of core, secondary and peripheral foodsdiscussed in Chapter 2 serves as a general guide.It must be recognized that there is increasingvariation in this pattern. It is possible that, infuture generations, meals may be quite differ-ent, although there are also signs of a ‘tradition-alist revival’, which may take us back to theold-established food patterns.

A healthy diet – how muchto eat?

In addition to deciding what foods to eat, eachperson makes a decision about the quantity toconsume. From experience we have learnedwhat is an adequate serving size for us and thisobviously varies between individuals.

Our ability to assess how much of a food wewould like to eat relies on learned responsesestablished during our childhood and added to whenever a new food has been introduced.The sensations arising from the stomach when a particular serving size has been eaten will beremembered and will help to determine ourbehaviour in the future. Other reflex pathways,linked to the metabolic consequences of themeal, may also be part of the regulatory process.It is believed that this type of learning is animportant component of the control of foodintake (as discussed in Chapter 2).

The variability of ‘normal’ serving sizesbetween individuals is a dilemma for thosestudying food intakes in populations. There is nosuch thing as an ‘average’ serving size, whichwould apply to everyone. However, for the sakeof expediency, such a measure is quoted andused in many contexts. However, in relation tothis ‘average’, it is recognized that different people will also have ‘large’ and ‘small’ servings.Interpretations of these are also subjective and,therefore, variable.

Make a list of foods that you usually eat duringthe course of a week. Divide them up into fourcolumns: foods eaten at breakfast, lunch, eveningmeal, and snack foods.■ Is this easy to do? If so, you have got strong

ideas about what foods are appropriate atwhat times, and in what meals. If you found it quite hard to do, this may be because youhave a much ‘freer’ food structure, and theitems in your diet may serve several roles.

■ Check with a partner how easy their list wasto write into columns.

■ Finally, check how much agreement there isbetween your list and your partner’s – do youconsider the same foods as appropriate at particular times?

Activity 3.1

❚ BASICS OF A HEALTHY DIET

38

Dietitians try to resolve this issue by usingreplica foods, which generally represent the‘average’ serving. Patients may then indicatewhether the amount they would consume issimilar to this or different. There is always, ofcourse, the tendency to claim that one’s intakefollows the average.

What are the features of a‘healthy’ diet?

This question is likely to produce a number ofdifferent responses from people, depending on their level of interest in nutrition and theirunderstanding of the principles of health.

Answers will fall into one or several of thefollowing categories.■ Eating more or less of particular foods.■ Eating more or less of particular nutrients.■ Eating specific foods that are believed to

have ‘healthy’ properties. (This may includetaking nutritional supplements or eatingorganically produced food.)

■ Adopting particular diet-related practices, aswell as lifestyle changes.

■ Having a ‘balanced diet’.Each of these will be discussed in turn to

consider how well they answer the question ofwhat are the features of a healthy diet.

Eating more or less of particular foods

This response derives from the belief that thereare ‘good’ foods and ‘bad’ foods, and that weshould eat less of the latter and more of the for-mer. Unfortunately, it is not a straightforwardmatter to classify foods in this manner; individ-ual foods are less important than the way inwhich they are combined in diets. However,foods that contain a lot of fat or sugar, or those which have been extensively refined orprocessed, are likely to be of less value in acomplete diet, since they reduce the nutrientdensity. This means that the remaining foods in the diet must contain more of the micro-nutrients to compensate.

This can be a particular problem in peoplewho have relatively small appetites, or who aresedentary and, therefore, have low energy needs,since their potential intake of the more nutri-tious foods in the diet will be limited.

Eating more or less of particular nutrients

This has been one way in which advice abouthealthy eating has been promoted. In manycountries, initial dietary guidelines includedadvice to eat less fat (especially saturated fat),reduce salt and increase dietary fibre. It is notsurprising, therefore, that these are now repeatedby consumers as the central principles of healthyeating.

However, people eat foods and not nutrients.Foods (with a very few exceptions) are not simply a source of one nutrient and, therefore,reducing the intake of a certain group of nutri-ents by excluding particular foods from the dietmay have consequences for other nutrients alsofound in those foods. For example, if milk anddairy products are excluded because of their fatcontent, this can have serious implications forintakes of calcium and riboflavin.

1 Observation: During the next few days, useany opportunities you may have to observepeople at mealtimes. Notice whether theamounts of food items they consume are similar to or greater/smaller than you wouldchoose.

2 Quantitative assessment: If you have accessto dietary or household weighing scales, makemeasurements of the typical serving size thatyou select of everyday foods. Ask members of your family or your colleagues/friends to do the same. Collate the information from asmany different people as possible.■ How much variation do you find?■ Are portion sizes for some foods more vari-

able than others?■ Can you offer explanations for this?■ What are the health implications of peo-

ple’s different concepts of ‘appropriate’serving size?

Activity 3.2

WHAT ARE THE FEATURES OF A ‘HEALTHY’ DIET? ❚

39

The corollary of this is that some foods con-tain a nutrient in quite large amounts. If this isnot made explicit, the intake of that particularfood may not be altered. For example, ordinaryhard cheese (such as Cheddar cheese) is recog-nized by most people as a source of protein andcalcium, important for growing children and forbones. However, it is also very rich in fat. Inlisting sources of fat, many people would omitto mention cheese, and will continue to eat itoften in quite large amounts. If changes aremade only to the most obvious sources of fat,such as the spreading fats, cooking oils and full-fat milk, but other sources including cheese,pastries, biscuits and cakes are not reduced,then the overall impact on total fat intakes willbe small.

As a consequence, more recent dietaryguidelines have moved away from this focus on nutrients and have reverted to giving adviceon foods that should be included in the diet,together with advice about quantities.

Eating specific foods that are believed to have ‘health-promoting’ properties

There is a perception that only certain foods arehealthy, and they should be included in the diet.Linked to this is the belief that, when thesefoods are present, it does not matter what elsethe diet contains. Thus, in practice, an individ-ual might be eating all the wrong proportions ofmacronutrients, but believes the diet is healthybecause it includes a high-fibre breakfast cerealand semi-skimmed milk. Clearly there is someconfusion here. A single food or two cannotmake a diet healthy, although they can begin toredress an unbalanced diet.

Another example in this category is theinclusion of nutritional supplements to correctdeficiencies in the food consumed. Although thenutritional content may well be improved by thesupplements, especially in terms of the micro-nutrients commonly found in supplements, thebalance of macronutrients may still be unhealthy.Again the consumer has a mistaken perceptionthat they are eating healthily.

Including ‘organically’ grown products in thediet may reduce the level of chemical additives

and contaminants consumed, but again doesnot necessarily make the diet nutritionally bet-ter balanced.

The remedy for an unbalanced diet that con-tains unhealthy proportions of the macronutri-ents and perhaps inadequate amounts of themicronutrients lies in a change in the foods con-sumed, and an alteration in the proportions ofthe different food groups. Improving an imper-fect diet can be likened to dealing with a plumb-ing problem in the house, such as a leaking pipe.It can be dealt with by putting a bucket under-neath, and living with the problem; this parallelsthe taking of supplements or adding one or two‘healthy foods’ to the diet. Alternatively, thehouseholder can call in the plumber and havethe pipe mended. Similarly, an individual canobtain nutritional advice, either from a dietitianor nutritionist, or from information booklets,and change their diet for the better. In the longterm, the latter will clearly be the more satisfac-tory solution.

Adopting particular dietary practices orlifestyle changes

A whole range of behaviours may be includedhere. Some diet-related examples, which aresuggested by people as ‘healthy eating’, mightinclude:■ eating regularly■ having breakfast■ cutting down on convenience or junk

foods■ eating home-cooked foods■ drinking water■ losing weight■ planning what to eat■ eating organic food■ eating less meat (especially red meat)■ eating more fish/fruit/vegetables.(A survey of your friends and family would pro-duce many more.)

Lifestyle changes might include:■ taking exercise■ not eating late at night■ giving up smoking■ reducing alcohol intake■ becoming vegetarian.


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Although the latter are not strictly ways ofobtaining a healthy diet, they may be perceived aspart of the healthy lifestyle, which includes diet.This is most clearly seen amongst people whobecome vegetarian, who often make changes notonly to dietary intake but also to many otheraspects of life, frequently adopting a more ‘envi-ronmentally sensitive’ lifestyle.

It is not being suggested here that to eathealthily one should adopt a vegetarian diet,although this is a belief held by some. Diets canbe healthy (and also unhealthy) whether theycontain meat and animal products, or not.

Eating a ‘balanced’ diet

Although this can be an appropriate definitionof what is meant by healthy eating, it is impre-cise and, as such, is open to many interpret-ations. Over the last 40–50 years, the concept ofa balanced diet has changed. Its earlier interpret-ation was of a diet that provided the macro-nutrients in sufficient amounts to preventdeficiency, with protein often seen as a priority.There was a belief that, if the macronutrientswere adequate, then the micronutrients would‘take care of themselves’. This may have beentrue when the diet contained mostly food closeto its natural state, with few processed andmanufactured foods on the market.

More recently, it was realized that simplymeeting the requirements for macronutrientsdoes not lead to good health, as evidenced bythe high rates of ‘Western diseases’, such ascoronary heart disease, cancer as well as obes-ity. Clearly, something was wrong with thisapproach.

It is only in the last decade that the ‘balance’concept has been clarified to show suggestedproportions of different food groups to beincluded in the diet. This aims to meet bothmacronutrient and micronutrient needs, as wellas achieving a balance of nutrients that couldpromote health. This has, therefore, involved achange in the concept of ‘a balanced diet’, whichhas perhaps not been recognized by everyone.In addition, levels of energy expenditure havefallen, so that energy intakes need to be less. It then becomes even more important to make

sure that what is eaten has the appropriate bal-ance of other nutrients.

In the UK, the Ministry of Agriculture,Fisheries and Food (MAFF) produced Eightguidelines for a healthy diet in 1990. These wereintended to be an update on diet and health for people with some knowledge of nutrition, togive guidance on the balanced diet. The guide-lines were as follows.1 Enjoy your food.2 Eat a variety of different foods.3 Eat the right amount to be a healthy weight.4 Eat plenty of foods rich in starch and fibre.5 Don’t eat too much fat.6 Don’t eat sugary foods too often.7 Look after the vitamins and minerals in your

food.8 If you drink, keep within sensible limits.

These were supported by a number of add-itional information leaflets about food labellingand food safety. These guidelines are now stillcurrent in the UK, following their re-issue in1998.

Similar dietary guidelines exist in othercountries and are reviewed regularly. In the USA,there is a 5-yearly review. The most recent in-depth scientific review resulted in an expansionof the guidelines from seven to ten. These areintended for children from age 2 years andhealthy adults. The new 2000 Dietary Guidelinesfor Americans are as follows (Johnson, 2000).■ Aim for a healthy weight.■ Be physically active each day.■ Let the pyramid guide your food choices.■ Eat a variety of grains daily, especially whole

grains.■ Eat a variety of fruits and vegetables daily.■ Keep foods safe to eat.■ Choose a diet that is low in saturated fat and

cholesterol and moderate in total fat.■ Choose beverages and foods that moderate

your intake of sugars.■ Choose and prepare foods with less salt.■ If you drink alcoholic beverages, do so in

moderation.A comparison with the UK guidelines shows

a great deal of common ground, as would beexpected, as both derive from the scientific basethat supports advice on healthy eating.

WHAT NUTRIENTS ARE NEEDED, AND IN WHAT AMOUNTS? ❚

41

What nutrients are needed,and in what amounts?

In practice, the majority of people have no ideaabout the actual quantities of nutrients theyrequire each day, and yet most manage toobtain approximately sufficient amounts tomaintain adequate health. Whether their healthis as good as it could be (i.e. ‘optimal’) is a mat-ter for debate.

Nutritionists require more specific informa-tion on which to base scientific and reasonableadvice. The starting point for these figures is thenutritional requirement.

Nutritional requirement

Each individual uses or loses a certain amountof each nutrient daily; this amount must, there-fore, be made available to the tissues eitherfrom the daily diet or from the body stores ofthat nutrient. If the nutrient is taken from bodystores, it must be replaced at a later stage, other-wise the stores will gradually become depletedand the person will be totally reliant on theirdaily intake. Eventually, a deficiency statemight develop, if the intake is insufficient.

The amount of each nutrient used daily is thephysiological requirement. It is defined as the

amount of a nutrient required by an individualto prevent signs of clinical deficiency. Thisamount varies between individuals; it could dif-fer from day to day due to different levels ofenergy expenditure. It may also alter with thecomposition of the diet owing to changes in effi-ciency of absorption or utilization of nutrients.

There are, however, a number of inherentproblems with this definition. First, it is arguedthat this approach, based as it is on the veryleast amount needed to survive without develop-ing a deficiency, leaves no margin of safety.Consideration could be given to the provision ofa nutrient store to act as a reserve in time ofphysiological stress or reduced intake. Second,it gives no guidance on how to determine therequirement for nutrients for which there is currently no recognized clinical deficiency. Thisapplies to fats (except essential fatty acids) andsugars. Third, there are no universally agreedcriteria of when clinical deficiency exists. Thisis because a clinical deficiency reflects one endof a continuum, making it difficult to defineprecisely, as indicated in Figure 3.1.

It is cumbersome to obtain individual valuesfor each nutrient requirement. One solution is to look at the average requirements of groups of similar people and to define a reasonable

Figure 3.1 The stages of developmentof a clinical deficiency. This is ageneral guide to the progressionfrom adequacy to deficiency. Insome cases, the biochemical end-point may be very difficult toidentify or there may be no specificsigns associated with deficiency.


42

minimum level. The age of the child is taken as abasis for defining ‘similar’ children; for pregnantwomen, the stage of pregnancy is taken as thecommon basis; for other groups of the population,age and gender are common criteria. This is theapproach used by the Panel on Dietary ReferenceValues of the Committee on Medical Aspects ofFood Policy, which produced the most recent setof data for the UK in 1991 (DoH, 1991). This Panelderived information about nutritional require-ments in a number of ways. These included:■ measures of the actual intakes of particular

nutrients in populations that are apparentlyhealthy;

■ the intakes of nutrients that are required tomaintain balance in the body;

■ amounts of a nutrient needed to reverse adeficiency state;

■ amounts needed for tissue saturation, nor-mal biochemical function or an appropriatelevel of a specific biological marker.The appropriate method has to be selected

for each nutrient, taking into account its meta-bolic activity, mode of excretion, storage in thebody and the availability of suitable biochemicalindicators. None of the criteria used in deter-mining the level of requirement is deemed per-fect, but is the best available with the currentstate of knowledge.

Distribution of nutritionalrequirements in a population

When measurements of requirements areobtained from a sufficiently large population,the results are assumed to follow a typical ‘nor-mal’ distribution curve. This indicates that, for themajority, the requirement is around the meanfor the group, but some have higher require-ments and some lower values. If the group issufficiently large, then half will fall above thesample mean and half below it; this is simply aproperty of the distribution and not somethingpeculiar to nutrition or requirements.

From requirements todietary reference values

Having established the range of nutritionalrequirements for a particular nutrient, it is

necessary to define more precisely what would be an adequate level of intake to meet theserequirements. Several options might be available(Figure 3.2). Setting the level at a point A, whichis above the range of individual requirements,would ensure that everyone’s needs were met butmight pose a risk in terms of excessive intakes, ifthe nutrient was harmful in large amounts. Therewould also be cost implications – should peoplebe encouraged to buy so much food to meet thishigh level? An alternative might be to set thelevel at point B, which is the mean. By definition,this would imply that this level of intake would besufficient for half of the population, but would be inadequate for the other half. This would not be satisfactory for most nutrients. However,point B, which is defined as the estimated averagerequirement (EAR), is used as the reference valuefor energy intakes. This is because it would clearlybe undesirable to advise people to consume alevel of energy that was above the needs of mostof the population. In addition, the reference val-ues are actually intended for use by groups.Within a group, there will be some whose energyneeds are above and some below the EAR. If thefood provided, or consumed, contains an amountof energy that reaches the EAR, and the individu-als eat to appetite, then one can assume that theirenergy needs are being met. If the mean energyprovided or consumed lies below the EAR, thissuggests that some of the group may not be

Figure 3.2 The normal distribution curve of nutrientrequirements in a population and levels used forsetting dietary recommendations.

FROM REQUIREMENTS TO DIETARY REFERENCE VALUES ❚

43

reaching their EAR and, conversely, a meanintake above the EAR implies an excessive intakeof energy amongst some members of the group.However, judgements about individuals cannot bemade by comparison with the EAR figure, as thisis a group mean.

In practice, for the majority of nutrients, thePanel followed the pattern of previous commit-tees and used a point that is towards the upperend of the distribution curve of nutritionalrequirements, at the mean � 2 standard devi-ations. Because of the particular properties ofthis type of distribution curve, this point (C)covers the requirement figures for 97.5 per centof the population. It could be argued that thisleaves 2.5 per cent of the population outside thelimits and, therefore, at risk of an inadequateintake. However, in practice, it was felt that anindividual would not have extremely highrequirements for all nutrients, and it was thusunlikely that anyone would consistently fail tomeet requirements across the range. Eating tosatisfy appetite would be likely to ensure ade-quate intake.

Therefore, to summarize, point C was identi-fied as the reference nutrient intake (RNI). Inaddition, the Panel identified point D, at thelower end of the requirement range. This repre-sents the mean � 2 standard deviations, andcovers the requirements of only 2.5 per cent of the population, who fall below this level.Again, it is possible that there are some peoplewho have nutritional requirements consistentlybelow this point and who may, therefore, meettheir needs at this level of intake. However, it ismore probable that, if someone is consuming anintake as low as this, they are not meeting theirnutritional requirement. This point has beencalled the lower reference nutrient intake (LRNI).It effectively represents the lowest level thatmight be compatible with an adequate intake.

The dietary reference value (DRV) tables(published by the UK Department of Health asReport 41; DoH, 1991), therefore, provide threedistinct figures for the majority of nutrients: theLRNI, EAR and RNI, which can be used as a yard-stick to give a guide on the adequacy of diets.The Panel chose a new name for these figures,moving from the recommended daily amount(RDA), which was used previously. It was felt that

this name had been too prescriptive, suggestingthat the amounts given referred to what individ-uals must consume. The corollary of this was thatintakes that fell below the RDA were deemed tobe deficient.

In setting the dietary reference values with arange of figures, the Panel intend the range tobe used and, therefore, to provide more flexibil-ity in assessing dietary adequacy. In addition,the DRV tables contain other data on dietaryrequirements for fats and carbohydrates, andsome micronutrients for which little informa-tion was available.

Fats and carbohydratesThe approach to dietary requirements based ondeficiency is not appropriate for nutrients hav-ing no specific clinical deficiency. Consequently,in the past, no RDA figures were set for fats andcarbohydrates. There is now considerable publichealth interest in fat and carbohydrate intakes,and a desire for guidance on intake levels. TheDRV Panel used their judgement, therefore,based on research evidence of health risks atparticular levels of intake, to arrive at popula-tion average figures for the components ofdietary fats and carbohydrates as well as non-starch polysaccharides. Rather than givingabsolute figures, the DRV values are expressedin terms of the percentage of total energy, whichideally should come from the various compon-ents (Table 3.1). To provide further guidance,individual minimum and maximum values arecited for some of the components.

Some micronutrientsIn the case of some of the micronutrients, insuf-ficient data were available to establish a normaldistribution of requirements and thence derivevalues for LRNI and RNI. In these cases, thePanel, wishing to give guidance, have provideda ‘safe intake’ figure, which is considered to besufficient to fulfil needs, but is not so high thatthere is a risk of undesirable effects.

In the USA, a similar approach has beenadopted in the revision of the RecommendedDaily Allowances that had been set in 1989.Since 1998, the National Academy of Scienceshas constituted a number of expert panels toprepare a comprehensive set of reference values


44

for nutrient intakes for healthy US and Canadianpopulations. A number of reports have presentedDietary Reference Intakes (DRI) for vitamins andsome minerals. These parallel the DRV figurespublished by DoH (1991) in the UK. The DRIincludes a number of values as follows.■ Recommended dietary allowance (RDA),

which covers the needs of most individualsin a particular life stage and gender group.

■ Estimated average requirement (EAR), whichrepresents the mean requirement of the indi-viduals in a population.

■ Adequate intake (AI) represents an amountfor a nutrient that is believed to satisfyneeds, but for which there is insufficientevidence to describe the full range of refer-ence intakes.

■ Tolerable upper intake level (UL) – the high-est level of a nutrient intake that is likely topose no risk of adverse health effects foralmost all individuals in the general popula-tion. As intake increases above UL, the riskof adverse effects increases.Although the figures presented in the US

tables are not always the same as those in theUK, they provide similar guidance on the rangeof nutrient intakes compatible with health.

If the UK tables are compared with those pro-duced by the Food and Agriculture Organization/

World Health Organization (FAO/WHO) or byother countries, differences both in the range ofnutrients listed and the amounts advised arefound. This implies two things. First, there aredifferences in needs between peoples of certaincountries, as a result of differing lifestyles andperhaps different genetic make-up of the popu-lation. Therefore, when tables of reference val-ues are used, they should be those relating tothe country in question. Second, opinions differbetween the committees drawing up the tablesin different countries as to the safety marginsthat should be added to the figures. As a result,final figures also differ. This does not mean thatsome are more ‘correct’ than others; it reflectsdifferences in emphasis and serves to underlinethe uncertainty surrounding such figures. It isimportant to remember that these figures arenever an ‘absolute’ when their uses are con-sidered. They are basically the ‘best judgement’based on the physiological and nutritional dataavailable at the time.

Practical applications

For individualsIt is important to remember that the DRV tablesare not designed for use to judge individualnutritional intakes for their adequacy. They

Dietary reference values for fat and carbohydrate for adults, as a percentageof daily total food energy intake (excluding alcohol)TABLE 3.1

Individual minimum Population average Individual maximumSaturated fatty acids 11Cis-polyunsaturated fatty acids 6.5 10

n-3 0.2n-6 1.0

Cis-monounsaturated fatty acids 13Trans-fatty acids 2Total fatty acids 32.5Total fat 35Non-milk extrinsic sugars 0 11Intrinsic and milk sugars 39Total carbohydrate 50Non-starch polysaccharides (g/day) 12 18 24

From DoH, 1991. Crown Copyright is reproduced with the permission of Her Majesty’s Stationery Office.

FROM REQUIREMENTS TO DIETARY REFERENCE VALUES ❚

45

should rather be applied to groups of healthyindividuals. However, since in practice they areused to assess individual diets, some words ofcaution are necessary.

Most people are unlikely to consume anamount of each nutrient to match the require-ment exactly. However, it is probable that thosewith higher needs consume more than thosewhose needs are lower. The higher the correl-ation of intake and needs, the lower the risk of deficiency there is in any one individual.Unfortunately, the information about individualneeds is not available and judgement must beused. The higher the intake level (i.e. the closerit is to the RNI), the lower the risk that it is inad-equate. On the other hand, levels approachingthe LRNI level are likely to carry a high risk ofbeing inadequate.

Thus, a firm statement about an individualdiet is only possible when the intake falls out-side the range of RNI to LRNI. Nevertheless, theDRV Panel estimated that the risk of deficiencyis about 15 per cent with an intake at the EAR,and falls to negligible levels when the intakeapproaches the RNI. However, it rises sharply atlow levels of intake, approaching 100 per centat the LRNI.

For groups of individualsGroup mean intakes eliminate the intra-individual variability and, therefore, allow moreconfident interpretation of results. When agroup mean exceeds the RNI, the likelihood ofmany members of the group having intakessubstantially below the RNI is small. Meansaround or below the RNI suggest that there aresome members of the group whose intake maybe inadequate. The lower the mean with respectto the RNI, the greater the chance that somemembers have an inadequate intake. This use isparticularly important in evaluating dietarysurvey data.

For dietary planningDRVs are used, for example, in institutions inplanning diets for groups of individuals. Inthese cases, the RNI should be taken as the tar-get (except for energy). Similarly, if a dietaryprescription for an individual is being planned,then the RNI should be the target, since there isno other information about the actual needs ofthe individual.

Figure 3.3 shows the results of a riboflavin intakestudy in a large group of boys. Three boys in thisgroup (boys A, B and C) were found to haveintakes of A, B and C mg respectively.

The following conclusions can be drawn fromthe results:■ With an intake of A mg, we can be fairly sure

that boy A is not reaching his nutritionalrequirement for riboflavin, since it falls at thelevel of the LRNI. He may already be showingsigns of clinical deficiency, such as dermatitis.If not, he should be investigated, and givenadvice on increasing his riboflavin intake.

■ Boy B’s riboflavin intake, of B mg, is below theEAR for the group. However, this does notnecessarily imply that he is receiving an inad-equate intake. He may simply be a child with a low individual requirement. On theother hand, if he is not growing normally orshowing signs of ill-health, his needs areprobably not being met and his intake shouldbe increased.

■ At first sight, boy C’s intake of C mg seems tobe quite adequate, as it almost reaches theRNI; it is quite likely that this is the case.However, the possibility could exist that hehas a very high requirement, which is notbeing met by the current intake, even thoughit appears quite high. It can only be assumedthat his intake is sufficient, if there is no evidence of inadequacy.

Figure 3.3 Distribution of riboflavin intakes in apopulation of 12-year-old boys.


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Food labellingTraditionally, food labelling has used the RDAvalue previously published in the UK. This cor-responds to the current RNI level and is, there-fore, sufficient or more than sufficient for 97.5per cent of the population. In using this figureon food labels, the manufacturer may under-estimate how much of the requirement for anindividual is actually being supplied.

For example, suppose a food label claimsthat the food product provides, in a typical serv-ing, 100 per cent of the RNI (or RDA) for vita-min C. Using the DRV figure, we can discoverthat it, therefore, supplies 40 mg. However, foran adult woman, the LRNI is only 10 mg, andthe EAR is 25 mg. Therefore, for an individualwhose needs are low, say 15 mg, this food prod-uct will actually supply 260 per cent of theactual needs. This is quite different from theclaim of 100 per cent. As a result of such dis-crepancies, the Panel suggested that it would bebetter if EAR values were used in food labelling.However, the DRV figure does provide a refer-ence point for the fortification of foods, and forthe development of new food products.

The Institute of Grocery Distribution (IGD)in the UK has proposed a set of Guideline DailyAmounts (GDA) for use in food labelling. Theseare based on the predicted daily consumption ofan average consumer eating a diet conformingto UK DRV (DoH, 1991) recommendations. Theagreed GDA are as follows.

These figures are being used in some labellingin the UK, and help the consumer to see moresimply how much fat and saturated fat the food contains as a part of the target dailyintake.

Additional labelling directives operate in theUK, related to EU rulings, which use RDA as thebasis for guidance. The RDA figures are EUagreed, and are not necessarily the same as theUK RNI or EAR figures. Thus, several yardsticks

are in operation, each providing somewhat dif-ferent information to the consumer.

Dietary planning

It is important that those who use figures fromthe dietary reference value tables should under-stand how they have been derived and, there-fore, what are their uses and limitations. Inpractice, however, this is not always possibleand, therefore, a means to translate the scien-tific information contained in the DRV tablesinto more accessible format is needed.

Meal planning tools

Many countries in the West have used mealselection guides for a number of years to helptheir consumers with healthy eating. Foodguides provide a framework to show how foodscan be combined together in a day’s eating toprovide an overall intake, which contains theappropriate range of nutrients. They achievethis by:■ grouping together foods that provide (gen-

erally) similar nutrients, and that may beinterchangeable in the diet;

■ making a quantitative statement about thenumber of ‘servings’ of foods from eachgroup to be taken daily.Food guides were first devised in the USA.

They first appeared in 1916 and consisted offive food groups – milk and meat, cereals, vege-tables and fruits, fats and fat foods, sugars andsugary foods. Further developments occurredbetween the 1940s and 1970s, with changes tothe number and components of the groups used.Such changes reflected an increase in theunderstanding of the role of diet in health anddisease prevention. In particular, more guidancewas given about the consumption of fat, sugarand alcohol in the later guides than their earliercounterparts.

Most countries that have developed such afood guide use either the concept of a pyramidor a circle to illustrate that there are variouscomponents making up a whole diet. The mostrecent version of the USA Food Guide is a pyra-mid (Figure 3.4). This indicates that the foods in

Men WomenCalories 2500 2000Fat (g) 95 70Saturated fat (g) 30 20

DIETARY PLANNING ❚

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the groups at the base of the pyramid should bepresent in the greatest amounts and ‘support’the diet. Progressive layers above this should beconsumed in smaller amounts. By implication,those at the top (fats, oils and sweets) should beused sparingly, and are the least important com-ponents of the diet. The Guide indicates thenumbers of servings as a range; individualswith lower nutritional needs (e.g. children)should take the lower number of servings. TheGuide also does not apply to infant feeding.

Note also that the Guide does not imply thatany single food is essential in the diet, no foodalone provides all the necessary nutrients. Whatis important, however, is to include variety in thediet. In this way, shortcomings in one food arelikely to be compensated by an adequate intakein another food. In 1999, a Food Guide adaptedfor children aged 2–6 years was published in

the USA. The nutritional messages are the sameas those in the original Food Guide Pyramid.However, the foods pictured are those commonlyeaten by children in this age group. In addition,the words used are shorter and the illustrationsshow active children, in an attempt to promotethe importance of physical activity. Most chil-dren in the USA have been found not to meet theguidelines depicted in the Pyramid, especiallywith respect to the grains, fruit and dairy groups.This is resulting in concern about nutritionalintakes, especially of sugars, saturated fats and very low calcium intakes. In addition, therising prevalence (i.e. the numbers of peopleaffected in the population) of overweight andobesity, that now affects over 20 per cent of children in the USA has led to this initiative, in an attempt to influence eating habits at ayoung age.

Figure 3.4 The USA Food Guide pyramid: a guide to daily food choices. (Adapted from The Food Guide Pyramid.US Department of Agriculture/US Department of Health and Human Services.)


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In the UK, a National Food Guide (theBalance of Good Health) was launched for thefirst time in 1994 (Figure 3.5). The design is atilted plate incorporating five food groups in thefollowing proportions.

The nutritional details of the groups used in the Balance of Good Health are presented inTable 3.2.

The emphasis in the UK Guide is on foods,rather than nutrients, and shows the importanceof considering the diet as a whole rather thanconcentrating on specific foods that may be‘good’ or ‘bad’. The format was selected after

extensive consumer research, which considereda number of possible designs and tested prefer-ence for them amongst consumers and theirperformance as nutrition education tools.

The purpose of the Balance of Good Healthis to allow all nutrition educators to provide aconsistent message and thereby to reduce theconfusion about the creation of a balanced diet.It is, therefore, intended that the Guide shouldbe used widely to provide simple messages ofbalance and proportion of the food groups in apractical way. In addition, the Guide is intendedto be sufficiently flexible to allow choices basedon personal preferences and dietary habits, andto take into account availability, costs, culturalnorms and ethnic diets. It is, therefore, notintended to be prescriptive.

As with any other food planning guide, theBalance of Good Health does not take intoaccount the needs of those on special diets,infants and children under 5 years, or frail elderlypeople. Individuals in these groups may need to

Segment size as per cent of whole plateBread, other cereals and potatoes 33Fruit and vegetables 33Meat, fish and alternatives 12Milk and dairy foods 15Fatty and sugary foods 8

Figure 3.5 The UK National Food Guide: the Balance of Good Health. (From Food Standards Agency 2001: Balanceof good health: information for educators and communicators. London: Food Standards Agency.) Reproduced bykind permission of the Food Standards Agency.

DIETARY PLANNING ❚

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Nutritional details of the five groups in the UK National Food Guide (the Balance of Good Health)TABLE 3.2

Name of food group Composition of food group Key nutrients found in groupBread, other cereals All breads made with yeast and other Carbohydrate

and potatoes breads NSPCereals, including wheat, oats, barley, Vitamin B complex

rice, maize, millet and rye together Calciumwith products made from them, Ironincluding breakfast cereals and pasta (Recommend:

Potatoes in the form usually eaten as ■ low-fat methods of cooking, and part of a meal (but not as a snack, sauces/dressings, spreadse.g. crisps) ■ high-fibre varieties to maximize

micronutrients)

Fruit and vegetables Fresh, frozen, chilled and canned fruit Vitamins C, E and carotenes and vegetables (antioxidant vitamins), folate

Fruit juices Minerals: potassium, magnesium, Dried fruit trace minerals

CarbohydrateNot included: potatoes, pulses, nuts NSP

Majority are low in energy

Meat, fish and Carcass meats, meat products Proteinalternatives (but not pastries and pies) B vitamins (especially B12)

Fish and fish products Minerals: phosphorus, iron, zinc, Poultry magnesiumEggs NSP (from pulses only)Pulses and nuts Long-chain polyunsaturated fatty

acids (in oily fish)Meat and its products may be

significant contributors to fat intake (low-fat alternatives available)

Milk and dairy foods All types of milk ProteinYoghurt CalciumCheese Fat-soluble vitamins (except in

low-fat varieties)B vitamins (riboflavin, B12)Not included: butter and eggs

Fatty and sugary Butter, margarine, fat spreads, Energyfoods oils and other fats Fat

Cream SugarCrisps and fried savoury snacks Essential fatty acidsCakes, pastries, biscuits Fat-soluble vitaminsChocolate and sugar confectionerySugars and preservesIce creamSoft drinks

NB: The Guide does not include composite dishes: these should be allocated to groups according to their main ingredients.


50

pay greater attention to the nutrient density ofthe foods consumed if their intakes are small.

The Guide also aims to help in achieving the dietary guidelines originally published by theUK Government in 1990 in the form of the Eightguidelines for a healthy diet (MAFF, 1990). There-issue of these incorporates the Balance ofGood Health as an illustration of how the twocan be used in conjunction.

How to use the Balance ofGood Health

The Guide is concerned with the proportions ofthe foods in the diet. The simplest way to use theGuide, therefore, is to calculate the proportion ofthe total daily diet provided by foods from thedifferent food groups in terms of numbers ofservings eaten during the day. Some concern hasbeen expressed that the definition of a ‘serving’or ‘portion’ is not made explicit. However, it

should be remembered that for any one individ-ual, servings of particular foods are consistentover time; it is the contribution of each of theseservings to the whole diet that is important.

Figure 3.6 illustrates how the Guide can beapplied to assess an individual diet. It is alsopossible to identify the shortcomings of the dietin this way, and use it as the basis for remedialadvice. Adding together the numbers of servingsgives the following percentages of the total:

Bread/cereal group 6 servings � 30 per centFruit and vegetables 4 servings � 20 per centMeat and alternatives 4 servings � 20 per centDairy foods 2 servings � 10 per centFats and sugars 4 servings � 20 per cent

It is, therefore, possible to see how this day’sintake complies with the Balance of GoodHealth. Clearly, there is not quite enough of thebread and cereals group, far too little fruit andvegetables and rather too much of the remaining

Figure 3.6 Example of a day’s food intake and the numbers of servings from the Balance of Good Health.

NUTRITION INFORMATION ❚

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three groups. In this way, it is possible to focuson which parts of the diet need attention andmake suggestions for replacing foods.

A consistent message

One of the main objectives of the Balance ofGood Health is to provide a consistent messagefor all consumers about a balanced diet. There isevidence of confusion about a number of issuesrelated to healthy eating. These can be foundamong many consumers as well as in the media, advertising and the catering industry. Inparticular, confusion exists in relation tointakes of specific nutrients or groups of nutri-ents. These include fat, complex carbohydratesand sugars, salt, alcohol and antioxidant nutri-ents. In addition, specific constituents of food,such as additives, or techniques used in foodprocessing, for example, irradiation, cause con-cern and are linked to ‘healthy eating’. Organicfoods are generally perceived as being ‘healthy’,even when their nutrient composition is similarto that of non-organically produced foods.Exotic ingredients or foods are sometimes cred-ited with exceptional nutritional properties; and(often unfounded) claims about ‘live’ yoghurt,honey, herb drinks and new ‘functional foods’all add to the confusion of the consumer.

Nutrition information

There are numerous booklets and leaflets nowavailable to the consumer produced by food

companies, retailers, hospital trusts and manyother organizations. How should these beviewed and what is the quality of the informa-tion they contain? Many of them are sound andvery informative. Some, however, can be mis-leading, often not by what they actuallyinclude, but by judicious omission of key points.

When reading nutrition information leaflets,ask yourself the following questions.■ Is the dietary advice being offered compat-

ible with a balanced diet, as described by theBalance of Good Health?

■ Is the advice stressing the importance of onenutrient or food, to the exclusion of or inpreference to others?

■ Is a particular product or brand being pro-moted?

■ Is there bias in the advice being givenbecause of other interests that the sponsor ofthe leaflet may have?

■ Does the leaflet promise unrealistic out-comes?

■ Does the advice suggest that you buy prod-ucts that you have never used before?

■ Is the advice being given appropriate to youand your lifestyle?

■ Is the leaflet written by a registered nutri-tionist or dietitian?

■ Is scientific evidence being quoted, includ-ing references to reputable sources of infor-mation?

■ Is there an address from which further infor-mation can be obtained?

If you can be satisfied that the evidence is bal-anced and unbiased, then the leaflet is likely tobe worthwhile and can be a useful source ofinformation. However, biased leaflets should notbe used, as these simply add to the confusion.

It is simply not true that nutrition profes-sionals are continuously changing their viewsand advice, as the media claim. Scientific debateis an important way of moving knowledge for-ward, and without it a subject stagnates andbecomes dated. New ideas and fresh approachesare essential to continually check that our theories can be supported and that the advicewe give is based on sound empirical evidence.The majority of nutrition experts do agree onthe basic advice about healthy eating. Where

Now carry out a similar exercise on your ownfood intake. You may have already kept a recordof a typical day, or several days’ food intake. Makean assessment of the proportions of your dietcoming from the various groups.■ What groups are overrepresented?■ Are some underrepresented?Use the Balance of Good Health to suggest alter-natives in the diet that could make the balancebetter.

Activity 3.3


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there may be disagreement, it may reflect par-ticular interests of the parties involved or relateto issues where the literature also conflicts.

The question of alcohol

The consumption of alcohol is not discussed inthe basic guidance on a balanced diet, as it isnot an essential component of the diet and doesnot feature in all diets. Yet the consumption ofalcohol is prevalent, with estimates suggestingthat almost 90 per cent of the population in theUK consume alcohol at some time each year.Alcoholic beverages are consumed as part ofmany social activities, but consumption canalso become excessive and result in physical,psychological and social harm to the individualas well as those around them. Economic esti-mates suggest that health and other problemsrelated to alcohol consumption, including timeaway from work, represent a heavy financialburden. However, there is also very substantialrevenue to the Government from the taxeslevied on alcoholic beverages.

Published recommendations relating toalcohol generally adopt the perspective of limit-ing the intake rather than actively promotingconsumption.

In order to quantify amounts of alcoholdrunk from a variety of different sources, astandard ‘unit’ of alcohol has been developed.In the UK, this is equivalent to 8 g or 10 mL ofethanol. This amount of ethanol is found in thefollowing measures of common drinks:■ 1⁄2 pint of standard-strength beer (284 mL)■ 1 measure of spirit (25 mL)■ 1 glass of wine (125 mL).Many other drinks are on the market that do notfit exactly into these categories and it can bedifficult, without adequate labelling, to identifyexactly how many units are present in a drink.

The definition of a unit differs between coun-tries, and in the USA, equals 12g of alcohol.

Benchmarks for safe levels of intake of alco-hol have been published, using the concept of a unit. These are that men should not exceed 3–4units per day and women should not exceed 2–3units per day. In addition, there should be some

drink-free days during the week. These bench-marks were introduced in 1995 to replace olderguidelines that stated safe intakes to be 21 unitsand 14 units per week for men and women,respectively. There has been an increase inbinge drinking, especially among young people,and amounts of this order were being consumedin one night. This was clearly not a safe intake,and the advice to spread alcohol consumptionover a greater period of time was introduced asa consequence.

With progressively higher intakes, there is agreater risk of harm occurring. Consequences ofexcessive alcohol consumption include damageto every system of the body, including the liver,digestive system, heart, brain and nervous sys-tem. In addition, nutritional intake is likely tobe affected and chronic overconsumption isassociated with a number of specific nutritionaldeficiencies. Even at moderate intakes, it islikely that alcohol contributes to the total energysupply and this may result in weight gain.Social consumption of alcohol accompanyingmeals has been shown to be associated with alarger food intake as well as the consumption ofhigher levels of fat.

However, moderate alcohol consumption hasalso been linked to beneficial effects, particu-larly in protection against coronary heart dis-ease. There is a J-shaped relationship betweenoverall mortality and alcohol consumption,with abstainers and heavier drinkers havinghigher mortality rates than those seen in moder-ate drinkers. Maximum health advantage forcoronary heart disease lies at levels of intakebetween 1–2 units per day. The reasons for theshape of this curve are still not agreed. In add-ition, the J-shaped relationship is now known to apply predominantly to men over the age of35 years and women after the menopause, withbenefits increasing in older age groups. Thelevel at which no harm is caused by alcohol alsoincreases with age, so that the young drinker ismost at risk. Mortality risk is increased in youngdrinkers at levels of alcohol consumption nor-mally considered to be ‘safe’; this may be asso-ciated with accidents and injury rather than thelong-term physical damage caused by alcoholitself.


53

On a population basis, there is no recom-mendation to increase alcohol consumption, foralthough abstainers might benefit from a smallamount of alcohol, the extra harm that could

ensue from increased drinking among heavierconsumers would not translate into an overallimprovement in health.

1 Eating healthily is not a matter of adding specific ‘health-giving’ foods to the diet, using specific foodpreparation techniques, avoiding additives or taking nutritional supplements. None of these will makethe diet healthy.

2 Choosing a healthy diet involves knowing what mixtures of foods to select and in what quantities.3 Adequate amounts of food must be consumed to meet nutrient requirements. These are expressed as

Dietary Reference Values and cover the needs of most of the population.4 The Food Guides show how a balanced diet can be created, by choosing from a wide range of foods,

in appropriate quantities.5 Alcohol intake can be beneficial to health when taken in small to moderate amounts. Benefits are more

likely in middle-aged and older people.

SUMMARY

1 A number of commonly eaten foods areperceived as being ‘healthy’ or ‘unhealthy’.a Compile a list of approximately 20 foods that

you consider fulfil these criteria.b Ask a number of friends to define the foods

as ‘healthy’ or ‘unhealthy’.c State whether different people choose the

same foods or whether there are differences(e.g. by age, gender).

d Account for the perceptions about thesefoods.

2 For what nutritional reasons might a vegetariandiet be considered ‘healthier’ than anomnivorous diet?

3 Explain why a nutritional deficiency state can be difficult to define precisely. What differentend-points are used to delineate deficiency?

4 Distinguish between an individual’s nutritionalrequirement and the reference nutrient intakefor a particular nutrient (e.g. vitamin C).

5 Explain why an intake below the level of the RNImay be nutritionally adequate.

STUDY QUESTIONS


Achterberg, C., McDonnell, E., Bagby, R. 1994: How to put the Food Guide Pyramid into practice.Journal of the American Dietetic Association 94, 1030–5.

DoH (UK Department of Health) 1991: Dietary reference values for food energy and nutrients in theUnited Kingdom. Report on Health and Social Subjects No. 41. Report of the Panel on DietaryReference Values of the Committee on Medical Aspects of Food Policy. London: HMSO.

DoH (UK Department of Health) 1995: Sensible drinking. The Report of an Inter-DepartmentalWorking Group. London: HMSO.

Fairweather-Tait, S.J. 1993: Optimal nutrient requirements: important concepts. Journal of HumanNutrition and Dietetics 6, 411–17.

Hunt, P., Gatenby, S., Rayner, M. 1995: The format for the National Food Guide: performance andpreference studies. Journal of Human Nutrition and Dietetics 8, 335–51.

Institute of Grocery Distribution 1995: Voluntary nutrition labelling guidelines to benefit the con-sumer. Watford: Institute of Grocery Distribution.


54

Johnson, R.K. 2000: The 2000 Dietary Guidelines for Americans: foundation of US nutrition policy.British Nutrition Foundation Nutrition Bulletin 25, 241–8.

MAFF (Ministry of Agriculture, Fisheries and Food) 1990: Eight guidelines for a healthy diet.London: Food Sense.

Mela, D.J. 1993: Consumer estimates of the percentage energy from fat in common foods. EuropeanJournal of Clinical Nutrition 47(10), 735–40.

Nestle, M. 1999: Animal v plant foods in human diets and health: is the historical record unequivo-cal? Proceedings of the Nutrition Society 58, 211–18.

the nutrients in foodand their role in health

PA R TTWO

57

proteins


❏ describe the composition and nature of proteins and identify protein-providing foods in the diet;❏ show how proteins are digested and metabolized;❏ identify the role of proteins in the body;❏ discuss the concept of indispensable amino acids and how this is reflected in measurement of protein quality;❏ explain the need for protein at different ages and in health and disease.

On completing the study of this chapter you should be able to:

❏ describe the basic structure of proteins and explain how they are altered by cooking;❏ describe the process of protein digestion;❏ explain the significance of indispensable amino acids and how foods may be combined to provide an

appropriate balance;❏ discuss the role of proteins and amino acids in the body, in health and disease, and the consequences of

protein deficiency;❏ explain the needs for protein at different stages of life and in trauma.

The word ‘protein’ is derived from the Greek andmeans ‘holding first place’. Proteins are essentialin the structure and function of all living things;without them no life can exist. Their importance,however, lies principally in the amino acids ofwhich they are composed.

Some people associate protein with strengthand muscle power, and perceive meat as beingthe most valuable source of protein. This view isonly partly true; proteins are an essential compon-ent of muscles, but this is only one of their manyfunctions in the body. Meat is a source of protein,but so also are many other foods, both of plantand animal origin. There is nothing special aboutprotein from meat.

There are millions of different proteins –plant, animal and human – but all are built upfrom the same 20 amino acids. The particularsequence and number of amino acids containedin a protein determine its nature. With 20 dif-ferent amino acids to choose from, and chains

which include perhaps several hundred differentamino acids, the variety is almost endless. Thereare over three million ways of arranging aminoacids in the first five places of a chain alone. Thevariety of proteins that exists is far greater thanthat of carbohydrates and fats. However, eachprotein has its own particular sequence of aminoacids, which is crucial for its properties andfunctions. If even one amino acid is missing ormisplaced in the chain, the properties of the pro-tein will alter. The sequence of amino acids iscontrolled by the genetic machinery of our cells,encoded in the DNA and RNA chains. This crit-ical relationship between the number of unitscontained and function does not apply in thecase of carbohydrates: they may contain more orfewer of the particular component unit (usuallya monosaccharide) without significant changesin properties.

The majority of the amino acids originatefrom plants, which are able to combine nitrogen

C H A P T E R

4

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from the soil and air with carbon and other substances to produce amino acids. These arethen built into proteins by plants. Humansobtain their proteins either directly by eatingplants, or by eating the animals (and their prod-ucts), which have themselves consumed theplants. This does not mean that our bodies con-tain exactly the same proteins as plants andanimals. The proteins we eat are broken down

into their constituent amino acids and arerebuilt, or some new amino acids are first made,before new proteins are made in our bodies. Ourbodies are able to make some amino acids fromothers, but there are certain amino acids (calledessential, or indispensable) that cannot be synthesized by the body and which must, there-fore, be supplied by the diet. This is shown inFigure 4.1.

Figure 4.1 Origin of human dietary protein.

AMINO ACIDS – THE BUILDING BLOCKS ❚

59

It is our need for these amino acids thatmakes it vital that we have adequate amounts ofprotein in our diet. If an individual fails to eatsufficient amounts of protein, the body’s ownstructural proteins are broken down to meetmetabolic needs for repair. In addition, otherprotein-requiring functions also fail, with result-ing illness and possible death. To judge the needsof an individual for protein, therefore, it is import-ant to understand how proteins are used in thebody and the magnitude of the daily turnover.

Amino acids – the buildingblocks

Amino acids are relatively simple substances.All have the same basic structure: a carbon(known as the � carbon), with four groups ofatoms attached to it:■ an amino group (–NH2)■ an acid group (–COOH) always present■ a hydrogen atom (–H) and■ a fourth group, which varies between differ-

ent amino acids and characterizes each one.This is the side-chain, identified as –R in the‘generic’ formula of an amino acid:

The simplest amino acid is glycine, in which theside-chain R is an H atom. Thus, the formula forglycine is:

(It is worth comparing this with the formula forthe simplest fatty acid, namely acetic acid: it isclear that the difference between these is small,with one of the H atoms in the fatty acid,

replaced with an NH2 group to produce theamino acid.)

It is possible to compare the next fatty acid withthe next amino acid, and see that again an Hhas been replaced by an NH2 group:

The nature of the side-chain will determine someof the properties of the amino acid and of pro-teins that contain a high proportion of theseacids. Side-chains may be aliphatic (open chainstructure) or aromatic (i.e. unsaturated ringstructure), acidic or basic (Table 4.1).

Except in the case of glycine, in which the � carbon has two H atoms attached, all otheramino acids have four different groups attachedto the � carbon. This implies that the molecule soformed can exist as two optically active isomersthat are the mirror image of one another: D and L

forms. This also occurs in monosaccharides, asdiscussed in Chapter 6. The majority of aminoacids in nature exist in the L form; however, some D amino acids do exist in foods, and a fewcan be metabolized by the body. Generally, meta-bolic reactions in the body distinguish between Land D forms of amino acids and D forms are usedless well. Some transamination of D-methionineand D-phenylalanine can take place to theirrespective L forms.

When amino acids combine to form proteins,they do so through the –NH2 group of one aminoacid reacting with the –COOH group of the adja-cent amino acid, splitting off H.OH (water) in theprocess. The link is known as a peptide link, andthe proteins thus formed are known as polypep-tides, or peptide chains. The polypeptide back-bone does not differ between different protein

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chains, it is the side-chains (R–) that provide thediversity.

A chain of amino acids may be written as:

When the whole chain is put together in three-dimensional space, the R– side-chains have to fittogether without colliding with one another.Some are attracted to each other; some arerepelled. Side-chains consisting of only carbonand hydrogen tend to come together, for theyexclude water. Side-chains with oxygen or –NH2

groups will mix with water, so these tend tooccupy adjacent places. Thus, the nature andlocation of the side-chains within a polypeptidechain will determine its arrangement. It will foldor coil in an attempt to bring together compat-ible side-chains. In addition, other weaker bonds(e.g. hydrogen bonds) also form to provide fur-ther levels of organization of the protein struc-ture. These will determine the strength andrigidity of the protein as well as dictating itsfinal shape. Proteins with different roles in thebody will have different shapes, most appropri-ate to their function. Their shape may, for exam-ple, be thread-like, helical or globular.

In addition, the shape of the protein may bealtered by changes in its environment, such asheat or pH change, which affect its stability.Once the change in shape has passed a certainpoint, the protein is said to be denatured. Thismeans that specific properties of the protein, suchas antibody or enzyme activity, are lost. However,the nutritional value remains unchanged, as theamino acids themselves are still present andunchanged.

Cooking processes cause denaturation of pro-tein – the change from raw to cooked forms issomething with which we are familiar. For exam-ple, there is a noticeable difference between araw and cooked egg, or the curdling of milk inthe presence of acid or bacteria in the productionof many dairy products. These changes occurbecause of the loosening of the weaker bondsholding the protein in shape so that its naturalshape is lost, and some of the moleculesrearrange themselves in new positions. Usually,cooking or food preparation processes do notaffect the basic peptide bonds.

Proteins in food

The overall proportions of amino acids in plant foods are different from those needed byhumans; those in foods of animal origin aremore similar. Many different sources of proteinexist, the main ones in the British diet being

The amino acids classified according to the nature of their side-chainsTABLE 4.1Aromatic amino acids Aliphatic amino acids Acidic amino acids and Basic amino acids

their amidesPhenylalanine Glycine Aspartic acid LysineTyrosine Alanine Asparagine ArginineTryptophan Valine Glutamic acid Histidine

Leucine GlutamineIsoleucine

SerineThreonine

CysteineCystineMethionineProline

}}

}

(branched-chain aminoacids

(OH in side-chain)

(S groups inside-chain)

DIGESTION AND ABSORPTION OF PROTEINS ❚

61

meat, milk, bread and cereals. However, proteincan also be provided by other animal products,such as eggs, dairy produce (cheese and milk-based desserts) and fish. Plant foods that areuseful sources of protein include all cereals andtheir products (including pasta and breakfastcereals), legumes, nuts and seeds. For manypeople of the world who follow vegetarian diets,the plant foods are the only sources of protein;clearly they can provide an adequate supply ofprotein. Roots and tubers do not have a highprotein content but, if they constitute a sub-stantial proportion of the diet, this protein canmake an important contribution.

Table 4.2 shows the amounts of protein con-tained in a range of foods. However, since someof the protein sources do not contain all of theamino acids needed by humans, it is important

that a range of protein sources is eaten to allowsmall amounts in one food to be compensatedwith another source. This is discussed further laterin this chapter in the section on protein quality.

Digestion and absorption of proteins

Proteins must be digested in order to release theamino acids of which they are composed so theycan enter the body pool and be used for cellgrowth, repair or protein synthesis. The chemicallinkages between amino acids are all peptidebonds, yet a number of different peptidases areneeded to cleave these bonds because of the dif-fering nature of the side-chains on the aminoacids adjacent to the bonds. Therefore, a singletype of peptidase could not split a protein chaininto its constituent amino acids in the same waythat a single lipase or amylase can split fat intofatty acids or starch to glucose. Several differentpeptidases act on the proteins of our foods, eachattacking bonds adjacent to particular side-chains on the amino acids. Other enzymes attackbonds at the ends of the peptide chain, taking offsingle amino acids, one after the other.

In the stomach, hydrolysis of the proteintakes place by the action of the hydrochloricacid secreted there. This denatures the proteinand allows the peptides to be attacked. In add-ition, the acid also activates the enzyme pepsino-gen into its active form of pepsin. This enzymeattacks a range of peptide bonds and, therefore,is able to split the long protein chain into aseries of shorter, polypeptide chains.

On passing from the stomach, the polypep-tides are further digested by enzymes secretedfrom the pancreas and activated in the duode-num. These include trypsin, chymotrypsin, col-lagenase, elastase and carboxypeptidase. Theseenzymes are able to split the chain at specificpeptide bonds, as well as removing end aminoacids. Final digestion is completed by enzymeslocated in the brush border of the small intes-tine, including aminopeptidases and tripepti-dases. These split the remaining peptides intosingle amino acids, or pairs of amino acids,which are absorbed and finally hydrolysed toamino acids in the intestinal mucosal cells.

Sources of proteinTABLE 4.2Food Protein Protein Energy

(g/100 g) (g/average fromserving) protein

(%)Wholemeal bread 9.4 3.4 17.3White bread 7.9 2.8 14.4Cornflakes 7.9 2.4 8.4Boiled rice 2.6 4.7 7.5Semi-skimmed milk 3.4 6.8 29.5Yogurt, low fat 4.2 5.3 21.5Cheese, Cheddar 25.4 10.2 24.4

typeEgg 12.5 6.3 34.0Beefburger 28.5 25.7 34.7Beef, stewed 15.1 39.3 44.4Roast chicken 27.3 27.3 61.7Pork chop 31.6 44.2 49.2Cod in batter 16.1 29.0 26.1Peanuts, salted, 24.5 6.1 16.2

roastPeanut butter 22.6 4.5 14.9Baked beans 5.2 7.0 24.8Peas 6.0 4.2 35Potatoes, boiled 1.8 3.2 10Cheese and 14.4 33.1 20.8

tomato pizza

Data calculated from Food Standards Agency (2002a, 2002b).

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There are a number of specific carrier mol-ecules that transport the products of proteindigestion across the intestinal mucosa into thebloodstream. Separate carrier systems have beenidentified for the basic, neutral and dicarboxylicamino acids and there is competition betweenthe individual amino acids for the carrier. Inaddition, there are carriers for small peptides.The process is summarized in Figure 4.2.

It is worth pointing out that ingestion ofsupplements, which may contain several aminoacids of the same chemical type, will result in competition for absorption. Thus, the aminoacid present in greatest concentration will beabsorbed preferentially, but the absorption of the others may be impaired. This may result inunbalanced amino acid absorption. Further,absorption of amino acids and peptides fromnatural, protein-containing foods occurs more

quickly and efficiently than that from an equiva-lent mixture of free amino acids.

In general, protein digestion is extremely effi-cient, and up to 99 per cent of ingested protein isabsorbed as amino acids. In young infants, how-ever, whole antibody proteins secreted in mater-nal milk are absorbed from the gut. These giveprotection against infections, particularly duringthe first days of life, when colostrum is secretedby the mother’s mammary glands. Colostrum isrich in immunoglobulins, which confer immunityto the child. It is also possible that proteins fromcows’ milk or wheat flour may, if given at thistime of life, set up antibody production in theinfant. This occasionally causes subsequent ‘foodintolerance’ or ‘food allergy’ (see Chapter 16).

Most of the amino acids pass into the blood-stream from the intestines, and travel to theliver in the hepatic portal vein. Some pass into

Figure 4.2 Digestion of proteins.

AMINO ACID METABOLISM ❚

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the liver cells, others go on to the general cir-culation. The liver is thought to monitor theabsorbed amino acids and to adjust their rate ofmetabolism according to the needs of the body.A small number of amino acids remain in thecells of the intestinal mucosa, for synthesis ofprotein and other nitrogen-containing com-pounds. Glutamine is thought to promote celldivision in the gastrointestinal mucosa, and isused by the intestinal cells as a primary sourceof energy. It is particularly important in times oftrauma to maintain gut integrity.

Amino acid metabolism

The cells of the body are able to synthesize thecarbon skeleton and add the side-chains of 12 ofthe 20 amino acids, using amino groups fromother amino acids; these are the dispensable (ornon-essential) amino acids. However, there areeight amino acids that cannot be made by thebody in this way and, therefore, have to be sup-plied in the diet. These are called the indispens-able (or essential) amino acids.

They are leucine, isoleucine, valine, lysine,tryptophan, threonine, methionine and phenyl-alanine. Histidine is also indispensable for children, and also, in some circumstances, foradults. It has been proposed that this classifica-tion is too rigid, as it is recognized that someamino acids may become indispensable in cer-tain circumstances (Table 4.3).

The body is able to convert many aminoacids from one to another. It does this by theprocess of transamination, which involves mov-ing an amino group from a donor amino acid toan acceptor acid (called a keto acid), which inturn becomes an amino acid.

The remnants of the donor amino acid (the car-bon skeleton) are then utilized in other meta-bolic pathways, usually to produce energy or inthe synthesis of fatty acids. Alternatively, theymay themselves receive an amino group, and bereconverted to an amino acid.

Amino acids may also be broken down bythe process of deamination, in which the aminogroup, having been removed, is incorporatedinto urea in the liver, and eventually excretedvia the kidneys in urine. The amount of ureaexcreted daily is a useful indicator of the rate atwhich protein turnover is taking place, and canalso be used to calculate the protein needs of an individual. The remaining carbon fragmentcan be converted to pyruvate and then glucose,in which case the amino acid is known as‘glucogenic’. Alternatively, if it leads to the for-mation of acetyl coenzyme A, and then ketonebodies or fatty acids, the amino acid is called‘ketogenic’.

Several amino acids are both glucogenic andketogenic, meaning that their carbon skeletonscan give rise to both glucose and fats. Only theamino acids leucine and lysine are purely keto-genic, and cannot be used to make glucose.

These exchanges allow the body to makemaximum use of its protein supplies, both fromthe diet and from that which is recycled withinthe body (see Figure 4.3).

The amino acid pool

The amino acid pool contains amino acidsobtained from protein in the diet and the amino

Amino acids that maybecome indispensableunder certain circumstances

TABLE 4.3

Amino acid Situation when it may become indispensable

Cysteine and In the neonatetyrosine May also spare methionine and

phenylalanineArginine In urea cycle disorders

Metabolic stressTaurine In neonates and during growth

Prolonged parenteral nutritionGlutamine May be needed in trauma,

cancer and patients with immune deficiencies

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acids released from breakdown of cells and gen-eral metabolic processes of renewal in the body.From this pool, the cells of the body can takethe amino acids they need to produce the pro-teins they require. If the pool does not containthe appropriate amounts needed, a cell has twopossible options:■ it can simply make less of the protein it

requires, limited by the amino acid presentin least amounts; or

■ it can break down some of its own protein to release the amino acids it requires forsynthesis.Obviously neither of these alternatives is the

ideal solution; in both cases less protein thanrequired is present in the cell, either because somewas broken down to make new protein or becausetoo little was synthesized. If this situation con-tinues, there will be a deterioration of function. Itis, therefore, important that the amino acid pool isadequate for the body’s needs. This also meansthat it must contain the indispensable aminoacids in the right proportions, so that synthesiscan take place. If one of these amino acids is in

short supply at the time that it is needed, perhapsbecause the diet did not contain much, thensynthetic reactions will be restricted to an extentdetermined by this amino acid. This is thentermed the limiting amino acid, and this conceptis used later in the chapter in the discussion ofprotein quality.

The total size of the amino acid pool hasbeen estimated at 100 g, including the plasmaand smaller amounts in the tissues. It principallycontains dispensable (non-essential) amino acids,since the indispensable amino acids are usedrapidly or, if present in excess, are deaminated.The pool represents the balance of the fluxbetween the incoming amino acids (from dietand tissue breakdown) and the use of aminoacids for synthesis of proteins or for deaminationand energy production. It has been estimated thatthe total amount of protein turnover in a day isin the region of 250–300g; this is greater ininfants and less in the elderly. The balance is regulated by the needs of the body and the size of the pool. If the pool becomes too large, thenmore deaminating enzymes will be activated and

Figure 4.3 Summary of amino acid metabolism.

AMINO ACID METABOLISM ❚

65

amino acids will be broken down and their nitro-gen excreted as urea. The carbon skeletons willbe used for energy or to synthesize fat.

Since the body has no means of storingexcess protein or amino acids, eating more pro-tein than the body requires results in breakdownof amino acids, with the production of fattyacids, glucose and urea, and heat. Since we gen-erally live in warm houses and wear appropriateamounts of clothes, this excess heat is not usedfor maintaining body temperature, but is largelydissipated as waste heat.

If insufficient protein is eaten, the body has touse its own ‘endogenous’ protein to provide theamino acids needed for the pool and, therefore, to maintain normal protein turnover. In time, thetissue proteins will be seen to waste, and the abil-ity of the body to maintain all of the functionsrequiring protein will deteriorate. Eventually, astate of protein deficiency will occur.

If insufficient energy sources are being sup-plied to the body in the form of carbohydrate orfats (even if protein intake appears adequate),then protein will be degraded and used for energy,since the body’s first priority is to meet its energyrequirements from whatever source is available.When this happens, the amino acids are con-verted to glucose (a process known as gluconeo-genesis) and used for energy. This means that theyare no longer available for synthesis. This is awasteful use of protein by the body and is seen toan extreme extent in untreated diabetes mellitus,as well as in situations of physiological trauma(such as fever, burns, fractures or surgery), espe-cially if food intake is reduced. The consequencesare a decline in muscle bulk as well as reducedlevels of plasma proteins, enzymes and con-stituents of the immune system. Thus, for aminoacid use to be optimal, the energy needs must alsobe satisfied, preferably from fat and carbohydratesources, which are, therefore, described as ‘spar-ing’ protein.

The greatest part of amino acid metabolismtakes place in the liver; other sites, however,include the skeletal muscle and, to a lesserextent, the heart, brain and kidneys. Muscle is themain site of metabolism of the branched-chainamino acids (leucine, isoleucine and valine),and produces large amounts of glutamine and

alanine, which can be used for energy in fastingor other emergencies. The kidneys are also animportant site of amino acid metabolism, includ-ing gluconeogenesis, and production of ammo-nia from glutamine, which is essential for themaintenance of acid–base balance. In addition,the kidneys are responsible for ridding the bodyof nitrogenous waste from protein catabolism.

The brain has transport systems for theuptake of neutral, basic and dicarboxylic acids,and there is competition between amino acids forthe carrier systems. Several of the amino acidsact as neurotransmitters or as their precursors:■ glycine and taurine are believed to be

inhibitory neurotransmitters;■ aspartate is thought to be an excitatory

neurotransmitter;■ tryptophan is the precursor of serotonin

(5-hydroxytryptamine), an excitatory neuro-transmitter;

■ tyrosine is used in the synthesis ofdopamine, noradrenaline and adrenaline(the catecholamines);

■ a number of neuropeptides are found in thebrain; these have a wide range of functions,including regulating hormone release,endocrine roles and effects on mood andbehaviour.

Thus, changes in uptake of amino acids or vary-ing levels in the brain can have diverse effects.

Control of protein metabolism

Amino acid and thus protein metabolism isunder the control of the endocrine system.Recent evidence suggests that the body has awell-defended system for metabolic adaptation,which protects essential functions and internalhomeostasis. This is necessary in the face ofvarying protein intakes and changing internaldemands. Protein synthesis is promoted byinsulin, which facilitates the uptake of aminoacids into tissues. On the other hand, glucagon,catecholamines and glucocorticoids have theopposite effect, and promote protein degrad-ation. Growth hormone is an anabolic agent forprotein. However, the exact effects of these hor-mones may vary between tissues and at differ-ent levels of nutrient intake.

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For example, the effect of insulin on periph-eral tissue uptake of amino acids is maximal forthe branched-chain amino acids, but minimalfor tryptophan. Thus, after a carbohydrate-containing meal, which stimulates insulin release,the uptake of tryptophan into tissues, includingthe brain, is increased, as competing aminoacids are no longer present. This is believed tostimulate serotonin synthesis in the brain andmay be responsible for the drowsiness experi-enced after carbohydrate ingestion. This alsocontributes to a reduction in food intake.

Uses of proteins

Proteins serve a large number of functions in thebody. Some are key components in structure,some are enzymes, hormones or buffers, othersplay a part in immunity, transport of substancesround the body, blood clotting and many otherroles (see Figure 4.4 for a summary).

Body composition

Protein is a key component of the structure ofthe body. Each cell contains protein as part ofthe cell membrane and within its cytoplasm.Muscles, bones, connective tissues, blood cells,glands and organs all contain protein. This protein is synthesized during growth, repaired,maintained and replaced during life, and formsa source of amino acids that can be drawn on inemergencies, although at the expense of the tis-sue it comes from. Only the brain is resistant tobeing used as a source of amino acids for emer-gency use. Thus, the protein in our body struc-ture is not static, but a dynamic constituent thatis in a state of continuous flux.

Formation of enzymes

Almost all enzymes are proteins and thus proteinsare instrumental in facilitating most of the chem-ical reactions that occur in the body. This includesthe digestion of nutrients (including protein), theregulation of energy production in cells and thesynthesis of all the chemical substances found inthe body. Enzymes are essential to normal life.

Homeostasis

The physiological mechanisms of the body aimto maintain a constant internal environment inthe face of continued changes that might dis-turb it. This is achieved by the action of variousproteins operating in specific ways.

HormonesMany of these consist of amino acids. They actas the messengers carried in the circulation, andcontrol the internal environment; for example,by regulating metabolic rate (thyroid hormones),blood glucose levels (insulin, glucagon), bloodcalcium levels (parathyroid hormone, calcitonin),the digestion process (secretin, cholecystokinin)(CCK) and response to stress (adrenaline).

Acid–base balanceProteins act as buffers in the circulation byaccepting or donating H� ions and therebymaintaining a fairly constant pH in the bloodand body fluids.

Fluid balanceBecause of their size and inability to leakthrough the walls of the blood vessels, proteinsin the plasma exert an osmotic effect that holds

Figure 4.4 Summary of uses ofprotein.

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fluid within the circulation. This prevents excesspooling of body fluids in the tissue spaces. Areduction in the levels of albumin and globulincauses oedema as a result of loss of fluid fromthe circulation into the tissue spaces.

ImmunityProteins play a key role in the function of theimmune system. They are needed for normal cell division to produce the cellular components.In addition, the antibodies and other humoralagents that are released are composed of aminoacids. Thus, a protein deficiency will result indefective immune function. This is seen clearlyin children suffering from protein–energy mal-nutrition, who have an increased susceptibilityto infection as a result of poor immune function.There is good evidence that certain amino acidsmay have a more specific role in immunonutri-tion. Among those being studied, glutamine,which is a precursor for glutathione, improvesgut barrier function and may be an essentialnutrient for a number of immune system cells.Glutamine has been described as conditionallyessential in critically ill patients, when there istrauma or physiological stress. Other aminoacids that have been studied in similar situationsinclude arginine and taurine.

Transport

Many of the substances that need to be carriedaround the body from either the digestive systemor stores to sites of action cannot travel in theblood alone, usually because they are insolubleor potentially harmful. When these substancesare attached to proteins, particularly albumin orglobulins, transport is facilitated. The level ofcarrier protein present at any time may deter-mine the availability of the particular substanceto the tissues. Haemoglobin is a transportingprotein, serving to carry oxygen in the body. Inthis case, it is the ability of the haemoglobinmolecule to take up a large amount of oxygenthat provides the advantage over oxygen trans-port simply in solution by the blood. Reducedavailability of haemoglobin (either because ofiron or protein deficiency) will affect the provi-sion of oxygen to the tissues.

In addition, transport proteins also carrysubstances across cell membranes; for example,during absorption in the digestive tract. As wellas facilitating transport, proteins may also bindwith some constituents of the body to provide asafe method of storage; for example, iron isstored in association with ferritin.

Blood clotting

Several proteins found in plasma play an essentialrole in blood clotting, including prothrombin andfibrinogen. Failure to synthesize these (for exam-ple, in deficiency of vitamin K, which acts as acofactor) will result in prolonged bleeding times.

Other functions

Although not its primary role, protein can serveas a source of energy when insufficient carbo-hydrate and fat are available to meet the body’sneeds. Proteins also form the major componentsof the hair and nails, as well as the structuralframework of bones.

It is also important to note that non-proteinnitrogenous compounds are produced fromsome of the amino acids. Glycine is used inhaem, nucleic acid and bile acid synthesis.Other examples include the use of tryptophan tomake nicotinic acid and tyrosine in catechol-amine synthesis.

Nitrogen balance

An overall indicator of protein metabolism inthe body is the nitrogen balance, which is thedifference between nitrogen intake and nitrogenoutput. When the balance is positive, protein isbeing retained in the body, indicating tissue synthesis. A negative nitrogen balance occurswhen there is a net loss of protein from the body,either because there is catabolism or becauseprotein or energy intakes are insufficient to meetthe daily needs (see Figure 4.5).

When nitrogen intake and output are in equi-librium, then protein is neither being gained norlost. Nitrogen balance studies do not, however,tell us where the protein is being stored or catab-olized, or what its functions are. Not all nitrogen

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flux relates to protein: there is some metabolismof non-protein nitrogen taking place, and someretention of nitrogen may represent increases inthis fraction rather than in protein content.However, it is generally assumed that the nitro-gen (N) in Western diets is largely of protein ori-gin, and the conversion factor of N � 6.25 isused to convert between nitrogen and proteincontent. This implies that all proteins contain 16per cent nitrogen; in reality the amount of nitro-gen in proteins varies between 15.7 per cent inmilk and 19 per cent in nuts.

Losses of nitrogen can occur from the bodyvia a number of routes. Faecal loss of nitrogenrepresents unabsorbed dietary nitrogen togetherwith residual nitrogen from the digestive juicesand mucosal cells shed into the tract. In health,these losses are small. Nitrogen is lost in theurine in the form of urea (mostly), ammonia,uric acid and creatinine. The urea contentreflects dietary intake and, therefore, decreasesas protein intake falls. Creatinine levels are rela-tively constant, as these are related to the musclemass, and represent its daily turnover. In add-ition, nitrogen is lost daily in skin cells, hair,nails, sweat and saliva and, although it is possi-ble to measure these by meticulous study, inpractice, a constant figure is used.

Balance studies carried out when the diet isdevoid of protein are used to indicate the obliga-tory losses of nitrogen. Values obtained in suchstudies give an average obligatory protein lossof 0.34 g/kg body weight for adults (or 55 mg ofnitrogen/kg body weight).

Nitrogen balance studies have been criticizedas imprecise for a number of reasons. Theseinclude:■ overestimation of intake;■ incomplete estimation of losses – gaseous

nitrogen loses are usually uncounted (breathand colonic gases);

■ uncertainty about adaptation to changes inprotein intake.However, despite these shortcomings, there is

still a role for nitrogen balance data until newermethodologies are sufficiently reliable androbust. These include the use of tracer-labelledamino acid oxidation studies. The most com-monly used isotope is 13C, with measurement oflabelled CO2 excretion. These studies allow fac-torial assessments of metabolic demands, effi-ciency of utilization and requirement. However,it is still problematic to arrive at informationrelating to whole-body protein turnover.

Protein quality

If a protein is to be useful to the body, it shouldsupply all of the indispensable amino acids inappropriate amounts. If this is not the case, anysynthesis that is required can only take place bybreaking down existing proteins. Alternatively,limited synthesis may take place until all of theamino acid present in least amounts has beenused up. The body cannot synthesize incompleteproteins, therefore, synthesis is limited by thisamino acid. Such an amino acid is termed ‘limit-ing’, and the protein from which it comes wouldbe described as having low quality. How canthis be quantified?

Milk or egg proteins have traditionally beenused as the ‘reference proteins’, as their aminoacid pattern most nearly conforms to that of totalbody protein. Most recently, the amino acid pat-tern of human milk has been set as the standardagainst which all other proteins can be judged fortheir efficiency of meeting human needs.

Different sources of protein have been shownto match the required amino acid pattern tovarying extents, and combining different plantfoods, for example, makes it possible to obtainthe necessary amino acids from several sourcesand achieve an overall balance (Table 4.4).

Figure 4.5 Components of nitrogen balance.

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Populations have naturally been doing this forgenerations; there is nothing new about it andmany traditional dishes reflect this.

In addition, it is possible to complementprotein foods of plant origin with foods derivedfrom animals to compensate for the limitingamino acid. In particular, milk and its productsprovide good complementary protein to partnerthe plant foods. Examples of such traditionalmixtures include bread and cheese, macaronicheese, rice pudding, cereal and milk.

Measuring protein quality

Chemical scoreThis compares the amount of each indispens-able amino acid in the test protein with theamount of this amino acid in the reference pro-tein; the chemical score is the value of this ratiofor the limiting amino acid:

Amount of amino acid in Chemical test protein (mg/g)

� 100score

�Amount of amino acid in reference protein (mg/g)

The reference scoring pattern for the mostfrequently limiting amino acids was developedby the FAO/WHO/UNU (1985):

The calculation does not take into accountthe digestibility of the protein and is, therefore,a very theoretical value. Digestibility is particu-larly an issue for many plant-based diets andsome cereals, for example, millet and sorghum,and needs to be considered especially for chil-dren in developing countries.

Biological valueThe biological value (BV) of a protein is a measureof how effectively a protein can meet the body’sbiological need. To make this measurement, thetest protein is fed to an experimental animal as the sole source of protein, and the nitrogenretention and loss are measured. The greater thenitrogen retention, the more of the protein hasbeen used. (Remember that, if a protein cannot beused because it contains limiting amino acids, itcannot be stored and, therefore, is broken downand the nitrogen excreted as urea.)

or more precisely:

For egg protein, BV is 100; and for fish andbeef the value is 75. It is generally agreed that aBV of 70 or more can support growth, as long asenergy intakes are adequate.

For both BV and chemical score, the resultfor a single food is of relatively little relevance

Amino acid Reference score (mg/g protein)

Leucine 19Lycine 16Threonine 9Valine 13Methionine � cystine 17

The use of complementary foods to make up for limiting amino acids in someplant foodsTABLE 4.4

Plant food Limiting amino acid Useful complementary food Example of mealGrains (or cereals) Lysine, threonine Legumes/pulses Beans on toastNuts and seeds Lysine Legumes/pulses Hummus (chickpeas

with sesame seeds)Soya beans and other Methionine Grains; nuts and seeds Lentil curry and rice

legumes/pulsesMaize Tryptophan, lysine Legumes Tortillas and beansVegetables Methionine Grains; nuts and seeds Vegetable and nut roast

BV �Nitrogen retained � 100

Nitrogen absorbed

BV �

Dietary nitrogen � (urinarynitrogen � faecal nitrogen) � 100

Dietary nitrogen � faecal nitrogen

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because most people consume a mixture offoods in their daily diet.

Millward (1999) reports that ongoing researchinto the adequacy of protein intakes in dietsaround the world has shown that, even withrevised amino acid scoring methods, the prob-lem of inadequate protein or severely limitingamino acids is not as widespread as commonlyassumed.

Protein requirements

Requirement figures for protein are calculatedon the basis of nitrogen balance studies, whichestimate the amount of high-quality milk or egg protein needed to achieve equilibrium. The safe level of protein intake was established byFAO/WHO/UNU (1985) as 0.75 g/kg body weightper day. In addition to nitrogen balance results,increments were included for growth in infantsand children, calculated from estimates of nitro-gen accretion. In pregnancy, protein retention inthe products of conception and maternal tissueswas calculated and, for lactation, the proteincontent of breast milk in healthy mothers wasused to obtain the reference value.

Uncertainty is expressed about the accuracyof these balance studies because they give resultsthat are considerably higher than minimumnitrogen losses in adults on protein-free diets.Also the duration of the studies may not be suffi-cient for adaptation to occur. Finally, it is unclearhow the amount of energy given to the subjectsaffects the results.

Figures recommended in the UK (DoH, 1991)for adults are calculated on the basis of 0.75 gprotein/kg body weight per day. Values obtainedusing reference body weights for adults areshown in Table 4.5. Current intakes in the UK areconsiderably higher than the values recom-mended here. The National Food Survey (DEFRA2001) shows that the mean daily total proteinintake was 67 g, of which 41.1 g was of animalorigin. This intake represents 147 per cent of themean RNI for protein and, even in the largesthouseholds, the intake is well above the meanRNI at 117 per cent.

Major food groups providing protein wereshown to be:

Milk products and cheese 21.3 per centof total

Meat and meat products 32 per centCereals and cereal products 26 per cent

It is assumed that, in the UK, there is a suffi-cient variety of different protein sources to elim-inate concerns about protein quality. However,for those individuals whose diet contains a con-siderable amount of unrefined cereal and vege-table, a correction for digestibility of 85 per centis to be applied.

Report 41 (DoH, 1991) suggests that it is pru-dent to avoid protein intakes that are in excess ofan ‘upper safe limit’ of 1.5 g/kg per day, suggest-ing that such high intakes may contribute tobone demineralization and a decline in kidneyfunction with age. It has been found that there isa linear relationship between increases in animalprotein intake and calcium loss in the urine,although the relationship with bone demineral-ization is still unclear. More recent evidence haslargely failed to support concerns about effects ofhigh protein intakes on kidney function, unlessthere is pre-existing renal disease. A number ofcross-sectional studies in the USA and Britainhave shown an inverse relationship between protein intakes and blood pressure and stroke.However, the possible mechanisms involved are

Dietary reference values forprotein for adultsTABLE 4.5

Gender/age Estimated Reference average nutrient

requirement intake(g/day) (g/day)

Males19–50 years 44.4 55.550� years 42.6 53.3Females19–50 years 36.0 45.050� years 37.2 46.5

From DoH, 1991. Crown copyright is reproduced with thepermission of Her Majesty’s Stationery Office.

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yet to be discovered, and intervention studieshave been unable to replicate these effects.

Finally, it should be noted that those individ-uals with high energy needs, such as athletes, con-suming a typical Western diet, are likely to ingestprotein in excess of this ‘upper safe limit’, unlessthey make adjustments to the balance of macro-nutrients in their diet. This should preferably beachieved through consuming more carbohydrate,rather than more fat, but may be impractical interms of the volume of food required.

Many questions remain to be resolved andnew issues are continually being raised in thisfield. Some of these are briefly discussed below.■ Newer research on individual amino acids

suggests that requirement figures for indis-pensable amino acids may need to beincreased and, therefore, the safe level of pro-tein intake may need to be revised upwards.Given the prevalence of undernutrition in the world, such a revision would have enor-mous implications in terms of global foodpolicies.

■ The distinction between essential and non-essential amino acids may become less clear-cut, as studies have shown that there is somepotential for amino acid synthesis from urearesidues, by the colonic bacteria. Factors thatmight influence this synthesis and availabil-ity to the host may need to be considered inthe future.

■ It is already clear that needs for specificamino acids vary between individuals and at

different times of life and conditions. Theability to cope with these life situations mayalso depend on optimal amino acid avail-ability and the presence of other nutrients.

Protein deficiency

Insufficient protein intake is a problem for manypeople of the world, especially the poor in manycountries. It is rarely their only nutritional problem; the diet is likely to be low in energyand fat, and may contain marginal amounts ofmany nutrients. In addition, there are likely to be social, economic and environmental problems,which increase the likelihood of infection andreduce the availability of health care. Low levelsof educational achievement are also likely to be found in these societies owing to a lack ofopportunity.

Children are most likely to suffer from pro-tein deficiency in a complex picture of protein–energy malnutrition, which can take a number ofdifferent forms. Classically, the two main formsare marasmus and kwashiorkor; there is consid-erable debate as to whether these are separateconditions or two ends of the spectrum of thesame condition. They have been seen to occur inthe same village and even in the same child atdifferent times, suggesting a common cause. Thechild exhibits growth failure, in particular, aslowing of linear growth, resulting in stunting(Figure 4.6). Usually the child is miserable and

Figure 4.6 Example of cases of protein deficiency.

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irritable. There is likely to be liver enlargement,possibly oedema, changes to the hair and skin;the eyes may be sunken and also show signs ofvitamin A deficiency. Susceptibility to infectionis increased, and the coexistence of infection andmalnutrition may precipitate death.

The exact causes of this clinical picture areunclear. Low protein intake can result in many ofthe signs, with low albumin levels resulting inoedema. It is possible that an imbalance of aminoacids may be responsible, as the syndrome doesnot occur in wheat-growing areas, but is com-mon where cassava, yams, maize and plantainare the staple. Most recently, it has been sug-gested that food contaminated with moulds maybe responsible, or that a lack of antioxidants pre-vents the body coping appropriately with the freeradicals produced by toxins or infections.

Treatment involves restoring the nutritionalstatus of the body, while treating infections, elec-trolyte imbalances and hypothermia, all of whichmay be present in a sick child with protein–energy malnutrition. In addition, the whole fam-ily may need to be educated about nutrition andhealth to provide long-term improvement and toprevent the condition recurring.

Protein deficiency as part of more general-ized malnutrition also occurs in the communityand particularly in hospitalized patients inBritain. When pre-existing illness, poor appetite,surgical or medical treatment and prolongedhospitalization coincide, there is the likelihoodthat insufficient nutrients will be consumed.Thus, although the process may not necessarilystart as protein deficiency, if food intakes areminimal, protein catabolism will quickly follow.

In addition, the catabolic response to traumaalso increases protein breakdown, contributingto the negative nitrogen balance. Particularlyvulnerable are overweight patients, in whomadiposity masks muscle wasting. Negativenitrogen balance may persist for some timebefore action is taken. Reports published duringthe last 20 years have indicated a prevalence ofmalnutrition in hospital patients ranging from20 to 50 per cent in different studies. Severalpolicy documents have been produced duringthis time and nutrition teams established inmany hospitals.

It is recognized that undernutrition hasmajor implications on the clinical outcome forthe patient. These include:■ increased post-operative complications and

poor wound healing;■ increased risk of pressure sores;■ poor immune response and increased sus-

ceptibility to hospital infections;■ reduced muscle strength, weakness, immo-

bility, inability to cough;■ apathy and depression;■ reduced quality of life;■ prolonged hospital stay;■ increased mortality.In addition to these, there are increased eco-nomic implications for the hospital.

The causes of undernutrition may be disease-related or arise for social or psychological rea-sons. In addition, they may have their origins in hospital services, routines and procedures. Thelatter may include the food provided, the timingof meals in relation to other procedures, and thefacilities and help available for eating. The dieteticand catering services can address some of these,others need to be addressed at the ward level.Protocols should be in place to identify and man-age patients at risk of undernutrition. The BetterHospital Food project (DoH, 2000), launched in2001 in the UK aims to improve meal provision,through greater choice and flexibility so that foodcan be provided to suit patient need and prefer-ences, and ensure adequate nutrition.

It is important, therefore, that patients areweighed regularly and that assessments of nutri-tional status are made, such as grip strength,mid-arm muscle circumference or plasma albu-min levels. Suitable provision and help with oralconsumption of foods or supplements is neededand more vigorous nutritional support via otherroutes when necessary. Careful monitoring of at-risk hospital patients is necessary, with all of the medical team needing an awareness of the potential problem. Increasing knowledgeand awareness of the importance of nutrition astreatment among doctors is seen as a corner-stone for any improvements. This has beenaddressed by the Royal College of Physicians(2002), but will take time to come into effect atward level.


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DEFRA (UK Department for Environment, Food and Rural Affairs) 2001: National food survey 2000.Annual report on food, expenditure, consumption and nutrient intakes. London: The StationeryOffice.


DoH (UK Department of Health) 2000: The NHS plan: a plan for improvement, a plan for reform.London: Department of Health.

FAO/WHO/UNU 1985: Energy and protein requirements. Report of a joint FAO/WHO/UNU ExpertConsultation. WHO Technical Report No. 724. Geneva: WHO.

Food Standards Agency 2002a: Food portion sizes, 3rd edn. London: The Stationery Office.Food Standards Agency 2002b: McCance and Widdowson’s The composition of foods, 6th summary

edn. Cambridge: Royal Society of Chemistry.Jackson, A.A. 2003: Human protein requirement: policy issues. Proceedings of the Nutrition Society

60, 7–11.Lennard Jones, J.E. 1992: A positive approach to nutrition as treatment. London: Kings Fund Centre.

1 Draw a flow diagram to show the movement ofamino acids within the amino acid pool whenthe body has adequate supplies of protein.Show how this changes when protein is in short supply.

2 Explain why a protein deficiency might result in:a oedemab an increased susceptibility to infection.

3 It has been suggested that Western dietscontain excessive amounts of protein.

a Keep a record for 1 week of how many times you eat protein-rich food. Use theinformation in Table 4.2 to help you.

b Are your sources of protein mostly fromanimal or plant foods, or a combination ofboth of these?

c Can you identify combinations of differentprotein sources in your meals, such as those discussed in the chapter?

d Compare your results with those of others in your group. What do you find?

STUDY QUESTIONS

1 Proteins are composed of combinations of amino acids, creating an enormous diversity of proteins.2 Twenty different amino acids occur in proteins. The body uses these very efficiently, and is able to

convert some of the amino acids into others. However, eight of them cannot be made in the body, andmust be provided in the diet; they are the indispensable amino acids. At certain times, for example, inyoung children, or in stress and trauma, other amino acids may become indispensable.

3 Proteins fulfil a great many functions in the body, acting as hormones, enzymes, carriers andmaintaining homeostasis.

4 Dietary sources of protein may be of animal or plant origin. The ability of the body to make full use ofthe amino acids supplied depends on the energy intake and the pattern of the amino acids in the protein.An inadequate amount of one amino acid may limit the usefulness of the whole protein, unless it iscombined with a complementary source, which provides the limiting amino acid.

5 Protein requirements are based currently on nitrogen balance studies.6 Intakes of protein in the UK are above the reference nutrient intake (RNI) in healthy adults. The hospital

patient may, however, be at risk of protein deficiency, which may compromise recovery.

SUMMARY

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McWhirter, J.P., Pennington, C.R. 1994: Incidence and recognition of malnutrition in hospital.British Medical Journal 308, 945–8.

Millward, D.J. 1999: The nutritional value of plant-based diets in relation to human amino acid andprotein requirements. Proceedings of the Nutrition Society 58, 249–60.

Royal College of Physicians 2002: Nutrition and patients, A doctor’s responsibility. London: RoyalCollege of Physicians.

Scrimshaw, N.S., Waterlow, J.C., Schurch, B. (eds) 1996: Protein and energy requirements sympo-sium. European Journal of Clinical Nutrition 50 (suppl. 1).

Waterlow, J.C. 1995: Whole body protein turnover in humans – past, present and future. AnnualReview of Nutrition 15, 57–92.

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fats


❏ describe the nature and characteristics of fats important in human nutrition;❏ explain the importance of the essential fatty acids;❏ discuss the role of fat in the diet and trends in fat consumption;❏ study the transport of fats in lipoproteins;❏ discuss the role of fat in the body;❏ discuss the part played by adipose tissue in metabolism.


❏ discuss the nature of various fats in the diet and the nutritional importance of the different types;❏ discuss the advantages and disadvantages of fat in the diet;❏ describe the current levels of fat intake in the UK;❏ discuss the importance of omega-3 fatty acids in the body;❏ explain the role of adipose tissue;❏ understand the general importance of fat in the body and its role in health.

All living cells contain some fat in their structure,since fatty acids are essential components of cellwalls and intracellular membranes. In addition,mammals and birds store fat throughout the body,especially between the muscles, around internalorgans and under the skin. Many fish have fatstored exclusively in the liver, but in the oily fish(like herring and mackerel) it is present through-out the flesh. In the plant kingdom, fats are foundin the fruits of various plants such as olives,maize, nuts and avocados. Plants manufacturefats by photosynthesis, the same process that theyuse to make carbohydrates. Animals use or storethe fat they ingest, or can synthesize fat from sur-plus energy taken in as carbohydrates or proteins.This does not generally apply in humans undernormal circumstances. Advice on healthy eatingencourages us to reduce our intake of certain

types of fats and increase others. Names such ascholesterol, polyunsaturates, omega-3s are usedby food manufacturers and can be very confusingfor many people. To be able to understand therationale and the details of this advice, it is neces-sary first to understand the nature of fats, andhow this is related to their behaviour in the body.Only then can we interpret the advice both forourselves and others.

What are fats?

Fats are substances that are insoluble in water,but soluble in organic solvents like acetone. In addition, fats are greasy in texture and arenon-volatile. When we think about fats in thediet, most people make a distinction between

C H A P T E R

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fats, which are solid at room temperature, andoils, which are liquid. Chemically, however,these two groups are similar; the major attrib-utes that produce the differences in solubilityare size of the molecule and types of bondspresent. To the chemist and biochemist, all ofthese compounds are ‘lipids’. In nutrition, themost important lipids are triglycerides (or tria-cylglycerols), which constitute over 95 per centof the fat we consume. In addition, there arephospholipids, sterols and fat-soluble vitaminsin the diet and body tissues. If we consider anaverage fat intake of 100 g per day, this wouldbe made up as follows:

90–95 g triglycerides4–8 g phospholipids

1 g glycolipids350–450 mg cholesterol

There are also other lipids in nature that are notimportant in nutrition.

Like carbohydrates, lipid molecules containcarbon, oxygen and hydrogen atoms linked in aspecific and unique way. The simplest lipids arethe neutral fats (triacylglycerols or triglycerides).

Triglycerides

These are the building blocks of most fats in thebody. Structurally, they are made up of a back-bone of glycerol to which three fatty acids areattached. Glycerol is a very simple molecule.When a fatty acid combines with glycerol, the linkage occurs between the –OH group in the glycerol and the –COOH group of the acidby esterification, with the loss of a molecule of water.

Usually three different fatty acids are attachedto the glycerol molecule, creating a huge diversityof triglycerides.

Triglycerides are readily broken down andresynthesized. A fatty acid can also be removedfrom the glycerol molecule by de-esterification,which occurs during the digestion of fats.Resulting products are diglycerides and mono-glycerides, containing two or one fatty acid,respectively. Fatty acids can be replaced onglycerol molecules by re-esterification. Thesetwo processes create particular triglycerides tomeet the specific needs of the body.

Fatty acids are chains of carbon atoms withhydrogens attached in the form of methylene(–CH2) groups. At one end of the chain is a methylgroup (–CH3), and at the other end an acidgroup (–COOH). The simplest of the fatty acids isacetic acid with the formula CH3.COOH; thus,the chain is only two carbons long. Most nat-urally occurring fatty acids contain even num-bers of carbons in their chain, normally rangingfrom 4 to 24 carbons. Thus, the basic formulafor a fatty acid is CH3.(CH2)n.COOH, where n isany number between 2 and 22.

Fatty acids with six or fewer carbons may bedescribed as ‘short chain’, those containing 8–12carbons are ‘medium-chain’, and those in whichthe chain is 14 carbons or more are ‘long-chain’fatty acids. The human diet contains mostly

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long-chain fatty acids, with less than 5 per centcoming from those having fewer carbons. Themost commonly occurring chain lengths are 14and 16.

No fat consists of a single type of triglyceride.In butter, for example, the main fatty acidsattached to glycerol are butyric, oleic and stearicacids, although there are 69 different fatty acidsactually present.

It is the identity of the fatty acids presentwithin a triglyceride that determines its physicalcharacteristics. Thus, a triglyceride made up pre-dominantly of short-chain fatty acids is likely tobe a hard fat, whereas one consisting of long-chain fatty acids will have a lower melting point,and may even be an oil at room temperature. In addition, the proportions of saturated andunsaturated fatty acids present will also affect itshardness.

Types of fatty acids

Fatty acids occurring in nature can be dividedinto three categories:■ saturated fatty acids;■ monounsaturated fatty acids with one double

bond; and■ polyunsaturated fatty acids with at least two

double bonds.In a saturated fatty acid, the carbon atom holdsas many hydrogens as is chemically possible; it is said to be ‘saturated’ in terms of hydrogen.In an unsaturated fatty acid, there are one ormore double bonds along the main carbon chain,known as ethylenic bonds. Each double bondreplaces two hydrogen atoms. If there is just onedouble bond, the acid is monounsaturated, iftwo or more double bonds are present, the fattyacid is polyunsaturated.

Implications of unsaturationThe location of double bonds in a polyunsatur-ated fatty acid is not random. Multiple doublebonds are separated by a methylene group, asfollows:

If the location of the first double bond is identified, the remainder can be predictedfrom this. A system of nomenclature has beendevised that classifies unsaturated fatty acidsinto families, according to the position of the firstdouble bond. These are the omega (also known asn-) families: 3, 6 and 9. The families of the com-mon fatty acids are given in Table 5.1, togetherwith the number of carbon atoms and, in the caseof the unsaturated fatty acids, the number ofdouble bonds present. Fatty acids from one fam-ily cannot be converted into another family, anyinterconversion can only occur within the samefamily.

Where double bonds exist, there is a possibil-ity of cis or trans geometric isomerism, whichaffects the properties of the fatty acid. Most naturally occurring forms are the cis isomers, inwhich the hydrogen atoms are on the same side ofthe double bond. Figure 5.1 shows the structuralarrangement of different fatty acids types. In cisconfigurations, the molecule is folded back,kinked or bent into a U-shape. In this arrange-ment, fatty acids pack together less tightly,increasing, for example, the fluidity of mem-branes. When the hydrogen atoms are arrangedon opposite sides of the double bond in transconfiguration, the molecule remains elongatedand similar to a saturated fatty acid. This allowsthe trans fatty acid molecules to pack moretightly together, and raises the melting point ofthe fat. To the consumer, this means that the fat is harder.

Trans fatty acids are produced as a result ofprocessing and are thus found in products con-taining hardened fats, such as hard margarine,pastries, biscuits and meat products. In addition,trans fatty acids are produced during transform-ations by anaerobic bacteria in the rumen of sheepand cows, so that some trans fatty acids may befound in meat and products from these animals,such as milk and dairy products. Evidence isaccumulating that trans fatty acids have adverseeffects in the body and this is discussed further inChapter 14.

A further consequence of unsaturation, particularly in polyunsaturated fatty acids, isthat the spare electrons are highly reactive

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and vulnerable to oxidation. In the presence of free radicals, such as ‘singlet’ oxygen or reactive hydroxyl groups, the double bonds can be attacked, leading to the formation of

lipid oxides or peroxides. These change theproperties of the fat, and may lead to malfunc-tion and disease. Free radicals arise in the body as part of normal metabolic processes

Figure 5.1 Spatial configuration of saturated, cis and trans unsaturated fatty acids.

Classification of fatty acids by saturation, chain length and familyTABLE 5.1Type of fatty acid Name Number of carbon atoms:

double bonds (fatty acid family)Saturated Butyric acid 4

Caproic acid 6Caprylic acid 8Capric acid 10Lauric acid 12Myristic acid 14Palmitic acid 16Stearic acid 18Arachidic acid 20

Monounsaturated Palmitoleic acid 16:1Oleic acid 18:1 (n-9)Eicosenoic acid 20:1 (n-9)Erucic acid 22:1 (n-9)

Polyunsaturated Linoleic acid 18:2 (n-6)Alpha-linolenic acid 18:3 (n-3)Arachidonic acid 20:4 (n-6)Eicosapentaenoic acid (EPA) 20:5 (n-3)Docosahexaenoic acid (DHA) 22:6 (n-3)

Note: In the shorthand system used in the table, the number of carbon atoms precedes the colon, the number of double bonds follows. The allocation to specific fatty acid families occurs on the basis of the position of the first doublebond in the molecule, counting from the methyl end. Thus in the n-3 family, the first double bond occurs on the thirdcarbon from the methyl end, in the n-6 and n-9 families, these occur on the sixth and ninth carbons, respectively.

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and can thus readily attack polyunsaturated fattyacids. The resulting products are themselveshighly reactive, triggering a chain reaction andproducing more highly reactive products. Thebody has a complex defence mechanism againstsuch reactions in the form of antioxidants,which exist both intracellularly and extra-cellularly, and whose function is to react withthe free radicals and thus inactivate them. Thereis more discussion about antioxidants inChapter 14.

Essential fatty acids

Although the body can synthesize most of the fat it requires, it has been known since theearly part of the twentieth century that certainof the polyunsaturated fatty acids cannot besynthesized and must be supplied in the diet. If they are excluded, a deficiency syndrome will develop, which in animals has been shownto include retarded growth and skin lesions,such as dermatitis. This deficiency can alsooccur in humans. Consequently, these fattyacids are known as ‘essential fatty acids’.Occasionally, you will find them referred to as‘vitamin F’.

The essential fatty acids are linoleic (18:2, n-6) and alpha-linolenic (18:3, n-3) acids.Vertebrates lack enzymes to introduce doublebonds at the n-3 and n-6 position, and cannot,therefore, synthesize members of these fatty acidfamilies. However, if acids containing these dou-ble bonds (i.e. the essential fatty acids) are pro-vided in the diet, other members of the familycan then be produced by a series of desaturation(adding a double bond by removing hydrogen)and elongation (adding two carbon atoms) reactions:

Moreover, there is competition between thefatty acid families for the enzymes involved,with the result that a predominance of one family (e.g. n-6 acids) in the diet can limit thesynthesis of some of the larger members of then-3 family. For this reason, both n-6 and n-3fatty acids should be supplied in sufficientamounts in the diet.

An intermediate product in the conversionof linoleic acid to arachidonic acid (n-6 family),is gamma-linolenic acid (GLA). This is suppliedin quite large amounts by some unusual plantoils, particularly evening primrose oil, borageand blackcurrant seed oils. Many claims aremade for the beneficial effects of these oils,especially evening primrose, although theredoes not currently appear to be an identifiedrole for GLA.

More recently, interest has focused on the n-3fatty acids contained in fish oils. These supplyvery long chain n-3 acids, such as eicosapen-taenoic and docosahexaenoic acids, which arenot made in large amounts in the body. They areparticularly important in the development ofthe nervous system and retina in young infants,and a dietary source is needed in very early life.The ability to convert the smaller n-3 acids toEPA and DHA does exist in the young infant,but probably is not sufficiently active to pro-duce adequate amounts.

Normally, breast milk produced by mothersconsuming mixed diets would supply sufficientamounts of DHA, but formula-fed infants mayreceive inadequate quantities, and some milksare now being formulated with additional long-chain polyunsaturated fatty acids. Pre-termbabies are particularly vulnerable to receivinginsufficient amounts of these, and again need toobtain a fortified feed to ensure their intake.

18:2 (n-6)Linoleic acid

18:3 (n-6)Gamma-linolenic

acid

20:3 (n-6)Dihomo-gamma-

linolenic acid

20:4 (n-6)Arachidonic acid

18:3 (n-3)Alpha-linolenic

acid

18:4 (n-3) . . . 20:5 (n-3)Eicosapentaenoic

acid (EPA)

22:6 (n-3)Docosahexaenoic

acid (DHA)

Diet

Diet

(Note: Some of the intermediate acids have been omitted from the n-3 series, for clarity.)

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80

The relative proportions of n-6 and n-3acids in the Western diet have changed in thelast 30 years for a number of reasons.■ There has been an increase in the consump-

tion of vegetable oils, such as corn and sunflower oil as a result of healthy eatinginitiatives, to replace the traditional con-sumption of butter and other animal fats.

■ Total intakes of meat from ruminant animals(beef and lamb) that are a source of n-3 fattyacids, have fallen. Furthermore, the n-3 acidcontent of the meat has also declined as the animals are fed less on grass and moreon alternative concentrates to maximizeproduction.

■ Consumption of oily fish (and total fish) hasbeen declining over this period, resulting inlower intakes of n-3 acids.Consequently, there is concern that insuffi-

cient quantities of n-3 acids can be synthesizedin the body, as there is too much competitionfrom the n-6 acids. This has potential implica-tions for the metabolic products derived fromthese acids and their effects in the body. There may be consequences within membranesthroughout the body, as well as effects on neuro-transmitter functions in the brain and on mood.

Evidence from a number of studies acrossEurope indicates that the ratio of n-6 to n-3acids is approximately 6:1. Proposals have beenmade in the USA and Europe that the intake ofn-3 acids should increase, without any furtherincreases in n-6 acids, to reduce this ratio.Strategies to achieve this and safety considera-tions need to be considered.

Further discussion of the possible beneficialeffects of n-3 fatty acids is to be found inChapter 14.

Conjugated linoleic acid (CLA)

A group of isomers of linoleic acid, containingdifferent geometrical double bond configura-tions, have become of interest. The double bondsare conjugated or contiguous, rather than meth-ylene-separated, as they are in linoleic acid. Thetwo double bonds can be in carbon positions 8and 10, 9 and 11, 10 and 12, or 11 and 13. Eachof the double bonds can also be in the cis or

trans configuration, and this results in a numberof possible isomers. The most studied of these isC18:2 c9t11 isomer. This isomer has also beencalled rumenic acid, as it is predominantly pro-duced in the rumen of cows and sheep. The maindietary sources of this acid are, therefore, dairyproducts and meat from ruminants. CLA hasbeen reported to have anticarcinogenic, anti-atherogenic and immune-modulating potential,although the mechanisms are unclear. Bodyweight gain, with reduced fat mass andincreased protein, has been shown in mice. CLAappears to be safe at doses up to ten times thosenormally found in the diet. Research into itsbioavailability and potential benefits of natu-rally occurring or supplemented CLA is ongoing.

Other lipids

Besides triglycerides, important lipids in nutri-tion are phospholipids and sterols. Phospho-lipids are closely related to triglycerides, as theycontain a glycerol backbone and two fatty acids.However, the third fatty acid is replaced by aphosphate group and a base. The commonestphospholipid, lecithin (also called phosphatidyl-choline), contains choline as the base. It is widelydistributed in cell membranes throughout thebody and is also a component of the surfactantin the lungs, which facilitates breathing by redu-cing surface tension in the alveoli. Other basesfound in phospholipids include serine, inositoland ethanolamine.

All phospholipids serve an essential func-tion in the body, as their structure contains botha hydrophobic (water hating) and a hydrophilic(water loving) area. This allows them to associ-ate with both lipid and aqueous compounds inthe body, and to serve as an emulsifying agent,allowing these two dissimilar parts to coexist.Their role is particularly important in cell mem-branes, and high concentrations are found inthe brain and nervous system. Sphingomyelin isa phospholipid occurring in the myelin sheath ofnerve fibres. All the phospholipids can be syn-thesized in the body and are, thus, not essentialin the diet.

Sterols are ringed structures containing car-bon, hydrogen and oxygen. The most prevalent

FATS IN THE DIET ❚

81

example of this group in animals is cholesterol(Figure 5.2), which is a waxy substance that canbe synthesized by the body from acetyl coenzymeA. The main site of synthesis is the liver, althoughall cells of the body can make it. The human bodytypically contains about 100g of cholesterol, ofwhich 7 per cent is found in the blood, and theremainder distributed in all cells of the body.Here, cholesterol plays a number of roles:■ maintenance of the structure and integrity

of cell membranes;■ regulation of the fluidity of cell membranes;■ facilitation of the communication between

the cell and its environment, including trans-port across the membrane;

■ limiting the leakage of Na and K ions acrossthe membrane;

■ synthesis of bile acids, which are needed forfat absorption;

■ synthesis of hormones, including the sexhormones, steroids and vitamin D.In the diet, cholesterol is only found in foods

derived from animals. Plant foods contain phyto-sterols, the most important being beta-sitosterol,which is found in nuts, cereals and fats and oils.Vegetarian diets are low in cholesterol, unlessthey include some animal products, like milk andeggs. Body cholesterol levels in an individual arekept fairly constant, with synthesis decreasing asdietary intake increases and vice versa. Absorp-tion of cholesterol is variable, ranging from 15 to60 per cent of dietary intake. Large intakes ofphytosterols may inhibit cholesterol absorptionand this has been utilized in a number of func-tional products developed to lower cholesterollevels. Cholesterol is excreted from the body inthe faeces, having been secreted into the digest-ive tract in the bile produced by the liver.

Levels of cholesterol in the blood are partlygenetically determined, so that effects of dietaryintake may be quite variable. Plasma cholesterollevels in some individuals respond minimally tochanges in dietary intake of cholesterol, while inothers the response is much greater. Raisedblood cholesterol levels are a major risk factor inthe development of cardiovascular disease and,for this reason, a great deal of research has beenundertaken to discover the factors which affectthem. These are discussed further in Chapter 14.

Fats in the diet

Nutritionists may describe fats in the diet as ‘visi-ble’ or ‘invisible’ fats (see Figure 5.3). Visible fatsare those that can be clearly seen in our food;these include the spreading fats, cooking oils andthe fat around pieces of meat. As this fat is obvi-ous, the consumer can quite readily make aneffort to reduce it – by using less spread on bread,by not using oil in frying and by trimming the fatoff meat.

Figure 5.2 Chemical structure of cholesterol. Figure 5.3 Sources of visible and invisible fats.

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Invisible fat is more difficult to remove. This is the fat that is often integral in a food product,for example, the fat in egg yolk, the fat containedwithin tissues in meat and fish, in nuts and, par-ticularly, in processed and manufactured foods,such as sausages, burgers, pies, biscuits, cakes,pastries and chocolate. It is clearly more difficultto reduce this fat – it involves either changingthe product by making it with less fat or simplyeliminating the food from the diet. Some successhas been achieved by food producers in pro-moting lower fat milk and dairy products, andlower fat versions of some processed foods. A major difficulty is that the consumer oftendoes not appreciate how much fat is contained ina food, because it cannot be seen. Moreover, thelabelling of foods may be often confusing, withessentially meaningless slogans, such as 90 percent fat free or 30 per cent less fat, providing no information about how much fat we are actually eating.

Some examples of the fat contents of selectedfoods are given in Table 5.2.

Trends in intakes of fats

Historical records suggest that fat intakes inmany parts of Europe increased quite markedlyat the start of the twentieth century, rising froma level of around 20 per cent of the total energyin the late nineteenth century, to values around30 per cent by the 1920s. Studies from this eraare not necessary comparable with today’smethods, but they do indicate a rapid increaseover a relatively short time. Expressed as a per-centage of the total energy intake, fat intake hasrisen steadily since data have been collected bythe National Food Survey. Levels in the 1940swere around 34 per cent of total energy.Throughout the 1950s and 1960s, they rose toreach 41 per cent and continued at a slower rateto reach 43 per cent by the mid-1980s. Levels

Food Fat (g/100 g) Fat (g/average Energy serving) from fat (%)

Cheddar cheese 34.9 14.0 75.5Cottage cheese 4.3 2.2 38.3Boiled egg 10.8 5.4 66Milk: full-fat 3.9 7.8 53.2Milk: semi-skimmed 1.7 3.4 33.2Milk: skimmed 0.2 0.4 5.6Cream: single 19.1 5.7 89.1Cream: double 53.7 16.1 97.4Butter/soft margarine 82.2 8.2 99.4Low-fat spread 37.6 3.8 92.7Beefburger 23.9 21.5 65.3Beef pie 19.4 28.1 56.3Lean beef, roast 6.3 5.7 28.1Cheese and tomato pizza 10.3 23.7 33.5Digestive biscuit 20.3 2.6 39.2Rich fruit cake 11.4 8.0 29.9Doughnut with jam 14.5 10.9 38.9Chocolate bar 30.7 16.6 53.1Potato chips 6.7 11.1 31.9Baked potato with skin 0.2 0.4 1.3


TABLE 5.2 Fat contents of selected foods per 100 g, per average servingportion and as per cent energy from fat

FATS IN THE DIET ❚

83

have gradually been falling since this time, andin 2000, the Department for Environment, Foodand Rural Affairs (DEFRA) (2001) found that fatcontributed 38.2 per cent of total energy intake.It is worth noting that carbohydrate intakeshave mirrored this trend, with an initial fall, fol-lowed by a rise in the percentage of energy fromcarbohydrate. The implications of these changesfor health are discussed in Chapter 8.

It is important to remember that the figuresdiscussed above reflect the percentage of energyfrom fat in the total energy intake. The actualamount of fat consumed has been decreasing, asnoted by successive National Food Surveyreports. There has been a greater reduction infat intakes in the higher than in the lowestincome group, so that fat intakes are now mar-ginally greater in this latter group. The data areshown in Table 5.3. On average, the differencein fat intake between social groups, regions andfamilies within the UK is relatively small. Muchgreater differences are seen if culturally differ-ent societies are compared.

One should remember, however, that therehas been a progressive trend towards eating out-side the home, which is more frequent in Group Athan Group D households. Therefore, the recordedintakes do not include all of the food consumedby individuals. Eating out was measured for thefirst time in 1994, and the National Food Surveyreports show that foods eaten out have a higherpercentage fat content than those eaten at home.

In addition to changes in the total fat intake,there has also been an alteration in the balanceof the saturated, monounsaturated and poly-unsaturated fatty acids in the diet. The changesreported by DEFRA (2001) in the percentage ofenergy from the main groups of fatty acids areshown in Table 5.4. These values reflect trends infood consumption patterns, with a decline in theconsumption of whole milk, butter, margarineand lard, and increases in the intake of oils andspreads made from vegetable oils. Many of thesechanges have been prompted by advice onhealthy eating in the last two decades and theresponse of food manufacturers.

Year Population mean Group A Group D

Fat (g) Energy Fat (g) Energy Fat (g) Energy (Calories) (Calories) (Calories)

1950 101 2474 109 2542 97 23791960 115 2630 120 2600 106 25401970 121 2600 124 2520 108 24701980 106 2230 106 2150 105 22401990 86 1870 86 1710 86 18902000 74 1750 68 1600 75 1720

Trends in total fat (g) and energy (Calories) intakes, per person per day,showing mean population figures and intakes in the highest (Group A) andlowest (Group D) income groups studied by the National Food Survey (DEFRA,2001). The figures do not include confectionery and soft or alcoholic drinks

TABLE 5.3

Percentage of energy from the main groups of fatty acidsTABLE 5.4Year Saturated Monounsaturated Polyunsaturated

fatty acids fatty acids fatty acids1972 19.3 15.9 4.31980 18.9 16.0 4.61990 16.7 15.3 6.72000 15.0 13.5 6.9

❚ FATS

84

Sources of fat in the British diet

Table 5.5 shows the main sources of fat and fattyacids in the British diet, based on data from theNational Food Survey 2000 (DEFRA, 2001). Therehave been some advances in the breeding andparticularly butchering of animals in the lastdecade, so that new analyses of meat available inthe UK show reductions in the fat content oflamb, beef and pork, with the greatest reductionsachieved in pork. To an extent it has also beenpossible to alter the fatty acid composition of the fat in meat by manipulating the types of fatsfed to animals. This is more successful in non-ruminants, such as pigs and poultry, than inruminants, as these tend to saturate fat by bacter-ial action in their rumen.

Sources of essential fatty acids

The parent acid of the n-6 polyunsaturated fattyacid (PUFA) family, linoleic acid occurs in meat,eggs and nuts (walnuts, brazil nuts, almonds andpeanuts). It also occurs in seeds used for oils andspread, such as sunflower, soya, corn, sesameand safflower. The parent of the n-3 PUFA fam-ily, alpha-linolenic acid is found in dark green,leafy vegetables and meat from grass-fed rumin-ants. Oils derived from nuts and seeds are also a source of this acid (as well as the nuts them-selves). Examples include walnuts, peanuts,almonds, soya, rapeseed and linseed. The longermembers of the n-3 family are found in oil-richfish, such as sardines, pilchards, salmon, trout,herrings, mackerel and fresh (not canned) tuna.

Cod liver oil is also a rich source, although not acommon component of the diet.

Various spreads, margarines and butters containdifferent amounts and proportions of fatty-acidtypes. Prepare a chart of the ones commonly foundin your local supermarket or grocery store, andcompare the percentages of total fat, proportionsof different types of fatty acids and the amount offat per serving, or per 100 g in each. You can alsoinclude some cooking oils in this survey.■ Which type of spread appears to have the

lowest fat content?■ Does this spread also have the lowest content

of saturated fatty acids?■ What are the implications of your results for

someone trying to eat less fat?

Activity 5.2

Look at a number of foods that are claimed tohave less fat, such as sausages, cheesecake, bacon,burgers, salad dressings. Work out how much fatthere is in a typical serving, or per 100 g.■ Is it less than in the comparable ‘normal fat’

product?■ How much less is it?■ How many fewer grams of fat will you eat by

substituting this food in your diet?

Activity 5.1

TABLE 5.5Food group Percentage of contribution to total

Fat Saturated Monounsaturated Polyunsaturated fatty acids fatty acids fatty acids

Fats and oils 26 21 28 41Butter 6 10 5 1.5Spreads/oils 16 6.5 18.5 34Meat and meat products 22 22 28 15Milk, dairy and cheese 17 28 14 4Cereals and cereal products 16 17 16 16

Sources of fat and fatty acids in the British diet (calculated from DEFRA, 2001)

DIGESTION AND ABSORPTION OF FATS ❚

85

Why do we eat fat?

People who are culturally accustomed to eatingfat, such as the populations of the Western world,find that food with a significantly reduced fatcontent is unpalatable. This is because Westernersare used to the way that fat enhances the palat-ability of food. Food containing fat creates a par-ticular ‘mouthfeel’, a feeling of creaminess andsmoothness when taken into the mouth, which isrelated to the presence of fat emulsions in a food.

In addition, fat enhances the flavour offoods, as many of the substances responsible for‘flavour’ and ‘odour’ are volatile fatty sub-stances, originating from the lipid in the food.Adding fat to a food can, therefore, enhance itssensory appeal. For example, frying or roastingfoods (such as potatoes) produces flavours thatcannot be obtained by boiling the same food.Hence the popularity of potato chips (Frenchfries). Aromas associated with oranges or coffeeare also oil-based. Sometimes the presence ofthese fat-based smells can be very unpleasant ina kitchen; cooking oil that has been used severaltimes, and thus contains a number of fat oxida-tion products, releases a very unsavoury smell.

Fat is a concentrated source of energy. Itsupplies 37 kJ/g (9 Calories/g), which is morethan any other macronutrient. It has the advan-tage that a large amount of energy can be consumed in a relatively small volume of food.This may be important for people with a smallappetite or those whose energy needs are veryhigh, such as athletes or those undertaking otherstrenuous activity. In addition, it can be helpfulwhen patients are being fed by a tube, where asmaller volume of feed is an advantage.

However, the disadvantage of the high energyconcentration is that it becomes very easy tooverconsume energy – a small amount of fat-richfood can provide unexpectedly high fat intakes.The converse of this is that, where people have

very little fat in their diet, they have to consumelarge volumes of food to meet their energy needs.For children, in particular, this volume may beunobtainable and this may be one of the con-tributory factors to undernutrition in develo-ping countries. Adding a small amount of oil to a traditional starchy rural diet can make a greatdeal of difference to overall energy intake.

As well as supplying energy in the diet, fatsalso provide a vehicle for other essential nutri-ents, in particular, the fat-soluble vitamins andthe essential fatty acids. The absorption of fat-soluble vitamins from the digestive tract dependson the presence and normal digestion/absorptionof fats. Thus, people on low-fat diets may be atrisk of insufficient intake of these vitamins. (SeeFigure 5.4 for a summary of these points.)

Digestion and absorption of fats

Fat digestion is uncomplicated. One type oflipase (a fat-splitting enzyme) can split the linkbetween glycerol and any fatty acid. A smallamount of lipase, called lingual lipase, is pro-duced in the mouth. This is probably of greatestimportance in infants, as it is particularly activein the breakdown of milk fats. Milk digestion isalso facilitated in breast-fed infants by the pres-ence of a lipase in the milk itself.

The main process of fat digestion starts inthe stomach, where the churning action breaksit down into a coarse emulsion. The emptying of fats from the stomach into the duodenumcauses the release of several hormones called

Compare the sensations in your mouth after amouthful of skimmed milk (very low fat), normalfat milk, single cream and double cream.

Activity 5.3

Figure 5.4 Why do we eat fat?

❚ FATS

86

enterogastrones, which inhibit further stomachemptying. In this way, the release of fats fordigestion in the intestine is slowed down, and afat-rich meal stays in the stomach for longer, cre-ating satiation. The main lipase is that from thepancreas, which splits fats in the jejunum into amixture of fatty acids and glycerol, together withsome monoglycerides.

However, fats are not soluble in the waterymixture of the small intestine and would nor-mally aggregate into large droplets. These needto be split up into tiny droplets by emulsifyingagents, which are both fat and water soluble. Inthe gut, this is carried out by the bile acids,which emulsify the fat and enable lipase to act.Bile acids are made in the liver from cholesterol,concentrated and stored in the bile ducts andgall bladder, and then secreted into the duode-num when the food enters from the stomach.Partly split fats and free fatty acids aid the bilesalts in emulsifying the neutral fats. The bileacids that have been used in fat digestion arereabsorbed in the ileum, and pass in the blood tothe liver, where they act as a stimulus for theirresecretion into the bile. They, thus, undergo whatis termed an enterohepatic circulation. Inter-ference with this circulation will alter the level ofbile acids and their precursor, cholesterol. The bilesalts that return to the liver act as an inhibitor tofurther synthesis from cholesterol. If fewer returnto the liver, then more synthesis of bile salts fromcholesterol can occur, thus lowering the level ofcholesterol in the blood.

Phospholipids are also broken down byremoval of their fatty acids, by the action of the enzyme phospholipase. Cholesterol esters in the diet are hydrolysed by esterases to removethe fatty acid and so release cholesterol forabsorption.

Once the fats have been split into their con-stituents, they merge into tiny spherical com-plexes, known as micelles, which diffuse easilyinto the intestinal cell (or enterocyte). Once insidethe enterocyte, the fat digestion products arereassembled into triglycerides, although not thesame as the original ones in the diet. These arethen coated with phospholipids and apolipopro-teins to produce chylomicrons. This ‘envelope’provides a means of stabilizing lipids in an

aqueous environment, such as the circulation. In addition to the triglycerides, the chylomicronsalso contain other fat digestion products, such ascholesterol and fat-soluble vitamins. Too large to diffuse into the blood capillaries of the gut wall, the chylomicrons pass into the lacteals ofthe lymphatic system, and eventually enter thebloodstream at the thoracic duct in the neck,where the lymphatic system drains into theblood. Fat digestion is summarized in Figure 5.5.

Some smaller fatty acids, containing 4–10carbon atoms, are able to pass into the bloodcapillaries in the gut, and so are absorbed directlyinto the hepatic portal vein, where they attach toplasma albumin and are transported to the liver.These types of fatty acids have the advantage ofbeing a little more water soluble; they are, there-fore, not so dependent on emulsification by thebile for their digestion. In some patients, wherethere is a fat digestion problem owing to a lack ofbile, introducing short-chain fats into the dietmay be a temporary way of adding dietary fat,which would otherwise not be tolerated. The twoways in which fat digestion products enter thebody are summarized in Table 5.6.

Fat digestion is normally very efficient, with95 per cent of ingested fat being absorbed. How-ever, in some instances digestion and/or absorp-tion will be defective. If fat is undigested orunabsorbed, it will appear in the faeces. This pro-duces a characteristic faecal appearance, withwaxy stools, which tend to be foul smelling and,because they float, are difficult to flush away.This condition is called steatorrhoea. Unabsorbedfats will remove other fat-soluble componentsfrom the body, in particular, the fat-soluble vita-mins, and chronic steatorrhoea may be associ-ated with a specific vitamin deficiency.

Causes of steatorrhoea may include:■ failure to produce lipase as a result of pan-

creatic insufficiency, or problems with theproduction or secretion of bile;

■ gallstones, which can block the secretion ofbile into the gut;

■ inefficient absorption of fat due to defects inthe surface of the small intestine, which maybe flattened or inflamed; and

■ ingestion of mineral oils, such as liquidparaffin, as a laxative.

TRANSPORT OF FATS IN THE BODY ❚

87

Figure 5.5 Digestion and absorption of fats.

Transport of fats in the body

Because of their hydrophobic nature, fats have to be carried around the circulation in associ-ation with hydrophilic substances, otherwise theywould separate out and float on the surface of

the blood, like the cream from the milk. Chylo-microns, which facilitate the entry of digestedfats into the circulation, are one example of suchan association. These are the largest and lightestof a group of aggregates collectively known as

❚ FATS

88

lipoproteins. Lipoproteins are classified accord-ing to their density and can be separated byultracentrifugation of a blood sample. At one endof the range are the large light chylomicrons,then, arranged in decreasing size, come very lowdensity, low-density and high-density lipopro-teins, usually referred to by their acronyms VLDL,LDL and HDL.

Fats in the blood are carried in lipoproteins,irrespective of whether they have originatedfrom the diet or been synthesized in the body. Inboth cases, the triglyceride and cholesterol estersare coated with a shell of phospholipid andapolipoprotein. The apolipoprotein provides an‘identity tag’ by which the body cells recognizethe particular type. The lipoproteins are not constant in their composition: they are dynamicparticles, which release and pick up their con-stituents as they travel around the body.

However, it is possible to describe the typicalcomposition of each type, as shown in Table 5.7.It can be clearly seen that the chylomicronscontain predominantly triglycerides and arethus very low in density. The major constituentsof VLDLs are also triglycerides. LDLs containmostly cholesterol and are its major carriers inthe body. HDLs are predominantly made up of

protein, with smaller fat contents than the othertypes. This accounts for their high density.There is also a difference in size, with the chy-lomicrons being the largest and the HDL thesmallest of the particles.

Chylomicrons start to appear in the bloodwithin 30 minutes of eating a fat-containingmeal, with a peak after approximately 3 hours.They cause an increase in plasma lipid levels,and serum samples taken during this time havea milky appearance because of this. Somechylomicrons may continue to enter into theblood after a fat-rich meal over a period of up to14 hours.

As chylomicrons circulate in the blood, fatsare removed from them by specific lipoproteinlipases in the blood vessel walls, especially inthe liver, skeletal muscle and adipose tissue, andfree fatty acids and glycerol are released. Thebody uses these products for particular meta-bolic processes needed at the time. This mayinvolve fuelling muscle contraction or perhapsbeing stored in the adipose tissue for subse-quent use. Chylomicrons may also pass some oftheir free cholesterol to HDLs.

The remnants of the chylomicrons are even-tually broken down in the liver and used to make

Summary of fate of fat digestion productsTABLE 5.6Short-chain fatty acidsMedium-chain fatty acids Absorbed directly into hepatic portal veinGlycerol

Triglycerides (reconstituted fromlong-chain fatty acids and monoglycerides) Made into chylomicrons; absorbed into lacteals,

Cholesterol carried via lymphatic system into the bloodPhospholipidsFat-soluble vitamins

Typical compositions of lipoprotein particles (as per cent)TABLE 5.7Triglyceride Cholesterol Phospholipid Protein

Chylomicrons 90 5 3 2VLDL 60 12 18 10LDL 10 50 15 25HDL 5 20 25 50

TRANSPORT OF FATS IN THE BODY ❚

89

other lipoproteins. The liver cells synthesize fat(endogenous fats) brought in from fatty acids;cholesterol is also synthesized. Eventually, thefats made in the liver are packaged as VLDLs andexported into the rest of the body.

As the VLDLs travel through the body, lipo-protein lipase removes their triglycerides, in muchthe same way as for chylomicrons. Both chylo-microns and VLDLs contain the apolipoproteinapo-CII, which activates lipoprotein lipase. Asthey lose triglycerides, the VLDLs become smallerand the proportion of cholesterol in themincreases. Thus, they are transformed into LDLs.

One other transformation also occurs. This isthe loss of some of the apolipoprotein, so thatthe remaining ‘identity tag’ is that of the LDLs.This is apolipoprotein B100 (apo-B100) and is vitalfor the normal metabolic functioning of LDLs.

The function of LDL is to act as the majorcarrier of cholesterol, taking it to the tissueswhere it is needed in cell membranes or for syn-thesis of metabolites, such as steroid hormones.Specific receptors for apo-B100 are present oncell surfaces. These allow the LDLs to attach tothe cell, and the whole LDL–receptor complex istaken into the cell, where it is broken down by

enzymes. The activity and number of receptorsites can vary, thus controlling cholesteroluptake by cells. In the genetically determinedcondition familial hypercholesterolaemia, sub-jects lack the LDL receptor, resulting in high circulating levels of LDLs.

HDLs are responsible for the removal of spareor surplus cholesterol as well as apolipoproteinsfrom cells and other lipoproteins; this is known as reverse cholesterol transport. When cholesterolis picked up by the HDLs, it quickly becomesesterified, which allows it to be taken into thehydrophobic core of the lipoprotein. In this way,the outer layer of the HDL maintains a diffusiongradient for more cholesterol to be picked up. Thissystem allows cholesterol to be removed from thetissues and taken to the liver. This completes the lipid transport cycle (Figures 5.6 and 5.7).

Because LDLs and HDLs are so intimatelyinvolved with cholesterol transport, they arebelieved to be closely associated with the devel-opment of atheroma and particularly of heartdisease. Consequently, factors influencing thecirculating levels of LDLs and HDLs have beenextensively studied. It is believed that they are influenced by a number of factors, including

Figure 5.6 Exogenous lipid transport.

❚ FATS

90

genetics, hormone levels, age, gender, smoking,exercise and diet. One such gene, which appearsto be particularly important, is that for apolipo-protein E (APOE). Several variants have beenidentified, which account for a proportion of thevariation in LDL levels within a population.Variants may also determine the response oflipoprotein levels to changes in dietary factorsand the rate of clearance from the circulation.

Factors affecting lipoproteins are discussedin more detail in Chapter 14.

Function of fat in the body

In considering the role of fat in the body, it isimportant to recognize that fat occurs through-out the body, as part of the structure of everycell membrane, as well as being found in dis-crete areas as adipose tissue. Fat is essential inbody composition and, as such, has manydiverse functions in the body. These are:■ structure■ storage■ metabolism.

It should be remembered, however, that thesecategories are not separate and distinct fromone another and there is considerable overlapbetween them.

Structure of membranes

The structure of biological membranes consistsof lipid molecules that are often associated

with other residues, such as phosphate groups orcarbohydrates, together with cholesterol and pro-teins. The exact nature of the membrane is verydependent on the types of fatty acids present,varying with their length, degree of saturationand spatial arrangement. In addition, various fatsoccur on the surface of the skin and contributeto its waterproof properties. Some of these fatsare quite unusual, containing chains with oddnumbers of carbon atoms, branched chains anddouble bonds in unusual locations. Free fattyacids, which are thought to have bactericidalproperties, may also be present.

Storage – the adipose tissue

The body is able to store fat as an energy reserve,in specialized cells, called adipocytes, which arefound in adipose tissue. Adipocytes make up onlyabout half of the total cell numbers within adi-pose tissue; fibroblasts, macrophages and vas-cular tissue are other important components.Adipose tissue plays a major role in metabolism(discussed below). Two types of adipose tissuehave now been identified – the predominantform, white adipose tissue (WAT) and brown adi-pose tissue (BAT), which occurs in much smalleramounts. Brown adipose tissue differs from WATin several respects, most noticeably in havingmany more mitochondria, blood capillaries andnerve fibres than the white tissue. This type of fatis much more widespread in newborn animals,and provides a means of heat generation at this

Figure 5.7 Endogenous lipid transport and metabolism.

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critical stage of life, before shivering mech-anisms develop. It used to be thought that brownfat then disappeared, but more recent researchsuggests that small amounts persist into adultlife, and may play a part in generating heat as ameans of ridding the body of surplus energy.

The WAT cells store fat as a single droplet,which fills almost the entire cell contents, push-ing the remaining organelles to the very edgesof the cell. The fat stored in the body is a reflec-tion of the type of dietary fat; thus, an individ-ual eating a diet rich in polyunsaturated fatswill have more of these in their adipose tissue.On the other hand, a person who has small fatstores and consumes little fat will have adiposetissue fats that are more typical of fat synthe-sized in the body containing mainly palmitic,stearic and oleic acids.

The number of fat cells has been estimated atabout 5 �1010 in a mature adult. There has beenconsiderable debate about the means of expan-sion of fat stores. This can occur by hyperplasia,which is an increase in cell number, or by hyper-trophy, which is an increase in size of existingcells. It had been believed that adipocyte numberswere set in early infancy, and would remain atthis level for life, but this is now known to beincorrect. The size of adipocytes is related to theirfat stores, so these will vary with the flux of fatinto and out of stores. As fat stores increase, it is postulated that new cells are formed from pre-adipocytes already present in the body. Whetheradipocytes can be lost on reduction of fat stores isstill under debate, although there is evidence thatapoptosis (programmed cell death) can occur, butthe significance of this in individuals is unknown.

It has also become clear that adipose tissuedepots to an extent may be self-regulatory, andthat depots in various parts of the body responddifferently to physiological demands. In partic-ular, there are differences between fat stored inthe abdominal region and that in the thighs andbuttocks. The fat adjacent to lymph nodes isproposed as having an important role in sup-porting the immune system, and may becomemuch larger in chronic inflammatory states at theexpense of other fat depots, resulting in changesin body fat distribution. This has been noted inHIV infection and Crohn’s disease.

The ability to store fat as an energy reserveoffers an additional benefit, that of insulationand protection. Adipose tissue covers some ofour more delicate organs, such as the kidneys,spleen, spinal cord and brain, to protect themfrom injury. This protective fat is used less read-ily as fuel in a fasting individual. Most of thefuel-storing adipose tissue is found under theskin, as subcutaneous fat. Here it also providesinsulation to facilitate the maintenance of bodytemperature. In hot climates, this can be a dis-advantage, with overweight individuals sweatingreadily to lose heat. On the other hand, sufferersfrom anorexia nervosa, who have little subcuta-neous fat, will feel cold even on a warm day, andwill dress in several layers of clothing both to provide extra warmth, but perhaps also to disguise their extreme thinness. The body alsostores fat-soluble vitamins in its adipose tissue.

Metabolic roles

Meeting the energy needs – fat metabolismThe provision of energy is probably the mostcommonly recognized function of fats. Fat is anenergy-dense fuel; more than twice as muchenergy is provided per gram of stored fat thancan be obtained from each gram of carbohydrateor protein. This means that our bodies can store alarge amount of reserve energy in a relativelysmall volume. If our major stores of energy werein the form of carbohydrate, we would eitherhave much smaller reserves or weigh much more!

The storage and release of energy from adi-pose tissue is under continuous hormonal control,mainly by insulin and noradrenaline. It has beenproposed that the adipose tissue is an essentialbuffer in the body to regulate fats whose levelsvary with intermittent food intake. This bufferingaction can fail, e.g. in obesity or in conditions oftoo little body fat, resulting in metabolic abnor-malities, such as insulin resistance (see below).

Fat storageThe adipocytes extract triglycerides from pass-ing lipoproteins by the action of the enzymelipoprotein lipase (LPL). This enzyme is activatedby insulin and is, therefore, most active in thepostprandial phase (after meals). The triglycerides

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are broken down by LPL, taken into the adiposetissue cell and then reassembled into newtriglycerides for storage. The storage and releaseof fat is a dynamic process, with a continuousflux of fats into and out of the cells. A great dealof fat storage occurs after meals, when there areincreased numbers of chylomicrons and VLDLsin the circulation. In theory, fat may be synthe-sized from carbohydrate, but this happens onlyin exceptional circumstances of extremely highcarbohydrate intakes and is very inefficient.Other sites in the body can also make fat, in par-ticular, the liver and mammary gland during lac-tation. However, the liver does not normallystore significant quantities of fat; a liver loadedwith fat is generally diseased. The mammarygland is able to synthesize shorter chain fattyacids, with lauric and myristic acids predominat-ing (C12 and C14).

Fat utilizationThe body uses stored fat as its major energy sup-ply, releasing non-esterified fatty acids (NEFA)into the circulation under the influence of nor-adrenaline released by the sympathetic nervous

system. At most levels of activity, fat provides a significant proportion of the energy used. It is only when we exercise very intensively (e.g.running the 100 metres sprint) that all the energycomes from carbohydrate, since fat cannot bemetabolized sufficiently quickly (see Chapter 16).The lower the level of activity, the greater the pro-portion of energy that comes from fat. However,some glucose continues to be used for metabolismas the brain, nervous system and red blood cellsrequire it. Under normal circumstances, glucoselevels are maintained by hormones such asinsulin, adrenaline and cortisol, which ensure thatsufficient is present to fuel these essential tissuesand organs. If there is no supply of glucose enter-ing the body, organs such as the liver are capableof making glucose from protein residues andglycerol from fat breakdown (see Figure 5.8).

Fat breakdown to supply ATP occurs by thesuccessive splitting of acetic acid molecules fromthe ends of long-chain fatty acids. These aceticacid molecules then enter the same commonpathway that serves carbohydrate metabolism.For complete oxidation, some carbohydrate mustbe present. If there is no glucose or glycogen,

Figure 5.8 The role of adipose tissue in metabolism.


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then acetic acid molecules combine in pairs toform ketone bodies. Once formed, ketone bodiesare sent to the peripheral tissues, where theycan be converted back to acetyl coenzyme Aand used in the normal Krebs (or citric acid)cycle. A mild rise in ketone body production(ketosis) will occur whenever fat mobilizationoccurs, for example, during moderate exercise,overnight fast and conditions associated with lowfood intake, such as acute gastroenteritis or thenausea and vomiting of early pregnancy. A moresevere type of ketosis causing mental confusionor coma, as well as physiological changes (mus-cular weakness and overbreathing), may occurin severe states of these kinds and also in dia-betes mellitus. In this case, insulin lack preventsnormal glucose entry into cells and thus glucoseoxidation. Symptoms associated with mild ketosisinclude lethargy, headache and loss of appetite.These are very general, however, and may becaused by many other factors.

If we fast, the body rapidly metabolizes bodyfat. Initially, there is also rapid breakdown oflean tissue as the body uses protein residues tomaintain blood glucose supplies. After a numberof days, however, the brain and nervous systemadapt to the use of ketone bodies for energy, and survival using fat stores becomes possible.Inevitably, a fatter person will be able to survivelonger than one with limited fat stores at theoutset.

Link with glucose metabolism – insulinresistanceResearch on the metabolic changes that occur inoverweight and obesity has identified closelinks between amounts of adipose tissue andsensitivity to insulin and, therefore, glucosemetabolism.■ Sensitivity to insulin has been shown to

decrease with increasing levels of body fat,even at relatively normal body mass index(BMI) levels.

■ Insulin normally inhibits the release ofNEFA from adipose tissue, but in obesity thisresponse is reduced per unit of fat mass.However, because there is more stored fat,the total amount of NEFA released is actu-ally increased.

■ The removal of triglycerides (as chylomicronsor VLDL) from the circulation by the action ofLPL may also be depressed by reduced sensi-tivity of this enzyme to insulin.

■ The overall consequence is a chronicallyraised level of circulating fats (lipaemia),which deposit in a number of tissues, includ-ing liver and skeletal muscle. This suppressesglucose utilization by muscle, stimulates theproduction of glucose in the liver and stimu-lates insulin release. High levels of NEFAmay also damage the pancreatic �-cells thatsecrete insulin. Thus, there is interferencewith the normal insulin-mediated glucosedisposal, owing to a failure of the buffercapacity of the adipose tissue (see Figure 5.9).

Adipose tissue and metabolic regulationAdipose tissue is now recognized as having arole as a source of many metabolic regulators,with more factors still being discovered. The mostimportant of these has been leptin, discovered in 1994, which is produced predominantly byadipose tissue, but has also been shown to be secreted by other organs like the stomach,mammary gland and placenta. Leptin receptorsare also found in adipose tissue but are princi-pally sited in the hypothalamus. Leptin has beenshown to interact with neuropeptides in the brainto inhibit food intake. It also plays a role inenergy expenditure, probably via BAT, and is asignal to the reproductive system in sexual mat-uration. Leptin release is under the control ofthe sympathetic nervous system.

There are many other factors released byadipose tissue with diverse actions and some asyet unidentified.■ Proteins involved in lipid and lipoprotein

metabolism include LPL and cholesteryl estertransfer protein, important in accumulationof cholesteryl ester in WAT.

■ Proteins that play a role in blood pressureregulation and blood clotting are also secreted,and may be a link with disorders of theseprocesses in obesity.

■ Immune function is also influenced by secre-tory products from the adipose tissue, includ-ing cytokines (most notably tumour necrosisfactor � (TNF�)) and complement system

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products. The cytokines in turn appear to havea regulatory role in various aspects of adiposetissue function. The immune system uses upto 15 per cent of the body’s resting metabolicrate, and it may be that the close relationshipbetween adipose tissue energy stores and theimmune system is a means of ensuring thatadequate energy can be provided when theimmune system is under stress. TNF� inhibitsfat storage and would, therefore, make fattyacids immediately available.

■ Metallothionein is a stress response proteinthat acts as an antioxidant, and may protectfatty acids in adipose tissue from damage byfree radicals during high rates of oxygenutilization.

Steroid metabolismCholesterol is essential in the body. It is the pre-cursor for the synthesis of the steroid hormones,

which includes those produced in the adrenalgland, as well as the sex hormones. It is also aprerequisite for the formation of vitamin D in theskin. In addition, cholesterol is used in the manu-facture of bile salts in the liver, which, as we sawearlier in this chapter, are vital in the normaldigestion of dietary fats. The bile salts can bereabsorbed from the lower gut and reused by theliver. Some, however, can be trapped in the fae-ces and removed from the body. In this case,more bile salts have to be synthesized from chol-esterol. Adipose tissue is a major site for storageof cholesterol.

Many of the steroid hormones are convertedto their active form in the tissue. This includesformation of oestradiol from oestrone, testo-sterone from androstenedione and oestrogensfrom androgens. The last of these can form an important source of female hormones in

Figure 5.9 Aspects of insulin resistance.


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overweight individuals, which may have posi-tive benefits in terms of maintaining bonehealth after the menopause, but also negativeconsequences in increasing the risk of hor-mone-dependent tumours.

Essential fatty acidsThere are two major metabolic roles for theessential fatty acids. The presence of essentialfatty acids in the membranes of cells and theirorganelles contributes to the stability andintegrity of these membranes. Signs of deficiencyinclude changes in the properties of membranes,particularly increases in permeability. These areaccompanied by reduced efficiency of energyutilization and, therefore, poorer growth. The n-3 acids are of particular importance in themembranes of the nervous system and brain, aswell as the retina. Docosahexaenoic acid (22:6)is particularly concentrated in the retina, andlevels increase in the fetal brain and retina inthe later stages of pregnancy. Development con-tinues in early childhood, and a supply of theselong-chain fatty acids is essential to optimizeneurological development.

In addition, essential fatty acids are the pre-cursors of a family of bioactive compounds calledeicosanoids, which act as metabolic regulators ina number of key functions. Two major pathwaysfor eicosanoid production exist. Prostaglandins,prostacyclins and thromboxanes are made by thecyclo-oxygenase pathway, and leukotrienes areproduced by the lipoxygenase pathway. Eicosa-noids are derived from fatty acids with 20 carbonatoms. Thus, the majority originate from arachi-donic acid (20:4), which is a member of the n-6fatty acid family and is produced in the bodyfrom the essential fatty acid, linoleic acid. How-ever, some are produced from eicosapentaenoicacid (20:5), which is a member of the n-3 family,made in the body from the essential fatty acid,alpha-linolenic acid. It is believed that a pre-dominance of n-6 acids in the body may prevent the formation of eicosanoids of the n-3 series.Prostaglandins and other eicosanoids are verypotent substances; therefore, they are produced atthe site of action and very quickly inactivated.They are made from essential fatty acids containedin the phospholipids of cell membranes. Thus,

although they may be described as ‘hormone-like’, they do not circulate in the blood in thesame way. Their release is triggered by a varietyof physiological stimuli, including hormones,such as adrenaline, antigen–antibody reactionsand mechanical damage or injury.

Prostaglandins have a range of diversefunctions, such as:■ lowering of blood pressure;■ blood platelet aggregation;■ diuresis;■ effects on the immune system;■ effects on the nervous system;■ rise in body temperature;■ stimulation of smooth muscle contraction;■ gastric secretion.

Some members of the eicosanoids haveopposing actions. For example, prostacyclinsare produced in the endothelial lining of thearterial wall and are powerful inhibitors of plate-let aggregation, as well as causing the arterywalls to relax. They, therefore, lower blood pres-sure. In contrast, thromboxanes are produced inthe platelets, where they stimulate aggregationand cause contraction of the blood vessel wall,thereby increasing blood pressure. It is, there-fore, important that these two eicosanoids arenormally balanced, to prevent major changes incirculatory function. Leukotrienes, on the otherhand, are pro-inflammatory.

The different fatty acid families give rise todifferent series of eicosanoids. Those producedfrom the n-3 family have less powerful effects onplatelet aggregation and vasoconstriction (haemo-dynamic functioning) and on inflammation thando the n-6 derived eicosanoids. This is believed tobe the explanation for the potential benefits offish oils rich in n-3 acids in relation to heart disease. This is discussed further in Chapter 14.

Increasing the levels of n-3 fatty acids in thebody has also been shown to displace some ofthe n-6 acids from cell membranes of white bloodcells. As a consequence, less pro-inflammatoryeicosanoids are produced as part of the immuneresponse. In addition, n-3 acids may affect otherparts of the immune response, such as cytokineactivation. These effects are of potential benefitin chronic inflammatory conditions, and supple-mentation with fish oils has been shown to

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reduce symptoms in subjects with rheumatoidarthritis. There are potential benefits also inasthma, psoriasis and Crohn’s disease, althoughmore research is needed in these areas.

How much fat should wehave in the diet?

For many nutrients, the answer to such a ques-tion would entail a consideration of the preven-tion of deficiency of the particular nutrient.However, in the case of fat, there is no recognizeddeficiency state that develops from the absenceof fat in general. The only problem arises from anabsence of the essential fatty acids. It should,therefore, be possible to set levels for guidance on intake of these fatty acids, in order to preventdeficiency. Evidence of the need for essential fattyacids comes from reports of linoleic acid defi-ciency in children and in clinical situations inadults. The dietary reference values report (DoH,1991) recommends that linoleic acid should pro-vide at least 1 per cent of total energy and alpha-linolenic acid at least 0.2 per cent. This amountsto between 2 and 5g of essential fatty acids daily,which can be readily achieved from a serving offish, seed oil used in cooking or green leafy vege-table. Since the publication of this Report, therehas been more interest in the possible healthbenefits of n-3 fatty acids and the implications ofthe ratio of n-6 to n-3 fatty acids. There are nofirm recommendations on a desirable ratio at thetime of writing, but it has been proposed thatlinoleic acid (n-6) should comprise a maximum of3 per cent of energy intake and total n-3 acidsshould be 1.3 per cent of energy. Thus, the ratio ofn-6 to n-3 fatty acids should be between 2:1 and3:1. Specific interest has focused on the diets ofpregnant women, where the status of long-chainpolyunsaturated fatty acids is correlated with

those in the baby. The importance of n-3 acidsfor neurological development in the fetus andinfant has been discussed earlier in this chapter,and women whose diets contain high levels of n-6 acids, or minimal amounts of n-3 acids maybe unable to supply their baby with adequate levels of n-3 acids, either via the placenta, or in breast milk. Premature infants may be espe-cially at risk, although term babies also need an adequate supply. The addition of long-chainfatty acids to formula milk is now permitted byEuropean and UK legislation, to improve intakesin infants. There is a need for more research inthis area.

The recommended levels of total fat and thedistribution of this fat into saturated, monoun-saturated and polyunsaturated fats is based onour knowledge of intakes in populations andevidence on the incidence of disease in thesepopulations, i.e. an optimum health approach.The main diseases that are considered in adviceon fat are atherosclerosis and cancer, and muchof the guidance on fat intakes aims to reducethe incidence of these diseases. Consequently,recommended levels in the UK are that totalfatty acid intake should average 30 per cent of dietary energy including alcohol. Of this, 10 per cent of total energy should be provided bysaturated fatty acids, 12 per cent by monounsat-urated fatty acids, an average of 6 per cent frompolyunsaturated fatty acids and 2 per cent fromtrans fatty acids. When calculated as total fat(including glycerol), these figures amount to 33 per cent of total dietary energy including alco-hol, or 35 per cent of energy from food.

Further discussion of the rationale for thesefigures and the links with atherosclerosis, coro-nary heart disease and cancer can be found inChapters 14 and 15.

1 The diet contains saturated and unsaturated fatty acids, arranged in triglycerides of varyingcomposition. The nature of the fatty acids influences the physical characteristics of the dietary fat. Inaddition, the diet contains small amounts of cholesterol and phospholipids.

2 Fat intakes in the UK have fallen in absolute terms in the last 40 years, but in relation to the total energyintake, levels remain at about 40 per cent of food energy. The majority of fat intake comes from fats, oils,meats and meat products.

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3 Fats increase the palatability of the diet and can contribute to overconsumption of energy, because of thehigh energy content per unit weight.

4 Digestion of fats requires the presence of bile from the liver. Failure of fat digestion results insteatorrhoea.

5 Fat is transported in the circulation in the form of lipoproteins, which vary in their content oftriglycerides and cholesterol.

6 Essential fatty acids are specifically needed in the diet in small amounts for membrane structure andsynthesis of eicosanoids.

7 Stored fat is an important energy reserve and serves to insulate and protect the body. It also hasimportant regulatory roles in metabolism and as a secretory organ for a number of bioactive factors.

8 Advice for the population in general is to reduce total fat intakes.

1 Both gamma-linolenic acid and alpha-linolenicacid contain 18 carbon atoms and three doublebonds. In what ways are they different and whyis this important?

2 What are the functions of the phospholipids andhow does this relate to their structure?

3 Suggest some explanations for the finding ofthe National Food Survey that food eaten

outside the home has a higher fat content than that eaten at home. What do yourexplanations imply about promotion of healthy eating?

4 Find out, by discussion, why people enjoyhaving fat in their diet. Do the reasons youobtain agree with those given in this chapter?

5 Under what circumstances might you expect anessential fatty acid deficiency to occur?

STUDY QUESTIONS


British Nutrition Foundation 1999: n-3 fatty acids and health. Briefing paper. London: BritishNutrition Foundation.

DEFRA 2001: National Food Survey 2000 Annual report on food expenditure, consumption andnutrient intakes. London: The Stationery Office.


DoH (UK Department of Health) 1994: Nutritional aspects of cardiovascular disease. London: HMSO.Food Standards Agency 2002a: Food portion sizes, 3rd edn. London: The Stationery Office.Food Standards Agency 2002b: McCance and Widdowson’s The composition of foods, 6th summary

edn. Cambridge: Royal Society of Chemistry.Frayn, K.N. 2001: Adipose tissue and insulin resistance syndrome. Proceedings of the Nutrition

Society 60, 375–80.Galli, C., Simopoulos, A.P., Tremoli, E. (eds) 1994: Effects of fatty acids and lipids in health and dis-

ease. World Review of Nutrition and Dietetics 76, 1–149.Macdiarmid, J.I., Cade, J.E., Blundell, J.E. 1994: Dietary fat: grams or percentage energy? Analysis

of the dietary and nutrition survey of British adults and the Leeds high fat study. Proceedings ofthe Nutrition Society 53, 232A.

Morton, G.M., Lee, S.M., Buss, D.H. et al. 1995: Intakes and major dietary sources of cholesterol andphytosterols in the British diet. Journal of Human Nutrition and Dietetics 8(6), 429–40.

Pond, C. M. 2001: Long-term changes in adipose tissue in human disease. Proceedings of theNutrition Society 60, 365–74.

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Roche, H.M., Noone, E., Nugent, A. et al. 2001: Conjugated linoleic acid: a novel therapeutic nutri-ent? Nutrition Research Reviews 14, 173–87.

Sanderson, P., Gill, J.M.R., Packard, C.J. et al. 2002: UK Food Standards Agency cis-monounsatu-rated fatty acid workshop report. British Journal of Nutrition 88, 99–104.

Trayhurn, P., Beattie, J.H. 2001: Physiological role of adipose tissue: white adipose tissue as anendocrine and secretory organ. Proceedings of the Nutrition Society 60, 329–39

Wise, A., McPherson, K. 1995: The relationship between individual beliefs and portion weights offat spreads. Journal of Human Nutrition and Dietetics 8(3), 193–200.

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carbohydrates


❏ describe the carbohydrates that are important in human nutrition, including simple and complex carbohydrates;

❏ review the digestion and absorption of carbohydrates;❏ consider the desirable levels of carbohydrate in the diet;❏ study the health implications of dietary carbohydrates.


❏ discuss the different types of carbohydrates in the human diet and explain their relative importance;❏ explain how different carbohydrates differ in their absorption, and the practical implications of this;❏ identify health aspects of both simple and complex carbohydrates, and the associated guidelines on dietary

intakes of the various types;❏ discuss the implications of sugar consumption with respect to dental health.

Carbohydrates are a group of substances foundin both plants and animals, composed of carbon,hydrogen and oxygen in the ratio of 1:2:1. Thename ‘carbohydrate’ was first used in 1844 bySchmidt, but the sweet nature of sugar hadalready been recognized for many centuries. It issaid that sugar was extracted as early as 3000 BC

in India; Columbus is credited with introducingsugar cane into the New World in the fifteenthcentury, and in the sixteenth century Elizabeth Iis reported to have had rotten teeth owing toexcessive consumption of sugar.

Foods providing carbohydrates are the cheap-est sources of energy in the world. For manysmall farmers in developing countries, they pro-vide not only the main food, but also a source of income for the family. In terms of the worldcommodity trade, carbohydrate-containing foods,predominantly cereals, represent a major part. Inaddition, we find foods containing carbohydratespleasant and attractive to eat, especially thosethat contain sugars.

In modern times, carbohydrates have tendedto be dismissed as of little importance in the diet,supplying only energy. In addition, carbohy-drates have been reputed to contribute to a number of diseases including dental caries, dia-betes, obesity, coronary heart disease and cancer,although some of these links are not proven.Some scientists suggest that, if sugar was a newlydiscovered food, with a major role as a foodadditive to increase sweetness, then it probablywould not obtain a safety licence and would bebanned. However, since the early 1980s, nutri-tionists have recognized the importance of com-plex carbohydrates in our diet, and these havebeen promoted as a major source of energy andnutrients in our diets, in preference to fat.

Some definitions

The empirical formula for carbohydrates isCn(H2O)n. The simple forms of carbohydrates arethe sugars, which are generally present as single

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units called monosaccharides, or as double unitscalled disaccharides. Chains of simple sugarswith 3–10 units are termed oligosaccharides.When the sugars are combined together in longerand more complex chains, they form polysac-charides. In addition, the diet may also containsugar alcohols, which are hydrogenated sugars,for example, sorbitol.

Most of the carbohydrates in the diet comefrom plants. They are synthesized from carbondioxide and water, under the influence of sunlight, by the process of photosynthesis. Thedisaccharide sucrose accumulates as the majorproduct of photosynthesis in the chloroplast.Germinating seeds can also convert fat andamino acids into sugar. All plant cells are alsoable to convert glucose and fructose into sucrose.

Monosaccharides

Monosaccharides are the simple sugars. Eachmolecule usually consists of four or five or, mostoften, six carbon atoms, generally in a ring form.In the hexoses, the six-carbon monosaccharides,which are the commonest in the diet, the ringcontains one oxygen atom and all but one of thecarbon atoms, the remaining carbon, hydrogenand oxygen atoms being located ‘above’ or‘below’ the ring (Figure 6.1). It is important tonote that glucose can exist in two isomeric forms: D-glucose and L-glucose (known as stereoiso-mers). However, only D-glucose is used in thebody. Fructose and galactose are the other nutri-tionally important monosaccharides; they canalso exist as stereoisomers. All three are six-carbon monosaccharides, or hexoses (‘hex’ mean-ing six, ‘-ose’ is the standard ending used for

carbohydrates). Fructose and galactose have thesame empirical formula as glucose, but differ inthe way the atoms are arranged in the ring. Otherarrangements are possible, and are found in vari-ous plant and bacterial carbohydrates.

Glucose (also called dextrose) is the maincarbohydrate in the body, although it only con-stitutes a small part of dietary carbohydrateintake. It is present in honey, sugar confec-tionery, fruit and fruit juices, vegetables, somecakes, biscuits and ice cream. It is a fundamen-tal component of human metabolism, being an‘obligate fuel’ (i.e. essential under normal cir-cumstances) for a number of organs, mostnotably the brain. Consequently, levels of glu-cose in the blood are controlled within narrowlimits by a number of hormones.

Traditionally, fructose (also called laevulose)has not been present in large amounts in thehuman diet. Naturally occurring sources includehoney, fruit and some vegetables. In recentyears, high fructose corn syrup has increasinglybeen used as a sweetening agent in beveragesand processed foods. This is derived from thehydrolysis of starch obtained from corn, initiallyto glucose and then by subsequent conversion tofructose. The syrup thus produced is inexpensiveand has almost entirely replaced sucrose inproducts such as soft drinks, canned fruit, jams,jellies, preserves and some dairy products. Themajor advantages of this syrup are that it doesnot form crystals at acid pH, and it has betterfreezing properties than sucrose. These changesare making fructose one of the major simplesugars in the Western diet.

After absorption, fructose is transported tothe liver, where it is metabolized rapidly. The

Figure 6.1 Structural formulae for three simple sugars.

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products can include glucose, glycogen, lacticacid or fat, depending on the metabolic state ofthe individual.

Galactose is not usually found free in nature,being part of the lactose molecule in milk.However, fermented milk products may containsome galactose that has been released. Onceabsorbed into the body, galactose may be incorp-orated into nerve tissue in growing infants or, if not required, it is transformed either intoglucose or glycogen for storage. In lactating(breastfeeding) women, galactose is synthesizedfrom glucose and included as lactose in the milksecreted by the mammary glands.

Other monosaccharides occasionally foundin foods include xylose and arabinose in whitewine and beer, mannose in fruit, and fucose (amethyl pentose sugar) in human milk and bran.

Sugar alcohols may also be present in food.The three most commonly found are sorbitol,mannitol and xylitol. They are absorbed andmetabolized to glucose more slowly than thesimple sugars. This confers the advantage of a slower rise in blood glucose levels, which iswhy ‘diabetic’ foods are sometimes sweetenedwith sorbitol. Although the rate of absorption isslower, the amount of energy they ultimatelyprovide is the same as from the simple sugar, sothey are of no benefit where energy reduction isrequired. However, the sugar alcohols are usefulin reducing dental caries, since they are not fer-mented by the bacteria in the mouth and, there-fore, do not contribute to acid production. Forexample, xylitol has been shown in a number ofstudies to have a cariostatic (caries-preventing)effect when included in chewing gum or candies.

The slow rate of absorption of the sugar alcoholcan, however, result in diarrhoea if large amountsare consumed in a short time.

Disaccharides

Disaccharides are formed when monosaccha-rides combine in pairs. Those of importance innutrition are sucrose, lactose and maltose. Ineach case, a molecule of water is lost when the two constituent monosaccharides combine, in a condensation reaction. This is illustrated inFigure 6.2, showing the formation of maltose.

Sucrose (sometimes called invert sugar) is thecommonest and best known disaccharide in thehuman diet. It is formed by the condensation ofglucose with fructose. It is obtained from sugarbeet or sugar cane, both of which contain sucroseas 10–15 per cent by weight of the plant. Thejuice extracted from these plants is purified andconcentrated, and the sucrose is crystallized outand removed. Byproducts of this process includemolasses, golden syrup and brown sugar. Sucroseis also contained in honey and maple syrup.Naturally occurring sucrose is also found in fruit,vegetables and some cereal grains. Sucrose isadded to a great many manufactured foods, bothsweet and savoury.

Lactose (milk sugar) is present in the milk ofmammals. In the West, most of the lactose isprovided by cows’ milk and its products. Inaddition, any foods that contain milk powder or whey, such as milk chocolate, muesli, instantpotato, biscuits and creamed soups, will containsome lactose. It is also found in human milk.Lactose consists of glucose and galactose.

Figure 6.2 The condensation of two molecules of glucose to form maltose. First an OH group from one glucose andan H atom from another glucose combine to create a molecule of H2O. Then the two glucose molecules bondtogether with a single O atom to form the disaccharide maltose.

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Maltose (malt sugar) is mainly found in ger-minating grains, as their starch store is brokendown. Its major source is sprouted grain, suchas barley or wheat used in the manufacture ofbeer. The ‘malt’ produced by the sprouting isthen acted on by yeasts to produce the familiarfermented product. Small amounts of maltosemay also be found in some biscuits and break-fast cereals and in malted drinks. Maltose con-sists of two glucose units.

Oligosaccharides

Oligosaccharides contain less than ten monomerunits to make up the molecule. They are presentin a number of plant foods including leeks, gar-lic, onions, Jerusalem artichokes, lentils andbeans. Generally, these sugars are considered tobe of minor nutritional significance. However,both the galactosyl-sucroses (raffinose, stachyoseand verbascose) contained in legume seeds and the fructosyl-sucroses in onions, leeks andartichokes are resistant to digestion in the uppergastrointestinal tract. Consequently, they passlargely unchanged into the colon, where fermen-tation occurs, resulting in the production ofvolatile fatty acids and gases and causing flatulence. This can be uncomfortable and may discourage the consumption of these foods.Nevertheless, there are health benefits from this

fermentation, and oligosaccharides have beenstudied and developed as possible components ofprebiotics or functional foods, which provide afood source for colonic bacteria (see Chapter 17).

Polysaccharides

Polysaccharides contain many (more than ten)monosaccharide units arranged in straight orbranched and coiled chains. These may be madeup of hexoses, pentoses or a mixture of these,sometimes with other constituents, such asuronic acid.

Traditionally, a distinction has been madebetween polysaccharides that are digestible, andtherefore ‘available’, such as starch, and the‘unavailable’ indigestible forms, such as cellu-lose, hemicelluloses and lignin, which were alsotermed ‘dietary fibre’. In recent years in the UK,these have been more clearly differentiated into:■ starches; and■ non-starch polysaccharides (NSPs).Both of these groups of polysaccharides are ofplant origin, comprising the store of energy inthe plant and its structural framework, respect-ively. A comparable carbohydrate store in ani-mals is in the form of glycogen, but its contentin the diet is negligible.

StarchStarch consists of linked glucose units arrangedin either straight or branched chains. Amyloseis the straight-chain form of starch. It containsseveral hundred glucose molecules linked byalpha-glucosidic bonds between carbons 1 and4 of adjacent glucose molecules. The linkage is formed by a condensation reaction, with theloss of a molecule of water. The branched-chaincomponent of starch, amylopectin, containssome alpha bonds between carbons 1 and 4,with additional bonds linking carbons 1 and 6,at intervals, to produce side-branches. In thisway, amylopectin may contain thousands ofglucose units in one polysaccharide unit (seeFigure 6.3). Most of the common starchy foodssuch as potatoes, cereals and beans containapproximately 75 per cent amylopectin and 25per cent amylose. The presence of a large amountof amylopectin allows the starch to form a

Look at a range of different manufactured prod-ucts in the supermarket or grocery shop. Identifyall the different names used to describe addedsugars. Compare them against the list given below.Sugar Sucrose Brown Invert

sugar sugarGlucose Sorbitol Laevulose LactoseMannitol Polydextrose Corn syrup CaramelHoney Molasses High fructose

corn syrupMaple Dextrose Fruit sugar MaltosesyrupFructose DextrinHow many of the foods that you looked at con-tain more than one of the above forms of sugar?

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Figure 6.3 Structures of starch andcellulose.

stable gel with good water retention. Alongwith naturally occurring starches in foods, suchas cereals, roots, tubers and pulses, food pro-cessing may add two further forms of starch

into the diet. These are extruded starch prod-ucts, such as savoury snacks and breakfast cereals, and modified starches, which are addedto foods as emulsifiers and stabilizers.

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Processed starchesIn general, the processing of starchy foods makesthem more attractive for human consumption.For example, the grinding of wheat grains tomake flour makes it possible to produce bread,cakes, biscuits, etc. Such rigorous processing dis-rupts the starch granules, releasing amylose andmaking it readily available to digestive enzymes,and thus increases digestibility.

However, if moist starchy foods are heatedand then cooled, the sols formed by amylose and amylopectin during the heating stage willbecome gels on cooling, which retrograde on fur-ther cooling into insoluble precipitates. Amylosegels retrograde more readily than amylopectingels, so their relative proportions are an import-ant determinant of the physical properties of the cooked food. Some retrograded starch canstill be digested, albeit more slowly. In particular,the retrograded amylose particles are especiallyresistant to digestion and form an important partof the starch that escapes digestion in the smallintestine.

Resistant starch is the name given to thecomponents of dietary starch that are resistantto the normal enzymatic digestion process inthe small intestine. They originate in three pos-sible ways.■ The physical structure of the food may pre-

vent access to digestive enzymes if the starchis surrounded by fat, or is in large lumpsowing to inadequate chewing. Once thesebarriers are removed during digestion, thestarch can be broken down.

■ The nature of the cell walls around the starchgranules may impede digestion. Walls incereals may be partly broken down by millingand grinding, in potatoes by mashing, but thecell walls in legumes are thicker and consti-tute a more resistant barrier. When starchyfoods are eaten with little disruption of cellwalls, digestion will be slowed.

■ Where the starch has become retrograded byheating and cooling, the enzymes are nolonger able to break the bonds. This starchwill travel undigested into the colon, where,together with the non-starch polysacchar-ides in dietary fibre, it plays a positive, beneficial role in health.

Non-starch polysaccharidesFor many centuries the belief has been held bysome that the non-digestible part of our dietderived from plant foods can have an influenceon health. In the early 1970s the concept of‘dietary fibre’ and its relationship with dis-ease was more clearly developed. Interest wasawakened by reports that the low prevalence inrural Africa of some intestinal disorders commonin the West could be associated with the highintakes of dietary fibre. Further, diverticular dis-ease of the colon, generally treated with a fibre-depleted diet, was found to improve greatly whena diet rich in dietary fibre was given. Evidencewas also presented that dietary fibre mightreduce the risk of other ‘Western diseases’, suchas coronary heart disease and diabetes. Theseideas were very attractive and were enthusiastic-ally received because they were offering newexplanations for the aetiology (i.e. the factorscontributing to its causation) of some commondiseases.

The ‘fibre hypothesis’, which was developedfrom these ideas, broadly stated that:■ a diet rich in foods containing plant cell wall

material (i.e. unrefined plant foods, includingcereals, vegetables and fruits) is protectiveagainst ‘Western diseases’; and

■ a diet that is depleted of such materials may in some cases cause ‘Western diseases’or in others be a factor facilitating their development.Unfortunately, the term ‘dietary fibre’ is mis-

leadingly simple. The original definition includedall material undigested by the endogenous secretions of the human digestive tract. This col-lective term covered a number of very diversecompounds, all having their origin in plants, buthaving different physiological and physicalproperties, and probably varying effects in thebody. As a result, general statements about theproperties of ‘dietary fibre’ might not apply forcertain constituents. A further problem ariseswith the analysis and quantification of ‘dietaryfibre’ in foods, to allow proper scientific study.One of the initial methods of analysis (Southgatemethod), included unavailable carbohydrate butalso lignin and some resistant starch. A numberof other methods for the measurement of fibre

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have been used in different parts of the world,giving quite different results in any single com-modity and increasing confusion.

In 1990, the British Nutrition FoundationTask Force recommended that the term ‘fibre’should become obsolete and much more pre-cise terminology, based on accurate analyticalmethods, be used. The Englyst method determinesnon-starch polysaccharides by a componentanalysis method using gas–liquid chromatog-raphy. In this way, it is possible to separatestarch, resistant starch and NSP, and to definethe physical and chemical properties of the var-ious complex carbohydrates in the diet. Themethod also allows the soluble and insolublefractions of NSP to be separated and quantified.From this, the specific biological effects will be more readily identified. However, it is impor-tant to recognize that results from studies maynot be directly comparable, if different analyti-cal methods have been used to quantify thedietary fibre.

A further complication is that this termin-ology is not widely accepted; the USA and someEuropean countries continue to use ‘dietary fibre’,

analysed by an enzymatic/gravimetric method(Association of Official Analytical Chemists;AOAC, 2000), which includes lignin and resist-ant starch. The results obtained by AOAC aretermed ‘total dietary fibre’. Food compositiontables in the UK (Food Standards Agency, 2002)provide NSP values for all foods where these areavailable. There is additional information avail-able about AOAC values for a smaller number offoods. It is recommended that these are used infood labelling to provide harmonization acrossEurope.

Although the term ‘high-fibre diet’ is actu-ally rather meaningless scientifically, it repre-sents a concept understood by the public and assuch will, therefore, be used at relevant pointsin the text.

Constituents of NSPNon-starch polysaccharides include a number ofpolymers of simple sugars, together with uronicacid. They are broadly divided into cellulose andnon-cellulosic polysaccharides. Their relation-ship to total carbohydrate in the diet is summa-rized in Figure 6.4.

Figure 6.4 The relationship of non-starch polysaccharides (NSPs) to other sources of carbohydrate (CHO).

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Cellulose is the principal component of cellwalls in plants. It is made up of glucose units,linked by beta 1–4 linkages, which are resistantto digestion. It has a very stable crystalline struc-ture, which gives it low reactivity (see Figure 6.3).

The non-cellulosic polysaccharides comprisehemicelluloses, pectins, beta-glucans, gums andmucilages. The sugars they contain include ara-binose, xylose, mannose, fucose, glucose, galac-tose and rhamnose. Those NSPs that containpredominantly cellulose tend to be insoluble; an increasing content of uronic acids increasessolubility. Wheat bran and, therefore, wholegrain wheat products contain a high proportionof insoluble NSP and only traces of uronic acids.Cereals such as oats and barley, however, areparticularly good sources of beta-glucans, whichare water-soluble polymers of glucose. Fruit andvegetables, in general, have more uronic acidsand pectin in their NSPs, and thus a higher pro-portion of soluble fibre than cereals.

Gums and mucilages are generally found inthe human diet as a result of manufacturingprocesses. Gums are extracted, for example, fromthe acacia tree or the Indian cluster bean, and areused as thickeners, stabilizers and emulsifiers bythe food industry. Mucilages from algae and sea-weeds are also used by the food industry as stabi-lizers and thickeners.

The soluble and insoluble NSP contents ofsome common foods are shown in Table 6.1. Itshould be noted, however, that the separationinto soluble and insoluble fractions is not chemi-cally very distinct and depends on the method ofextraction used.

The National Food Survey (DEFRA, 2001)found that the British diet contained 12.6 g ofNSP per day, with a range of 5–19 g and 7–25 greported in men and women, respectively.Vegetarians and vegans tend to have greaterintakes of NSP. Mean values of NSP intake forthe USA are 15 g/day, with a higher intakerecorded in men. Other urban populations inaffluent countries are reported to have similarintakes, but slightly higher intakes have beenrecorded in rural populations. This probablyreflects a greater energy intake, related tohigher energy expenditure levels. In the UK, theNSP is provided by:

Cereals and cereal products 47%Vegetables and potatoes 36%Fruit 11%

Digestion of carbohydrates

The purpose of digestion is to make all dietarycarbohydrates into small units (mostly of glucose)

Non-starch polysaccharide (NSP) content of somecommon foods, showing soluble and insoluble fractionsTABLE 6.1

Food Total NSP Soluble NSP Insoluble NSP (g/100 g) (g/100 g) (g/100 g)

White bread 1.5 0.9 0.6Wholemeal bread 5.8 1.6 4.2Weetabix 9.7 3.1 6.6Oatcakes 5.9 3.5 2.4Rice, white 0.2 Trace 0.2Apples 1.6 0.6 1.0Bananas 1.1 0.7 0.4Peanuts 6.2 1.9 4.3Baked beans 3.5 2.1 1.4Lentils 1.9 0.6 1.3Potatoes 1.2 0.7 0.5Carrots 2.5 1.4 1.1

Adapted from Englyst et al. (1988). Reproduced with kind permission of Blackwell Science Ltd.

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which can be absorbed across the mucosal wall ofthe digestive tract and used by the cells in metab-olism. Digestion is brought about by both physi-cal and chemical means. Biting and chewing inthe mouth, and churning by the stomach, ensurethat pieces of food are broken down into a semi-liquid chyme, so that enzyme action can occur.

Sugars

The diet contains simple sugars not only of dif-ferent sizes but also in different physical states.Some are consumed in their natural state, con-tained within the cells of the food plant. Theseinclude all the simple sugars found in fruits andvegetables. We eat them with the cell walls andother plant material with which they are asso-ciated. Eating them often requires a certainamount of effort in biting, chewing and diges-tion. These sugars have been termed ‘intrinsic’,and are generally considered to have little or noundesirable effects on our health.

In addition, the diet also contains sugarswhich are free, that is, extracellular or not con-tained within cells. These come from milk, wherethe lactose is free in solution, from honey, whichcontains free fructose and glucose, and from the large number of foods that contain addedsugars. These sugars are ‘unpackaged’ and readilyavailable both for bacterial action in the mouth,and for rapid absorption and metabolism. Thename ‘extrinsic sugars’ has been given to thisgroup. Those present in milk are not consideredto cause detrimental effects to health. However,the ‘non-milk extrinsic sugars’, which includesucrose, corn syrup and synthetic fructose inrecipes and manufactured foods and drinks,have potentially damaging effects for health.These will be considered in more detail later inthe chapter.

Whether sugars are intrinsic or extrinsic willdetermine how much cellular breakdown has totake place before they are released. Apart fromthis, the simple monosaccharides require nodigestion before being absorbed. Disaccharides,such as lactose and sucrose, require to be split bytheir specific enzymes, lactase and sucrase, intomonosaccharides before they can be absorbed.These enzymes are to be found in the brush

border of the mucosal cells of the duodenum andupper jejunum. Studies of the process of diges-tion show that the digestion of sucrose and lac-tose is virtually complete in the small intestine.

However, some individuals lack the enzymelactase and are thus unable to complete thedigestion of this sugar. This may arise for twodifferent reasons. The most common is ‘primarylactase non-persistence’, which is a normal dis-appearance of lactase from the mucosal cellsafter infancy. This occurs in many ethnic groupsaround the world whose customs do not includethe use of milk beyond infancy. Caucasians areone of the few groups who continue to producelactase throughout life; even so, the ability todigest lactose declines with age. In the UK, lac-tase non-persistence has been recorded in 55 percent of ethnic Indians and 82 per cent of ethnicAfro-Caribbeans. If milk is consumed by some-one with lactase non-persistence, the lactoseremains in the intestines, attracting water andcausing a feeling of distension, abdominal dis-comfort and diarrhoea. These signs result fromfermentation of the lactose by intestinal bacteria,producing large amounts of gas and acid. Milkderivatives such as yogurt, in which the lactosehas been fermented, do not cause these problems.In addition, small amounts of milk may be toler-ated if introduced gradually. The use of probioticpreparations that contain milk-fermenting bac-teria can also facilitate tolerance to milk.

Lactase deficiency may also arise as a sec-ondary condition, resulting from damage to theintestinal mucosa by some other disease process,such as malnutrition, HIV infection and parasiticinfestations. Deficiencies of sucrase may alsooccur, but these are rare.

Starch

In the mouth, salivary amylase (ptyalin) acts oncooked starch granules. It is not clear how farthis digestion progresses and whether there aredifferences between people who eat their foodvery quickly and those who chew each mouthfulthoroughly. It is also possible that this earlybreakdown of starch in the mouth may make asignificant difference to overall digestibility. Theenzyme travels down to the stomach, mixed with

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chewed food. It is now thought likely that, pro-tected by starch and some of its degradationproducts, salivary amylase continues to be activeuntil the chyme reaches the small intestine.

Here, pancreatic amylase continues the break-down of starch, acting on 1–4 linkages in bothraw and cooked starch. Amylose in starch isdegraded to mainly maltose and maltotriose, withsmall amounts of glucose produced; amylopectinsare broken to oligosaccharides by the time thechyme reaches the distal part of the duodenum.

Digestion is completed by oligosaccharidasesbound to the surface of the brush border cells;these are substrate specific and liberate glucoseas the end-product of the digestion process.

Some starch is resistant in varying degrees to digestion by amylases. A classification of thedigestibility of starch has been proposed (seeTable 6.2). It must be remembered, however, thatdigestibility is variable and probably dependenton the composition of the meal.

Also the nature of starch granules varies fromone food to another, some being more susceptibleto the action of amylase than others. Most readilydigested are the starches of most cereals, sweetpotato and tapioca. Starch from raw potato andunripe banana is resistant, but cooking of thepotato and ripening of the banana increasesdigestibility. Starch in peas, beans and yams ismost resistant to digestion by amylase. Dietaryoligosaccharides, found in onions, garlic andleeks, artichokes, beans, peas and some cerealsare not broken down or absorbed in the smallintestine, and pass further along the bowel

together with resistant starch (although they arenot starch molecules).

Resistant starches that escape digestion inthe small intestine become available for fermen-tation in the colon by the bacterial flora. Theresult of this process is an increase in faecalmass owing to the multiplication of the bacteria,production of short-chain fatty acids (acetic,propionic and butyric acids) and a decrease incolonic pH. In addition, CO2, H2 and some CH4

are produced. These contribute to a sensation ofbloating and flatulence. It has been estimatedthat between 20 and 30 per cent of the potentialenergy contained in the resistant starch becomesavailable to the body in the form of short-chainfatty acids absorbed from the colon. Figure 6.5summarizes the digestion of carbohydrates.

Non-starch polysaccharides

In the mouth, high-fibre foods generally requiremore chewing. This slows down the process ofeating and stimulates an increased flow of saliva.The saliva contributes to the volume of the swal-lowed food bolus. Once in the stomach, the fibre-rich food tends to absorb water and the solublecomponent starts to become viscous. Both ofthese changes delay stomach emptying. In thesmall intestine, the soluble fibre travels slowlybecause of increased viscosity; this prolongs theperiod of time available for the absorption ofnutrients. The fibre may also bind some divalentions in the small intestine, making them unavail-able for absorption at this point.

Classification of starch according to digestibilityTABLE 6.2Type of starch Example of occurrence Probable digestion in small intestineRapidly digestible Freshly cooked starchy food RapidSlowly digestible Mostly raw cereals Slow but completeResistant

Physically inaccessible Partly milled grains and seeds ResistantResistant granules Raw banana and potato ResistantRetrograded Cooled, cooked potato, bread and Resistant

cornflakes, savoury snack foods

From Englyst, H.N. and Kingman, S.M. 1990: Dietary fibre and resistant starch: a nutritional classification of plant polysac-charides. In: Kritchevsky, D., Bonfield, C., Anderson, J.W. (eds), Dietary fibre. Reproduced with kind permission of Plenum Press Publishing Corporation, New York.

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Once in the large intestine, the soluble fibrebecomes a food source for the growth and multiplication of the bacterial flora. The con-sequences of this are exactly the same asdescribed above for resistant starch. Thus, both

resistant starch and soluble NSPs contribute toincreasing bulk in the large intestine, and theproduction of fatty acids and gases.

Insoluble fibre, which has reached the colonlargely unchanged, swells by water holding, and

Figure 6.5 Digestion of carbohydrates.

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adds further to the volume of the colonic con-tents. The faeces, therefore, are both bulkier andsofter because of the increased water content.

Absorption of carbohydrates

After digestion, the resulting monosaccharides areabsorbed from the gut lumen across the mucosainto the blood by one of three mechanisms:■ simple diffusion;■ facilitated diffusion; or■ active transport.

The latter two processes allow faster absorp-tion of the simple sugars than could be achievedby simple diffusion alone. This becomes particu-larly important in the later stages of absorption,as concentrations in the gut lumen fall. Activetransport involves the breakdown of ATP andthe presence of Na�.

Absorption of sugars causes a variable rise inblood sugar. When given individually, glucoseand maltose produce the greatest increase, fol-lowed by sucrose, lactose, galactose and fruc-tose. The effects are not necessarily the samewhen these sugars are consumed as part of ameal. The level of glucose in the blood rises to amaximum in about 30 minutes and falls to fast-ing levels after 90–180 minutes. The rate of riseto the maximum and the rate of fall vary withthe nature of the meal, and are related to thedigestion rates occurring in the small intestineand the speed of release of glucose.

It is possible to measure the relative effectsof different carbohydrate foods on the bloodsugar level. The rise in blood glucose followingingestion of a portion of a test food containing50 g of available carbohydrate is compared withthe effect on blood glucose of a 50 g availablecarbohydrate portion of a standard, such as glu-cose or white bread. Comparison of the areasunder the two glucose curves obtained producesa ‘glycaemic index’ (Figure 6.6).

The glycaemic index of a large number offoods has been determined. Glycaemic responsesvary between individuals, but the ranking ofresponse to different foods can be predicted fromthe standard results. Foods grouped according totheir glycaemic index are shown in Chapter 16.

Diets with a low glycaemic index have beenshown to have various health benefits, includingreduction of blood lipids and improved bloodglucose control in diabetic subjects. They alsoenhance satiety and increase athletic endurance.More research is needed to increase the evidencebase on relationships between glycaemic indexand health, in specific conditions and for thegeneral population. There are moves to introducelabelling of products with their glycaemic index,although there needs to be public educationabout the significance of this measure before anysuch initiative.

By definition, we would not expect the non-starch polysaccharides to be absorbed. However,these compounds do not travel through thedigestive tract completely unchanged. Physicalbreakdown and bacterial fermentation are themain changes that alter both the soluble andinsoluble fibres as they pass through the digest-ive tract. Some of the fatty acids released as aresult of fermentation are absorbed and provideusable energy.

Figure 6.6 Rise in blood glucose after eating, and thecalculation of glycaemic index.

■ Why might diets with a low glycaemic indexbe beneficial in diabetic subjects?

■ What foods should be recommended?■ Why might diets with a low glycaemic index

help to promote satiety?■ In what ways might diets with low glycaemic

index be beneficial in endurance athletes?

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Metabolism of carbohydrates

In discussing carbohydrate metabolism in thebody, it is simplest to consider glucose, fructoseand galactose. These travel in the bloodstreamfrom the small intestine to the liver, where theyare stored as long chains of glucose units in the form of glycogen. The liver stores one-thirdof the body’s total glycogen (about 150 g). The remainder of the glucose may pass on to themuscles, where it is also stored as glycogen.Storage of glycogen is encouraged by insulin,the hormone produced by the � cells of the pancreas. Liver glycogen is readily transformedback into glucose whenever the blood sugarlevel falls below about 4 mmol/l. Thus, glucosecan continue to supply energy to the brain,

central nervous system and other organs whetherthe person has eaten or not. The glucose fromthe blood passes into these tissues where it isoxidized and energy is released by means of oneof several pathways (glycolysis, tricarboxylicacid cycle, hexose monophosphate pathway),depending on circumstances. A number of vita-mins are needed to achieve this oxidation, mostnotably thiamin, riboflavin and nicotinic acid.Insulin is also needed to facilitate the entry ofthe glucose into tissues (see Figure 6.7). Muscleglycogen is not used to maintain blood sugarlevels, rather its role is to provide energy directlyfor muscle contraction.

Glycogen is stored in association with waterand is a bulky way of storing energy. Thus, the

Figure 6.7 Metabolism ofcarbohydrates.

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body only contains enough glycogen to provideenergy for relatively short periods of time,although new research suggests that glycogenstores are well controlled. Longer term energystores are maintained in the form of fat and, as alast resort, as protein. If we take in more carbo-hydrate than we need, the body will use the glu-cose to fill its glycogen stores and then couldconvert the remaining glucose into the more per-manent storage form – fat. Unlike the limitedstorage capacity for glycogen, the body can storeunlimited amounts of fat. In practice, this doesnot occur in humans to any significant extent andcarbohydrate metabolism is stimulated to utilizethe excess carbohydrate. As a consequence,energy from fat is not used and fat may be stored.Fat synthesis from carbohydrate only occurswhen extremely large amounts of carbohydrateare consumed over a period of days.

Why do we needcarbohydrates in the diet?

From the above discussion, it is clear that carbo-hydrates are an important source of energy forthe body, providing glucose for immediate useand glycogen reserves (see Figure 6.8). All thecells of the body require glucose and some, suchas the brain, nervous system and developing redblood cells, are ‘obligatory’ users of glucose. We are able to make some glucose from proteinsand fats in the process of gluconeogenesis. Thisenables the body to survive when the glycogenstores are depleted and no carbohydrate has beeneaten. Almost all the body’s amino acids (those

known as glucogenic) and the glycerol part oftriglycerides (about 5 per cent of the weight offat) but not the fatty acids can be converted toglucose. However, using protein to make glucoseis potentially harmful, since tissue protein maybe broken down. This happens in starvation bothin the early stages before the body adapts tousing more fats for essential energy, and in thefinal stages when body fat stores have beendepleted, and the body’s structural protein isbeing used for energy.

A further problem arises when there isinsufficient carbohydrate available to completefat metabolism. In the absence of carbohydrate,acetyl coenzyme A accumulates and condensesto form ketone bodies. This state, known asketosis, is associated with mild disturbances ofcellular function and is an early indication ofinsufficient carbohydrate availability in thebody. So, even though glucose can be producedfrom non-carbohydrate sources, the processesare inefficient and potentially harmful, andindicate a specific need for carbohydrate in thediet to supply energy.

Carbohydrates are also used in the synthesisof various metabolically active complexes.Glycoproteins are important components of cellular membranes, in particular on the extra-cellular surface. They are also found as circulat-ing proteins in blood or plasma. Glycolipids,such as sphingolipids and gangliosides, haveroles at receptor sites on cells and in synaptictransmission.

Mucopolysaccharides have important water-holding or binding properties in many sites of

Figure 6.8 Why do we needcarbohydrates in the diet?

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the body; they occur in basement membranesand in intercellular cement and form an integralpart of cartilage, tendon, skin and synovial fluid.Disorders of mucopolysaccharide metabolismhave been associated with a number of diseasestates. Little is currently known about the influ-ence of dietary sugars on these compounds oron specific quantitative requirements.

How much carbohydrateshould we have?

The intake of dietary carbohydrate must not onlybe sufficient to provide the necessary energy forthe survival of the body, but must also containsufficient specific sugars to allow the synthesis ofessential complex molecules. However, this isdifficult to quantify; it is much easier to calculatethe amount of protein needed by the body tomaintain nitrogen balance, and the amounts offat to supply the essential fatty acids.

The only true requirement for carbohydratesthat current knowledge has identified is for theprevention of ketosis. Estimates of the minimumamount of carbohydrate needed by an adult arein the range of 150–180 g carbohydrate per day.This does not necessarily need to be suppliedentirely from the diet: 130 g could be synthe-sized by gluconeogenesis, with the remaining50 g provided exogenously from food. The totalfigure represents 29 per cent of the total energyexpenditure.

Studies on pregnant rats indicate that a min-imum amount of carbohydrate, up to 12 per centof glucose, is needed to sustain pregnancy andlactation and avoid high mortality rates in theoffspring. This points to other specific require-ments for synthesis of carbohydrate-containingcomplexes.

In the UK, the recommendations made aboutcarbohydrates use an ‘optimum’ intake approach,which includes an amount sufficient to: preventketosis; avoid starvation but not induce obesity;avoid adverse effects on the large intestine, andon lipid and insulin metabolism; and to avoidcaries. In addition, the intake should contributeto an enjoyable diet. The sources of carbohydrateshould be as unprocessed as possible, as anyincrease in the degree of processing is linked with

possible adverse effects. The dietary referencevalues report suggests that:■ dietary carbohydrate should supply 50 per

cent of energy;■ sugars not contained within cellular struc-

tures (the non-milk extrinsic sugars) shouldconstitute no more than 10 per cent of theenergy; and

■ the balance should be made up from com-plex carbohydrates and other sugars, suchas those in fruits and milk.Dietary guidelines published in other coun-

tries on the whole adopt a similar approach tosugar intake with a level of approximately 10per cent being recommended. Some scientistsbelieve that such a low level is not achievablealongside the goal to lower fat intakes. Studiesof the British diet have shown that a reciprocalrelationship exists between intakes of fat andrefined sugars, and that lowering the sugarintake is likely to cause an increase rather thanthe desired reduction in the intake of fats. Thishighlights one of the dilemmas associated withlooking at individual nutrient components ofthe diet to compile ‘whole diet’ guidelines.

The National Food Survey 2000 (DEFRA,2001) showed the reciprocal trend in carbohy-drate and fat intakes in the UK over the past 60 years, with a decreasing percentage of theenergy from carbohydrate being accompaniedby an increased percentage from fat. Recently,this trend has reversed and, currently, carbohy-drate percentage is rising, as fat percentagefalls. The most recent survey showed that car-bohydrates provided 46.6 per cent of totalenergy. The total intake of carbohydrates was218 g from household food, which contained131 g of starch and 87 g of total sugars (includ-ing 47 g of non-milk extrinsic sugars). A further21 g of carbohydrate was consumed from foodseaten outside the household. These figures show that the proportions of carbohydratesconsumed in the UK do not match the dietaryguidelines.

Carbohydrates and health

There is a great deal of confusion surroundingthe links between carbohydrates and health.

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Opinions about carbohydrates include thefollowing:■ ‘they are fattening’;■ ‘they provide instant energy’;■ ‘they are bad for the teeth’;■ ‘they are essential to life’’.In order to evaluate these views, it is necessaryto distinguish between the various types of carbohydrates in the diet, since each behavesdifferently in the body.

Health aspects of sugars

In general, moderate amounts of sugar in thediet give us pleasure without harming health. Itis only when amounts eaten become large andpossibly displace more nutrient-dense itemsfrom the diet that there is potential for harmfuleffects. Their concentration in the mouth haspotential to damage the teeth and the rate atwhich the digestion products of sugars enter theblood can have consequences for metabolism.Each of these possible health consequences willbe evaluated.

Do they supply ‘empty calories’?This term implies that sugars provide nothing but energy, as they contain no other nutrients.Intrinsic sugars eaten in association with cellwall material are slowly released during diges-tion. It is not easy to consume large amounts ofintrinsic sugars, as they come packaged alongwith plant cell wall materials, for example, infruit. In this case, intrinsic sugars are associatedwith other nutrients, such as vitamin C, caroteneand potassium. The non-milk extrinsic sugars, inparticular sucrose (but also other simple sugars

added during food manufacture), can be presentin some foods, such as sugar confectionery orsoft drinks, where they might be the only nutri-ent. In this case, sugar would supply only energy.If the sugar is present in large concentrations inonly a small volume of food, large amounts canbe consumed without our being aware of it. In anactive individual whose daily energy needs areperhaps 12.6MJ (3000Calories), large amountsof sugar may make little difference to the overallnutrient content of the diet. This is because manyother foods are being eaten to provide the neces-sary energy. Several studies, both in childrenand adults, have shown that when a high sugarintake is part of a high energy intake, micronu-trient intakes are not compromised. However, insomeone who has only a small energy require-ment perhaps of 6.3 MJ (1500 Calories), a highintake of sugar would allow little space in therest of the diet for nutrient-rich foods. In thiscase, the diet may well be short of essentialmicronutrients.

Nevertheless, a subject with a small appetiteshould not be prevented from eating sugar, assmall amounts might enhance the palatabilityof the diet and might encourage a greater over-all food intake. This is particularly applicable toolder people or those with illnesses affectingappetite.

Does sugar lead to overweight?Worldwide studies tend to show that obesity in a population rises as sugar intake increases.However, this is an oversimplification, since therelationship may not be causal. In general, fatintakes are much better correlated with theoccurrence of obesity than are sugar intakes.Epidemiological surveys of different populationshave repeatedly observed an inverse relationshipbetween reported sugar consumption and thedegree of overweight.

It is also possible to show that removingsugar from the diets of volunteers causes weightloss and, if sugar is unknowingly substituted by artificial sweeteners (thus leaving the sweettaste), energy intake is reduced and not com-pensated by an increase in other foods. Theseresults imply that including sugar in the dietinflates the energy intake.

Perform a small survey, asking your friends andfamily what they believe about carbohydrates, inrelation to health. Is there a difference in answersaccording to the gender of the respondent ortheir age?

When you have completed the study of the fol-lowing section, return to your answers and checkhow many correct opinions were expressed.

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Further information comes from studies onthe satiating effects of carbohydrates. After con-sumption, digested carbohydrates can influencea number of physiological mechanisms involvedin satiety. These studies show that, although thesensory characteristics of sweet carbohydratesencourage consumption at the outset, carbo-hydrates later act as effective appetite suppres-sants, reducing hunger ratings and subsequentfood intake.

On balance, therefore, it seems that sugarsare not a major culprit in the development of overweight. It should be remembered that 1 gof carbohydrate provides 16 kJ (3.75 Calories),compared with 37 kJ (9 Calories) per gram of fat,17 kJ (4 Calories) per gram of protein and 29 kJ(7 Calories) per gram of alcohol.

Dental cariesAlthough the 1980s saw a fall in the incidence oftooth decay in many parts of the UK, this declinehas stopped, and incidence is again increasing.Caries in early childhood affects one in ten of all3–4 year olds in the UK. There is regional vari-ation, and in Scotland, 50 per cent of childrenaged 3.5–4.5 years had experienced caries. In 30per cent of these it had extended into the dentalpulp. Extensive evidence suggests that the mostimportant dietary factors in the causation ofdental caries are simple sugars. In the surveysmentioned, there was a higher incidence ofcaries in children who used a sweetened com-forter. In older children, a study of 12-year-oldsin England found that 50 per cent had no decay.

Numbers of decayed teeth continue to increaseinto adulthood, with averages from surveys inthe UK reported to be:

16–24 years 10.8 decayed, missing orfilled teeth

25–34 years 16.035–44 years 19.0

These figures demonstrate that caries is a prob-lem for all age groups, but may also reflect therecent improvement in dental health among theyounger adults, compared with the older groupshown here.

Teeth are generally covered in a layer ofplaque made up of bacteria (Streptococcusmutans is the prevailing species) and sticky poly-saccharides. The dietary sugars provide the sub-strate for the multiplication of oral bacteria andthe production of acid as a fermentation product.The acid causes a fall in pH within 5–10 minutes;as the pH reaches a critical value of 5.4, the toothenamel begins to demineralize. Fortunately,buffers in the saliva work to restore normal pHlevel, generally within 30 minutes of the con-sumption of sugar. However, if sugar consump-tion occurs at frequent intervals, the teeth areexposed for prolonged periods of time to the lowpH, resulting in damaging demineralization andthe development of caries (see Figure 6.9).

The evidence comes from a number of dif-ferent types of study.■ Observations of the rate of dental caries in a

population and its relationship with sugarconsumption show a close correlation. This

Figure 6.9 Development of dentalcaries and the role of diet.

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applies when different countries are com-pared or when comparisons are made at dif-ferent times in the same country. From thesedata it has been possible to show that, on apopulation basis, an increase in the averagedaily intake of sugar by 20g/day is associatedwith one extra decayed/missing/filled tooth.

■ Studies on isolated communities have shownthat, where sugar consumption is negligible,dental caries is unknown. Introduction ofsugar into the diet is accompanied byincreased incidence of tooth decay.

■ Intervention studies, in which sugar intake ismanipulated, both in terms of quantity andtiming of consumption, have shown a clearrelationship with dental caries.

■ Most recently, studies in which oral pH hasbeen measured following consumption ofsugar-containing foods and drinks show therapid fall in pH that follows sugar intakeand that results in dissolution of the toothenamel. Experiments in animals confirm thepivotal role of sugars in the process; artifi-cial sweeteners in foods are not associatedwith development of decay. Studies ofplaque microorganisms in culture providefurther evidence of their ability to generateacids from sugar substrates.All of these studies confirm that the most car-

iogenic (caries-causing) sugars are the non-milkextrinsic sugars, which are present on the toothsurface without cell walls. Also relevant are theconcentration of the sugar, the period of contactand the frequency of consumption. Thus, a lowconcentration that passes through the mouthvery quickly will have much less effect than aconcentrated source of sugar present in a stickyform that remains in the mouth for a long time. A further factor is the amount of saliva producedto wash away the sugar remnants and buffer theacid. More saliva flows at the end of a meal thanwhen a small sugary snack is eaten. Thus, lessdamage will be caused to teeth if sugar is con-sumed with meals. Glucose and fructose are fer-mented at a similar rate to sucrose, but theiroverall impact on dental health is less as they areconsumed less often and in smaller amounts.

In contrast, starch is poorly fermented by theoral bacteria and is, therefore, less acidogenic.

Cooked staple starchy foods, such as rice, pota-toes and bread are, therefore, of low cariogenic-ity. Uncooked starch is of very low cariogenicity,but also is rare in human diets. Some foods contain cooked starch together with substantialamounts of added sugars. These will be cario-genic to the same extent as a similar quantity ofsucrose.

Recommended intakes of sugar for dental healthTwenty-three national expert committees aroundthe world have set targets for the intake of addedsugars, the average being 10 per cent or less ofenergy intake. This is also the recommendationmade by the UK Dietary Reference Values Report(DoH, 1991).

The dose–response relationship betweencaries and extrinsic sugar consumption showsthat sugar levels should not exceed 60 g/day foradults and teenagers. For younger and pre-school children, these intakes should be propor-tionately reduced. Thus an intake of 30 g/daywould be advised for a pre-school child. Inaddition, the European guidelines state thatsugar consumption should be no more than fouroccasions per day. Above this frequency, thereis an increased risk of dental caries.

Advice relating to reducing caries risk from sugar consumption was compiled by theCommittee on Medical Aspects of Food Policyin their report on ‘Dietary sugars and humandisease’ (DoH, 1989). The main points are sum-marized as follows.■ The consumption of non-milk extrinsic

sugars should be decreased and replaced by fresh fruit, vegetables and starchy foods.

■ Those providing food for families and com-munities should seek to reduce the frequencywith which snacks are consumed.

■ For infants and young children, simple sugars should not be added to bottle feeds;sugared drinks should not be given in feederswhere they may be in contact with teeth forprolonged periods; dummies or comfortersshould not be dipped in sugars or sugarydrinks.

■ Schools should promote healthy eating pat-terns both by nutrition education, and by


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providing and encouraging nutritionallysound food choices.

■ Elderly people with teeth should restrict theamount and frequency of consumption ofnon-milk extrinsic sugars because their teethare more likely to decay owing to exposureof tooth roots and declining salivary flow.

■ When medicines are needed, particularly longterm, ‘sugar-free’ formulations should beselected by parents and medical practitioners.

■ Dental practitioners should give dietaryadvice, including reduction of non-milkextrinsic sugar consumption, particularly tothose who are prone to dental caries. Tofacilitate this, the teaching of nutrition dur-ing dental training should be increased.

Diabetes mellitusEvidence linking diabetes mellitus with carbo-hydrate consumption and especially sucroseconsumption is far from conclusive. Non-milkextrinsic sugars, because of their rapid rate ofdigestion and absorption, can result in a rapidincrease in blood glucose and high levels ofinsulin. However, restriction of sugar intake may form part of the management of diabeticpatients. Non-insulin-dependent diabetes melli-tus, which develops more commonly in olderpeople, is linked with overweight and it can thusbe supposed that excessive intake of any sourceof energy may increase the risk of its develop-ing. A diet rich in complex carbohydrates andcontaining non-starch polysaccharides is recom-mended in the management of diabetes.

Metabolic consequences of sugar intakeWhen sucrose is fed to subjects at levels of18–33 per cent of total energy intake, a numberof changes occur in the serum profile. It isbelieved that these result from a rapid influx ofsugars into the circulation. The changes include:■ increased fasting plasma triglycerides in

men and post-menopausal women;■ decreased HDL cholesterol;■ increased fasting insulin levels.

It is suggested that these effects are particu-larly noticeable in a subsection of the popula-tion, possibly about 15 per cent, who are deemed‘carbohydrate-sensitive’. These changes in serum

lipids and insulin have all been associated withdisease, although a direct casual link with sugarsis not proven. Diseases that may be implicatedinclude coronary heart disease, diabetes, gall-stones, hypertension and kidney stones.

Other consequences for healthA number of other conditions have been linkedwith a high sugars intake, although the evidenceon these is scant. People who suffer from Crohn’sdisease have consistently been reported to have ahistory of a high sucrose intake, compared withcontrols. Although a precise mechanism is as yetunproven, it is possible that sugars in high con-centrations may affect intestinal permeabilityand damage the mucosal wall, leading ultimatelyto gastrointestinal disease. There is also a sug-gested relationship between sugars and hyper-active, criminal or delinquent behaviour.

There is a widespread belief that ingestion ofglucose or a carbohydrate-rich food can improveintellectual performance. This is difficult to eval-uate as there are many aspects of mental func-tion that can be measured and the effects ofglucose are not consistent. However, reactiontime tests, information processing, word recalland memory tests have all been shown toimprove after a glucose drink. Variations in glu-cose control may also affect mental function.The evidence for these results and mechanismsmediating the findings, however, remain elusive.

SummaryThe present household intake of total sugars inthe UK amounts to 87 g/head per day (DEFRA,2001) and includes 47 g of non-milk extrinsicsugars (NMES). The food groups contributing tototal and NMES intakes are shown in Table 6.3.These figures do not include the additional 20 gof NMES consumed outside the home, from softand alcoholic drinks and confectionery.

Overall, 22 per cent of total energy comesfrom sugars, although there are substantial dif-ferences between the age groups. For instance,breastfed and bottle-fed infants may obtain 40 per cent of their total energy from sugars. Thisgradually declines to 26–29 per cent among pre-school children and 19–25 per cent in older chil-dren. Levels of intake among adults fall between

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17 and 21 per cent of energy, although studies onunemployed adults found levels up to 25–28 percent of total energy intake coming from sugars.

At these levels of intake, it is unlikely thatsugars increase the risk of cardiovascular dis-ease, high blood pressure or diabetes. There isalso no sound evidence that sucrose causesbehaviour problems. However, people with sugarintakes in excess of 200 g/day should replacesome with starchy food. Finally, sugars can con-tribute to obesity and overweight, as can almostany other food, if consumed in excess of energyneeds. People who are trying to reduce theirweight should reduce their sugar intake as wellas their total food intake.

Health aspects of starch

For many years, starchy foods had a bad nutri-tional image. This started to change in 1977,when the McGovern Report (Select Committee onNutrition and Human Needs, 1977) recommendedthat complex carbohydrates should be increasedto compensate for the reduction of fat needed tocut heart disease rates. Starchy foods have manynutritional advantages. Foods such as potatoes,bread and other cereal products, nuts, pulses andseeds provide not only complex carbohydrate inthe form of starch, but also non-starch polysac-charides and other nutrients, such as protein, ironand the vitamins B and E.

Starchy foods had a reputation for being‘fattening’ and were often the first items to becut out of weight-reducing diets. In fact, theyhave a lower energy density and a higher satietyvalue than most foods with a significant fatcontent. For example, a plate of potatoes or ofrice contains the same amount of energy as four

average biscuits, yet most of us can imagine thedifference in the feeling of fullness produced.Increasing the consumption of starchy foodscan reduce the proportion of fat in the diet.

An economic advantage of starchy foods isthat they are inexpensive. Where people have tolive on a low income, they can be very valuablenutrient-rich foods.

During passage through the digestive tract,the products of starch digestion are releasedslowly. Consequently, the effects on blood sugarlevels are small and these foods tend to have alower glycaemic index. It is for this reason thatstarchy foods are particularly advantageous inthe management of diabetes. Resistant starchpresent in starchy foods has properties similar tothose of non-starch polysaccharides and, there-fore, shares some of the health benefits of thisgroup of carbohydrates.

In the UK, the average domestic consump-tion of starches amounts to 131 g/person perday (DEFRA, 2001). This represents 28 per centof total energy intake. The major food sourcesof starch are:

Cereals and cereal 74% of totalproducts

Potatoes 10% of total

Intakes of starchy foods are almost 50 percent higher in men than women. This may reflectthe prevailing belief among women that starchyfoods are ‘fattening’; however, it may also reflectthe higher total energy intake of men. The dietaryreference values report (DoH, 1991) suggests thatstarchy foods should comprise 37 per cent of thetotal energy intake. It can thus be seen that, ingeneral, the UK diet is lacking adequate amountsof complex carbohydrates.

Food groups contributing to total and non-milkextrinsic sugars (NMES) intakes (DEFRA, 2001)TABLE 6.3

Food group Contribution to Contribution to total sugars (%) NMES intake (%)

Cereals and cereal products 24 29Sugars and preserves 21 40Fruit 19 13Milk and milk products 19 —


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Health aspects of non-starchpolysaccharides

Figure 6.10 summarizes the effects of non-starch polysaccharides on the digestive tract.From this, it is possible to consider the proposedhealth benefits of NSPs.

In the mouth, the presence of NSP can pro-mote dental health. This may be the result of thephysical effects indicated in the figure, as well asthe different foods eaten on a higher fibre diet.

The presence of NSPs in the stomach cancontribute to the sensation of satiety, and pos-sibly help in weight maintenance. The increasedviscosity resulting from soluble NSP slows empty-ing from the stomach. The association of nutri-ents with cell wall material results in a longerdigestion process, before nutrients are liberated.

In the duodenum, the viscous contents moveslowly and release their nutrients over both alonger time and a greater length of the gut. This

Figure 6.10 Summary of the effects of non-starch polysaccharides in the digestive tract.

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means that the rise in blood levels of nutrients isprolonged and attains lower peaks. The majorapplication of this rests in the management ofdiabetes, where better control of blood sugarlevels can be achieved. Both soluble and insol-uble sources of NSP can play a role. It has beensuggested that between meals blood glucose levels may be regulated by insoluble NSP intake, although further research is required.

Most of the effects of NSPs occur in the largeintestine. Bowel contents are increased in volumeby a number of mechanisms. This facilitatespropulsive contractions of the large intestine andreduces the transit time. As a result, less pressureis needed to move the bowel contents. This isbelieved to be of benefit for a number of boweldisorders, including constipation and diverticulardisease. (In diverticular disease, there are smallpockets, or hernias, formed in the mucosa of thecolon, which may become inflamed. It is thought that high pressure in the bowel may contribute to their formation.) It has also been proposed that regular consumption of an NSP-rich dietmay reduce the risk of appendicitis, and may be of benefit in some cases of irritable bowel syndrome.

If intakes are low, the converse effects areseen, with small volumes of bowel contents,which move slowly and allow harmful residuesto persist. Some metabolites may be absorbedand have metabolic consequences (e.g. on chol-esterol metabolism). The increased pressure gen-erated in moving bowel contents may damagethe colonic mucosa. Finally, the alkaline pHencourages growth of anaerobic bacteria, whichare associated with the production of more harm-ful metabolites, including some carcinogens.

Unabsorbed NSP has the facility to bindother substances. This is the result of chargedparticles on its surface as well as the mesh-likestructure, which can physically trap other mol-ecules. Consequently, possibly harmful metab-olites or residues can be eliminated from thebowel with the NSP residues. This includes bilesalt metabolites, cholesterol, drug and hormoneresidues, and possible carcinogenic byproductsfrom the diet. While these are still present in thebowel, their concentration may be reducedbecause of the greater water content associatedwith the NSP. Thus, NSP may be of benefit in

prevention of gallstones, coronary heart diseaseand various cancers.

Although many of these mechanisms appearpossible, it is difficult to obtain conclusive evi-dence of the preventive role of NSP in manydiseases. This is mainly because:■ an increased intake of NSP is often associ-

ated with other ‘healthy’ aspects of the diet,such as lower fat intakes;

■ many of the diseases mentioned take manyyears to develop; therefore, studies need tobe prolonged;

■ the diseases may be multifactorial in originand NSP may be only one of several factorsinvolved; and

■ techniques to measure NSP intakes accur-ately are still being developed.Nevertheless, epidemiological data do sug-

gest that in populations where NSP (or fibre)intakes are higher, bowel disorders are less. It ison this basis, especially in relation to constipa-tion, that the dietary reference value report(DoH, 1991) makes the recommendation thatNSP intakes should be on average 18 g/day, withan individual range from 12 to 24 g/day. Thiswould increase the average stool weight by 25per cent to a level of 100 g/day. Population stud-ies indicate that, at higher stool weights, there isa reduced risk of bowel cancer, gallstones anddiverticular disease.

In addition to these effects, there is consist-ent evidence that an increase in the NSP intakeof the diet, without an increase in energy, isassociated with a modest weight loss. This mayaverage 1.9 kg over 3.8 months, and is of a simi-lar magnitude to those observed when percent-age of fat is reduced in the diet. The effects arenoted with consumption of high-fibre foods orfibre supplement. The exact mechanism con-tributing to the effect is unclear, but may be acomposite net result from: energy dilution in thefood, extra chewing required, gastric distension,gastric emptying, and nutrient absorption ratesand caloric excretion in faeces. On this basis, it is suggested that an increase in fibre intakes, inline with recommendations, could make animportant contribution to weight management.

Foods that provide fibre (or NSP) are thewholegrain cereals, fruits and vegetables, and itis recognized that many other nutrients and


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non-nutritional factors are also provided besidethe NSP content. For this reason it is difficult toattribute effects of a diet rich in these foodssolely to its fibre content. However, many stud-ies do show that wholegrain cereal intakes arelinked to lower incidence of chronic diseasesand it is probable that some of this effect isrelated to fibre intakes. For example:■ a significantly lower risk of mortality from

heart disease in a number of cohorts, islinked to the regular consumption of at leastone serving of wholegrain cereal per day;

■ at least one daily serving of wholegraincereal is associated with a reduced risk ofcancer, especially gastrointestinal cancer,probably through direct effects in the bowelor through a role in weight control;

■ evidence from population-based and clinicalstudies suggests that regular consumption ofwholegrain cereals in the diet may be aneffective way of lowering the risk of develop-ing Type 2 diabetes, through better gly-caemic control.In summary, there are many advantages to

be gained from an adequate intake of NSP. Thesemay be effected directly by the consequences of NSP in the digestive tract, or by some of the associated nutrients and other phytochemi-cals, which are associated with NSP in foods.Following dietary guidelines to eat more starchycarbohydrate foods and fruit and vegetables willensure adequate levels for health.

1 Carbohydrates may be classified by size and by digestibility.2 The simple sugars are readily digestible, and are important in the diet as a source of energy and for the

manufacture of carbohydrate complexes necessary for the structure and function of the body.3 Excessive intakes of simple sugars (in amounts greater than 200 g/day) are undesirable. However,

amounts smaller than this do not specifically and uniquely cause overweight or diabetes. Dental caries,however, is linked to the intake of simple sugars, especially if eaten at frequent intervals. Nevertheless,the Dietary Reference Value report recommends a maximum of 10 per cent of energy from non-milkextrinsic sugars.

4 Starches may be digestible or resistant. The digestible starches release glucose more slowly than dosimple sugars. In addition, food sources of starch generally contain other nutrients. Starches are,therefore, considered to be desirable in the diet. Resistant starch escapes digestion in the smallintestine but is fermented by bacteria in the large intestine. This is believed to be of benefit to health.

5 Non-starch polysaccharides can be classified as soluble or insoluble. The soluble NSPs contribute toviscosity in gut contents, and slow the absorption of nutrients. The insoluble NSPs retain water andincrease bulk in the large intestine. Both forms have beneficial effects for health, both within thedigestive tract and for general metabolism.

SUMMARY

1 a Draw up a table to compare the sources andproperties of intrinsic and extrinsic sugars.

b How do these sources of sugars differ intheir metabolic effect in the body?

2 a Account for the variable digestibility of starchfrom different sources in the diet.

b Why are starchy foods encouraged in the diet?3 Healthy eating advice recommends a reduction

in the intake of non-milk extrinsic sugars to 10 per cent of total energy.

a What changes in the diet would be needed toachieve this?

b What effect might these changes have onother components of the diet?

4 a Suggest practical and realistic ways in whichan increase in starchy carbohydrates intakemight be promoted.

b What other benefits might follow from thechanges you suggest?

STUDY QUESTIONS

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Ahrens, U. (ed.) 1998: Oral health, diet and other factors. British Nutrition Foundation Task ForceReport. London: British Nutrition Foundation.

Association of Official Analytical Chemists 2000: Official methods of analysis, 17th edn. Gaithersburg,MD: AOAC.

Blaak, E.E., Saris, W.H.M. 1995: Health aspects of various digestible carbohydrates. NutritionResearch 15(10), 1547–73.

Bolton-Smith, C., Woodward, M. 1995: Antioxidant vitamin adequacy in relation to consumption ofsugars. European Journal of Clinical Nutrition 49(2), 124–33.

Conning, D. (ed.) 1993: Biological functions of carbohydrates. London: British Nutrition Foundation.DEFRA 2001: National Food Survey 2000 Annual report on food expenditure, consumption and

nutrient intakes. London: The Stationery Office.DoH (UK Department of Health) 1989: Dietary sugars and human disease. Report on Health and

Social Subjects No. 37. Report of the Panel on Dietary Sugars. Committee on Medical Aspects ofFood Policy. London: HMSO.

DoH (UK Department of Health) 1991: Dietary reference values for food energy and nutrients in theUnited Kingdom. Report on Health and Social Subjects No. 41. Report of the Panel of DietaryReference Values of the Committee on Medical Aspects of Food Policy. London: HMSO.

Englyst, H.N., Bingham, S.A., Runswick, S.A. et al. 1988: Dietary fibre (non starch polysaccharides)in fruits, vegetables and nuts. Journal of Human Nutrition and Dietetics 1, 247–86.

FAO (Food and Agriculture Organization) 1998: Carbohydrates in human nutrition. Report of a jointFAO/WHO Expert Consultation. Rome: FAO.

Food Standards Agency 2002: McCance and Widdowson’s The composition of foods, 6th summaryedn. Cambridge: Royal Society of Chemistry.

Howarth, N.C., Saltzman, E., Roberts, S.B. 2001: Dietary fibre and weight regulation. NutritionReviews 59(5), 129–39.

Jackson, A.A. 1992: Sugars not for burning. In Eastwood, E., Edwards, C., Parry, D. (eds) Humannutrition: a continuing debate. London: Chapman & Hall, 82–99.

Naismith, D., Nelson, M., Burley, V. et al. 1995: Does a high-sugar diet promote overweight in chil-dren and lead to nutrient deficiencies? Journal of Human Nutrition and Dietetics 8(4), 249–54.

Richardson, D.P. 2000: The grain, the wholegrain and nothing but the grain: the science behindwholegrain and the reduced risk of heart disease and cancer. British Nutrition FoundationBulletin 25, 353–60.

Select Committee on Nutrition and Human Needs, United States Senate 1977: Dietary goals for theUnited States (McGovern Report). Washington, DC: US Government Printing Office.

Sheiham, A. 2001: Dietary effects on dental disease. Public Health Nutrition 4(2B), 569–91.

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energy needs


❏ discuss the components of energy balance: energy intake and energy output;❏ study energy intake and how it can be measured;❏ study energy output and its component parts;❏ consider the different requirements for energy in various individuals in different activities.


❏ describe the amounts of energy obtained from different macronutrient sources;❏ identify different ways in which energy intake can be measured;❏ discuss the components of energy output and their relative contribution to the total.

Energy is the essence of life – without it, wecould not survive. We need energy for all thebasic physiological functioning of the body, particularly at cellular level in active transportpumps, but also more apparent functions, suchas breathing, digestion and excretion. The mostenergy-demanding organ is the brain. In addi-tion, our muscles require energy to function –the heart to keep blood circulating to all the tissues, and our skeletal muscles to maintainposture, balance and mobility. For any activity,whether to do with our occupation, leisure orsport, more energy must be supplied. Even whenwe are asleep we are using energy. Also, in theearly years of life and during pregnancy, add-itional energy is required for growth.

This energy has to be provided from themacronutrients in our food, which are brokendown to their constituent parts by digestion andmetabolized in the tissues. Some of the energywill be used immediately (according to an oxida-tive hierarchy – see Chapter 8) and some stored.If more is eaten than is needed, there is a netincrease in the body’s energy content and thesize of the stores increases. Conversely, if thecurrent energy needs are greater than the intake

of energy, then some will have to be providedfrom stored energy. These are the fundamentalsof energy balance.

Units of measurement ofenergy

Two different units of measurement have beenused in nutrition to quantify energy, reflectingthe development of understanding of this subject.Traditionally, energy was perceived as heat andmeasured in calories, where one calorie of heatraised the temperature of 1mL of water through1°C. Measurements of energy in nutrition were in units of 1000Calories, or kilocalories (oftenshown as kcalories or Calories for simplicity).

The unit preferred by nutritionists today isthe kilojoule (or megajoule for larger amountsof energy), which is the SI unit for the measurement of energy. The joule was origin-ally defined as the amount of energy exertedwhen a force of 1 newton was moved through adistance of 1 metre. Like the calorie, it is a smallunit (1 Calorie � 4.18 joules), and so normallyappears as the kilojoule (kJ � 1000 joules), orthe megajoule (MJ � 1000 kJ) in nutrition.

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The Calorie is still widely used by the public,appears on food labels, and underpins mostweight control diets. For this reason, it has beenvery difficult for nutritionists to move entirelyto the SI measurement of energy. Food labellingin the UK, however, shows energy contents inboth units.

It is interesting to note that the unit of elec-trical energy consumption, the watt, is alsolinked to the joule. Something using electricalenergy at 1 joule/second is using 1 watt of electricity. The rate of energy use of a typicalman, 11 MJ (or 2600 Calories) per day, is about100 joules/second, or 100 watts. Feel the heatgiven out by a 100 watt light bulb, and remem-ber that you are giving out that much heatyourself!

Energy intake

This is the first part of the energy balance equa-tion and includes a study of both the quantity offood eaten by an individual, as well as its energycontent. The determinants of when and howmuch food people eat are discussed in Chapter 2,and you are recommended to refer to this sectionto consider the physiological basis of foodintake.

Energy content of foods

Different foods provide different amounts ofenergy for a given weight. This is determined bytheir content of macronutrients. Carbohydrate,fat, protein and alcohol in a food contribute toits energy content. The micronutrients, vitamins,minerals and water do not contribute to energy.In order to study energy intake, the nutritionisthas to know the energy content of foods thatmay be eaten, digested, absorbed and then oxi-dized in the body. Various methods have beendeveloped to obtain these values.

Bomb calorimeterIn a laboratory, the amount of energy containedin a food is determined with a bomb calorimeter(Figure 7.1). This is a steel vessel with a tight-fitting stopper. It is filled with oxygen underpressure and a weighed amount of the food is

placed into the crucible within. The whole appara-tus is sunk in a water bath of known volumeand temperature. The food is ignited electricallyand burns explosively as the energy held in thechemical bonds is released in the form of heat.The heat of combustion is measured from therise in water temperature.

An alternative measurement is to determinethe amount of oxygen used during the combus-tion, since this is converted to carbon dioxideand water in combining with the carbon andhydrogen molecules of the food.

Examples of heats of combustion obtainedfrom a bomb calorimeter are:

These represent the gross energy of the food,which is greater than the true quantity ofenergy obtained by the cells of the body for anumber of reasons. Small amounts of the poten-tial energy are lost during the processes ofdigestion and absorption, which are not 100 percent efficient, even in health. Estimates suggestthat digestion rates are as follows:

Carbohydrates 99%Fats 95%Protein 93%

Figure 7.1 The bomb calorimeter.

kJ/g Calories/gStarch 17.2 4.1Glucose 15.5 3.6Fat 39.2 9.37Protein (egg) 23.4 5.58

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In illness, the losses may be substantially greaterowing to vomiting, diarrhoea and inefficientdigestion and absorption.

Proximate principlesThe amount of energy that the body receivesfrom a food, called the metabolizable energy,can be calculated from values known as ‘proxi-mate principles’. These are based on extensive,meticulous experimental work, some of whichdates back to the early years of the twentiethcentury. Such was the accuracy of this work thatfew changes have had to be made to the valuesobtained with the more sophisticated techniquesnow available. The proximate principles providea value for the amount of energy that is availa-ble for metabolism from each macronutrientcontained in a food. Thus, after analysing a foodto determine its content of fat, protein, ‘availa-ble’ carbohydrate (starch and sugars) and alco-hol, it becomes possible to calculate the amountof energy provided for each 100 g of the food.These are the figures that appear in the foodcomposition tables used in the UK (FoodStandards Agency, 2002b) shown in Table 7.1.

The contribution to metabolizable energyfrom non-starch polysaccharides is discounted inthe calculation of energy used in the food tables,although they are partially fermented in the largebowel to short-chain fatty acids by bacteria.Thus, the calculated metabolizable energy maybe slightly lower than the true value, if someenergy is obtained from non-starch polysacchar-ides. On the other hand, a diet rich in non-starchpolysaccharides may interfere with the absorp-tion of some of the other macronutrients, therebyreducing the metabolizable energy obtained.

On balance, the effects may actually cancel eachother out.

In addition, there may be losses of metabol-izable energy in illness. For example, in poorlycontrolled diabetes, energy in the form of glu-cose is lost in the urine; in nephrotic syndrome,large amounts of protein, another potentialsource of energy, are excreted.

This method allows us to calculate the amountof energy the body can derive from any combin-ation of the macronutrients, in effect, therefore,any food. Using this approach, it is also then pos-sible to find out what proportion of the totalenergy taken in has actually been provided by theindividual macronutrients. Dietary guidelines aregenerally formulated in these terms. Data forselected foods are shown in Table 7.2.

Most foods do not contain the ideal propor-tions of the macronutrients as given in dietaryguidelines. It is the combination of different foodswithin a complete diet that determines whetherthe balance of the diet is right. For this reason, itis misleading to speak of ‘bad’ foods and ‘good’foods in terms of the proportions of energy theysupply from the macronutrients. All foods can beuseful, when combined with others in a mixeddiet. However, if a diet contains too many foodsthat all have a similar pattern of energy provision,perhaps containing high percentages of energyfrom fat, then the total diet risks being too high infat. It is, therefore, only an overdependence onparticular types of food, resulting in a diet whichis a long way from that suggested by dietaryguidelines that might be termed ‘a bad diet’. Itshould be remembered, however, that even such adiet can be redeemed by including foods thatredress the balance of macronutrients.

The energy conversion factors used in the currentUK food composition tablesTABLE 7.1

kJ/g Calories/gProtein 17 4Fat 37 9Carbohydrate (available 16 3.75

monosaccharide)Alcohol 29 7

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Diet surveys

Information about the energy content of foodscan be applied in a practical way to assess energyintakes of groups of the population. Usually thisis performed using survey techniques. Many suchstudies have been undertaken, using the method-ologies described in Chapter 1. However, it mustbe remembered that it is very difficult to obtainaccurate information about what people actuallyeat. In recent years, it has become clear that, in most surveys of food intake, the subjects have underreported their consumption levels. For example, the ‘Dietary and nutritional surveyof British adults’ (Gregory et al., 1990) found the mean energy intakes of the subjects to be10.2MJ (2450Calories) in the men and 7.02MJ(1680Calories) in the women. These figures arelow compared with the dietary reference values.In fact, when dieters and those who were unwellwere excluded from the sample, 40 per cent ofthe women and 27 per cent of the men were calculated to have an energy intake that was lessthan 1.2 � basal metabolic rate. This clearly pro-vides insufficient energy for any significantamount of activity as part of the daily lifestyle,and is unlikely to be the true picture. In the light

Percentage of energy from carbohydrate, protein and fat in selected foodsTABLE 7.2Food Total energy content Energy (%) from

of 100 g serving (kJ)Protein Fat Carbohydrate

Wholemeal bread 922 17 10 73Cornflakes 1601 8 2 90Boiled rice 587 8 8 84Milk, semi skimmed 195 30 32 38Cheese, Cheddar type 1725 25 75 0Butter/margarine 3042 1 99 0Low-fat spread 1519 7 91 2Egg, boiled 612 35 65 0Beef stew 570 45 42 13Chicken, roast 742 63 37 0Baked beans 355 25 6 69Peanuts 2491 17 79 5Peas 291 35 11 54Potatoes, boiled 306 10 1 89Chocolate 2177 6 52 42


Susan has a diet that provides her with a total of8.8 MJ (2100 Calories) per day, but wishes to know if it contains the appropriate proportions of themacronutrients in line with dietary guidelines. Onanalysis, the nutritionist finds that the diet contains:

Carbohydrate 200 gProtein 95 gFat 100 gAlcohol 10 g

The energy obtained from these macronutrients can, therefore, be calculated and expressed as apercentage of the total amount of energy in thediet.Carbohydrate: 200 � 16 � 3.2 MJ. Therefore, percent of total is 3.2/8.8 � 100 � 36%.Protein: 95 � 17 � 1.6 MJ. The % of total is1.6/8.8 � 100 � 18%.Fat: 100 � 37 � 3.7 MJ. The % of total is 3.7/8.8 �

100 � 42%.Alcohol: 10 � 29 � 0.29 MJ. The % of total is 0.29 /8.8 � 100 � 3%.Check these figures against the dietary guidelines(Chapter 3), and draw some conclusions aboutSusan’s intake.

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of evidence on the prevalence of overweight andobesity in the population, it was concluded thatthese values must be an underestimate of the trueintakes.

Results from the 2000 National Food Survey(DEFRA, 2001) report that the total amount ofenergy consumed per person was 1878 Calories(including household food and food eaten out).The percentages of the total energy supplied bythe different macronutrients (excluding alcohol)were:

Carbohydrates 46.6Protein 14.6Fats 38.2

Contribution from food groupsIt is also possible to obtain information from theNational Food Survey (DEFRA, 2001) about howthe major groups of foods contribute to ouroverall energy intake. The percentages of totalenergy intake from each of the groups are:

Cereals and cereal products 33(Including bread 7;biscuits, cakes 9)

Meat and meat products 14

Fats and oils 10Vegetables (including potatoes) 10Milk, dairy and cheese 13Soft/alcoholic drinks and 7

confectionery

All other food groups contribute less than 10per cent of the total energy.

Careful inspection of these figures showsthat the majority (about 80 per cent) of theenergy in the UK diet is actually obtained fromstaple foods, such as bread, cereals, pasta, pota-toes, meat, fruit and vegetables. Of the remain-der, 10 per cent is supplied by foods that containonly fat (fats and oils), and nearly 10 per centby foods that contain only simple carbohydrate(sugars), such as sugar, soft drinks and confec-tionery. These are the foods that could be termed‘empty energy’. The majority of energy in thediet is accompanied by micronutrients.

Energy output

The second part of the energy balance equationrelates to the usage of energy by the body inperforming its various functions and activities.

Using your own diet record, calculate the percent-age of the energy in your diet coming from thedifferent macronutrients.■ How do your figures compare with the dietary

guidelines?■ Can you identify particular foods in your diet

that are contributing to an especially high/lowintake of one of the macronutrient groups?

Compare your results with those of other stu-dents; if possible, produce a table of results for awhole group.■ How similar are the results?■ Which macronutrient is the most variable?■ What difference does including alcohol in the

total energy intake make to the individualmacronutrient percentages? (Check in thedietary reference values report (DoH, 1991) tosee how the guidelines vary when alcohol isincluded or excluded.)

Activity 7.2

Compare the figures given below from theNational Food Survey for the proportions of thedietary energy provided by the macronutrientswith those given in Chapter 3 as part of thedietary reference values for the UK.Which nutrients are overrepresented?Now look at how the total energy intake is madeup from the major food groups.■ How does this compare with the Balance of

Good Health recommendations? (See Chapter 3for details.)

■ Can you identify the food/food groups thatare consumed in excessive amounts, andthose that need to be increased?

■ What would happen to the total intake ofenergy and of other nutrients if one of thegroups was omitted completely from the diet?(Look at each group in turn when consideringyour answer.)

Activity 7.3

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The components of energy output or expenditurehave been studied extensively and will be con-sidered in turn (see Figure 7.2). They are:■ basal metabolic rate;■ thermogenesis (related to food intake);■ physical activity;■ growth (at certain stages of life).

Measurement of energy output

The body converts the energy of food into ATPwith an efficiency of approximately 50 per cent,with the remaining energy being lost as heat.When the ATP itself is used by the body to dowork a further loss of heat occurs, equal toapproximately 50 per cent of the energy in theATP. Finally, the work itself generates heat. Inthis way, it can be seen that a body’s total heatproduction gives a measure of the amount ofenergy that has been used.

Because of this, it is possible to use calorim-etry, or the measurement of heat, to quantify theamount of energy expenditure. If heat is meas-ured directly, the technique is known as directcalorimetry. However, in many cases, it is notpractical to do this, and an indirect approach isused, based on the utilization of oxygen. This isvalid because the rate of oxygen consumption is proportional to the amount of ATP synthesis,and each mole of ATP synthesized is accom-panied by production of a given amount of heat.It is thus reasonable to use measurements ofoxygen consumption to calculate heat produc-tion within the body.

It is possible to see from the chemical equa-tions for the oxidation of carbohydrates andfats how much oxygen is used and how muchcarbon dioxide is produced.

Glucose oxidation:C6H12O6 � 6O2 → 6H2O � 6CO2

� 15.5 kJ/g of energy

Starch oxidation:(C6H10O5)n � 6nO2 → 5nH2O + 6nCO2

� 17 kJ/g of energy

Fat oxidation:e.g. glyceryl butyro-oleostearate (the mainfat in butter)

C3H5O3.C4H7O.C18H33O.C18H35O � 60O2

→ 43CO2 � 40H2O � 39 kJ/g of energy

It can be seen that, for carbohydrate oxidation,the volume of carbon dioxide produced equalsthe volume of oxygen used. When fat is oxi-dized, however, the volume of carbon dioxideproduced is about 70 per cent of the volume ofoxygen consumed. These values are usuallyexpressed as a fraction: CO2 produced/O2 con-sumed, known as the respiratory quotient (RQ).The RQ for carbohydrates is 1.0, and for fatsaverages 0.71 (different fats have slightly differ-ent values). The non-nitrogenous portions ofproteins are, on the whole, intermediate in com-position between fats and carbohydrates and,for protein, the RQ is usually given as 0.83.

The RQ value can be used to discover theamount of energy production for each litre ofoxygen consumed, since this is also predictablefrom the equation. Normally, the body uses amixture of substrates for its metabolism, and themetabolic mixture being used can be determinedfrom a measurement of RQ. Thus a value close to0.7 suggests that mainly fats are being metab-olized; conversely, a value close to 1.0 wouldindicate carbohydrate-fuelled metabolism. Inpractice, the usual metabolic mixture providesan RQ of around 0.8.

In summary, if one can determine oxygenusage and/or carbon dioxide production, it ispossible to calculate the amount of energyreleased during metabolism. With informationabout both oxygen and carbon dioxide, it is

Figure 7.2 The components of energy output.

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possible to derive the actual RQ that applies.However, if only one of the gases has beenmeasured, an RQ of 0.8 is assumed (as this repre-sents the average metabolic mixture). It is esti-mated that not adjusting for the actual RQprobably introduces an error of 3–4 per cent,which is generally acceptable for most purposes.

Tables 7.3 and 7.4 provide the RQ and oxygenutilization values used in these measurements.

Direct calorimetryThe original human calorimeter was designed byAtwater and Rosa in 1905. This was the size of asmall room, and contained a bed and stationaryexercise bicycle. The walls were well insulated toprevent any heat loss, and all heat dissipated bythe subject was transferred to circulating waterin the walls of the chamber. Increases in watertemperature could be measured, and these repre-sented the subject’s heat loss.

In addition, the gases flowing into and out ofthe chamber could be analysed, giving add-itional information about the subject’s metab-olism. Such calorimeters are still in use today. The

major difference lies in the methods by whichthe heat output is measured in the walls of thechamber; modern calorimeters use microchipsand computers for this. There is also a reductionin size, with some modern calorimeters being thesize of a phone booth or even smaller.

The major drawback of the human calorim-eter (apart from its cost) is that it only allows alimited amount of activity, and is thus notusable for ‘real-life’ measurements.

If the calorimeter is large, the length of timetaken for any changes in heat to be measurableis longer. At a minimum, a calorimeter of 1.6 m3

provides a response in 3 minutes; one with asize of 20 m3 takes 2 hours to show a response.The accuracy of measurements with a directcalorimeter is of the order of 1–2 per cent.

Indirect methodsRespiratory gas analysisThe principle of indirect calorimetry is based onthe relationship between oxygen use and carbondioxide production, described above. To applythis, the method used must be able to measure

Energy yields obtained from the oxidation of different substratesTABLE 7.3Nutrient Oxygen consumed Carbon dioxide Respiratory Energy equivalent

(litres/g) produced (litres/g) quotient (kJ/kcal per litre of oxygen)

Starch 0.829 0.829 1.0 21.2/5.06Glucose 0.746 0.746 1.0 21.0/5.01Fat 2.019 1.427 0.71 19.6/4.69Protein 0.962 0.775 0.81 19.25/4.66

The effect on energy yield of different metabolicmixtures and respiratory quotient (RQ)TABLE 7.4

RQ kJ per litre Energy (%) derived fromof oxygen

Carbohydrate Fat0.71 19.6 1 990.75 19.8 16 840.80 20.1 33 670.85 20.3 51 490.90 20.6 68 320.95 20.8 84 161.00 21.1 100 0

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either or possibly both of the gases over a periodof time. Equipment used for this purpose rangesfrom the large and stationary to more portableversions. Obviously stationary equipment canonly be used when subjects are resting; moremobile activities require portable equipment.

Originally, the respiration chamber itself wasused, with the gases inspired and expired by thesubject sampled and analysed. More recently, ahood or small plastic tent is placed over therecumbent subject to collect the gases, whichthese days pass straight into automated ana-lysers linked to computer printouts, to provideinstant data. This type of measurement is usefulin hospital patients who may be confined to bed.The equipment must be mobile and moved to thebedside.

Mobile equipment has largely been of the‘backpack’ variety, worn by the subject duringphysical activity. The necessary link betweenthe equipment and the subject’s respiratory sys-tem has been by way of a corrugated tube,mouthpiece and nose clip. This is not especiallycomfortable, and can both limit the duration ofthe measurement and affect the normal patternof breathing.

Isotope methodsAlternative approaches have been developed inrecent years. The most significant of these is thedoubly labelled water technique, using stableisotopes of hydrogen and oxygen (2H and 18O).The subject drinks a small volume of labelledwater. The hydrogen equilibrates in the bodywater pool (producing hydrogen-labelled water),the oxygen in both the water (as oxygen-labelled water) and in the carbon dioxide pools.Thus, the 18O is contained in both the carbondioxide and water, and the 2H is contained onlyin the water; therefore, the labelled oxygen islost from the body faster than the hydrogen.

The rates of loss of the isotopes are generallymeasured in a series of samples of body fluid,such as urine, over a period of days (up to 21).The difference between the rates of loss of thetwo isotopes, therefore, represents the loss of car-bon dioxide, and can be used to calculate carbondioxide and, hence, heat production. In turn, thiscan be used to derive energy expenditure.

Several assumptions are made with this tech-nique, most notably about isotope fractionationin the body. In addition, as oxygen usage is notmeasured, the RQ has to be estimated. However,if a concurrent food intake record is kept, thenan RQ value from the intake can be calculated,assuming there is energy equilibrium.

This technique provides a useful, safe andnon-intrusive way of measuring carbon dioxideturnover, and hence metabolism over periods oftime. As a result, a large amount of informationhas been derived in recent years about energyexpenditure in groups of subjects that previ-ously have been difficult or unethical to study,such as the elderly, pregnant and lactatingwomen, and young infants and children.

Measurements of 24-hour energy expend-iture can be made by a relatively novel isotopetechnique, the bicarbonate–urea method. Thetechnique uses the isotope dilution principle.Labelled CO2, given subcutaneously as bicarbon-ate, is diluted by endogenous CO2; the extent of this dilution is measured by the isotope activ-ity in urinary urea, produced over a 24-hourperiod. This allows the CO2 produced in the body to be calculated, and energy expenditurefound using values for the energy equivalent of CO2.

Other methodsA number of other techniques have been used tomeasure energy expenditure, including:■ activity diaries;■ heart rate monitoring;■ skeletal muscle recording (electromyography);■ pedometers (to record movement);■ energy intake studies for subjects in energy

balance.All of these give less reliable results, but may beof value when groups of subjects are beingstudied, to provide more general data.

Some of the methods listed above can pro-vide estimates of the intensity of exercise orpatterns of activity during a period of exercisethat may provide useful additional information.Activity diaries are prone to omissions, espe-cially of small habitual movements, that may beimportant over a 24-hour period, and may over-report structured or intense activity.

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131

Application of measurements of energyexpenditure

In the case of individuals in hospital, it is oftenvitally important to know the exact amount ofenergy required by the body. For example,patients who are being fed intravenously havelittle opportunity to regulate their intake accord-ing to appetite. Their clinical state, for example,after major surgery, or the treatment beingadministered may have a dramatic impact ontheir metabolism, and energy needs may be aslittle as 50 per cent of those calculated, or up to 150 per cent of this value. There is, therefore,a serious risk of underfeeding or overfeeding, if exact energy expenditure is not known. Thisis particularly a hazard in overweight and obesepatients, in whom layers of adipose tissue maymask a significant loss of lean tissue.

Components of energyoutput

Basal metabolic rate

The single largest component of a person’s dailyenergy output is the basal metabolic rate (BMR).In a sedentary individual it may represent 65–70per cent of total energy expenditure. BMR isdefined as ‘the sum total of the minimal activityof all tissue cells of the body under steady stateconditions’.

This generally means that BMR is measuredwhen no digestion or absorption of food is tak-ing place (at least 12 hours after eating), and in asubject who is in a state of physical and mentalrelaxation. If measurements are made within ashorter time interval after a meal, the valueobtained is called the resting metabolic rate, as itwill be somewhat higher than the true BMR. Thegreater part of the energy is used in driving theosmotic pumps that maintain the differencesbetween extracellular and intracellular fluids,and for the synthesis of proteins and othermacromolecules. Only about 10 per cent of thetotal basal energy is used for internal mechani-cal work, including the functioning of the heart,respiratory system and digestive tract. Tables ofBMR values generally give figures as Calories orkilojoules per kilogram body weight, per hour.As a general rule, the BMR for men averages4.2 kJ (1.0 Calories) per minute and for women3.75 kJ (0.9 Calories) per minute. Metabolism in subjects during deep sleep (called minimalmetabolic rate), may be 5–10 per cent lower than BMR.

Various factors, both external and internal,can affect the BMR of an individual, and theseare now considered (see Figure 7.3).

Body weightSince basal metabolism reflects the energyneeded to sustain the function of the body, it is

Figure 7.3 Factors affecting basalmetabolic rate.

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clear that the larger the body, the greater will bethe BMR. Weight is thus a critical determinant ofBMR. Measurements on many subjects confirmthis relationship. However, the two major com-ponents of body weight make a different contri-bution to the total BMR, with lean body massbeing considerably more metabolically activethan fat mass. The metabolic activity of lean tis-sue is relatively constant between individuals, soif BMR is expressed as kilojoules or Calories perkilogram of lean body mass only, the result issimilar for all individuals. It is the proportion offat mass in the total body weight that modifiesthe final figure.

GenderThe BMR for women is lower than that for menbecause of differences in the proportions ofbody fat to lean. In women, the body fat contentis, on average, 10 per cent higher than in men,with a consequently lower lean mass and thuslower BMR. This gender difference is apparentby the age of 2 years.

A further aspect is the energy demand madeon the mother’s body during pregnancy and lactation to support the growth of the fetus.Changes occur to the maternal BMR to allow fora more efficient use of energy, and these aredescribed more fully in Chapter 11.

AgeThe BMR (per kg) is highest in young infants andfalls throughout the remainder of the life cycle. The decline is relatively slow in children andadolescents, in particular, but once adulthoodhas been reached, there is a gradual progressivedecline of approximately 2 per cent per decadeafter the age of 30 years. This is related to theamounts of metabolically active tissue presentat different ages, as well as the rapid rates ofgrowth in early infancy and adolescence. It isalso higher in young infants because of theneed to maintain body temperature. As peopleage and become more sedentary, the amount oflean tissue declines, with a parallel fall in BMR.However, if a person retains a high level ofactivity, the decline in BMR with age is muchsmaller as the lean tissue mass is more effec-tively preserved.

A failure to acknowledge and adapt to thedeclining energy needs may, in a proportion ofthe population, explain the increase in bodyweight that tends to occur in the middle years of life.

DiseaseBoth diseases and their treatments may have aninfluence on the BMR. Since the thyroid hor-mones are regulators of the metabolic rate,undersecretion or oversecretion by the thyroidhas a major influence on metabolism. Fever andtrauma tend to increase metabolism. Stress canalso increase energy expenditure in the shortterm. Various drugs or pharmacological agentshave an effect on metabolism and many increasethe rate, for example, caffeine, nicotine andamphetamines. Some drugs, such as beta block-ers and antidepressants, may reduce metabolism.Undernutrition also depresses metabolic rate.

Measuring BMR in people who are ill may,therefore, not give accurate results, if confound-ing factors are not allowed for. BMR may vary atdifferent stages of the disease; thus, the point inits time course when BMR is measured could beimportant. Anxiety, blood transfusions, effect ofpre-test treatments or feeding regimes may allinfluence the outcome of a BMR measurement.In translating the BMR result into a total energyexpenditure, it should also be remembered that abedridden patient will have a much lower levelof physical activity, so that energy requirementsoverall may be less than in health, even if BMRis elevated.

Other factorsThere are a number of other factors that may havean influence on metabolism, including genetics,climate and ethnicity. These are all difficultareas to study and, although some examples ofdifferences arising from genetic or ethnic varia-tion have been reported, other studies fail toshow such differences. Most Westerners respondto changes in climate by adjusting their cloth-ing and the level of heating or air-conditioningin their environment. When people are preventedfrom doing so, then metabolism is seen toincrease both at low and at high environmentaltemperatures.

CALCULATION OF ENERGY EXPENDITURE ❚

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Thermogenesis

As mammals, including humans, are warm-blooded, our bodies need to generate heat tomaintain body temperature (thermoregulatorythermogenesis). This requires energy and will bea variable aspect of our energy balance. Mostly,we exist in environments at a comfortable, orthermoneutral, temperature so that little extraenergy is used to keep warm, although before the widespread introduction of central heatinginto homes, it is probable that more energy was used to maintain body temperatures. Eatingaffects energy expenditure because the bodyuses energy in eating, digesting and absorbingthe food, transporting the nutrients and incorp-orating them into the cells. It represents the inef-ficiency of the body’s processing of its foodintake. This is usually called the ‘thermic effect’of food or ‘diet-induced thermogenesis’. In thepast, this was known as ‘specific dynamic action’of food, and was thought to derive specificallyfrom proteins. However, all the macronutrientsof the diet contribute to this heat production,although fats contribute least and proteins themost. It varies between individuals and alsobetween meals of different size and composition,but as a general guide is believed to amount to10 per cent of the total energy eaten in a meal.Thus, if a meal containing 3 MJ (750 Calories) is eaten, the amount of energy available to the body for use will be 10 per cent less thanthis. Thermogenesis also occurs as a result ofcold exposure, hormonal state or drug intake,although these are difficult to quantify.

Physical activity

This is the aspect of our total energy expend-iture over which we have most control. We canchoose to undertake a range of different activ-ities during the course of a typical day, walkingto work or school, taking part in sports, havinghobbies for our spare time that involve move-ment. On the other hand, we can drive or takethe bus to work, we can sit during our break andlunch hours and, on returning home, spend theevening in front of the television. Clearly, suchcontrasting lifestyles will be associated withdifferent levels of energy output.

It has been shown by careful measurementsthat the amount of energy expended in activity isrelated to the size of the body being moved and,consequently, to the BMR. Therefore, two indi-viduals, both weighing 60kg, will expend a simi-lar amount of energy performing the same task.In contrast, a person weighing 100kg will usetwice as much energy in a given task as a 50kgperson. This is an important finding, as previouscalculations of energy expended in activitiesmade no reference to the size of the person per-forming them. Many figures have been derivedthat quantify the average amount of energy used,in relation to the BMR, for specific activities.These are known as physical activity ratios(PARs), which represent the energy costs of activ-ities. In the USA, these are called METs (meta-bolic equivalents), and this acronym is also seenin many training and fitness contexts in the UK.By expressing these in terms of the BMR, onevalue for each activity can then be applied to allindividuals regardless of age, size or gender,since these will already have been taken intoaccount in the calculation of the BMR itself.

In deriving the PARs, some generalizationshave to be made. A certain amount of activity iscommon to most people; this includes the gen-eral ‘personal maintenance’ activity associatedwith washing, dressing, preparing and eatingfood and generally moving about from room toroom in the home environment. It is assumedthat this makes similar demands on the body forall individuals, and a factor of 1.4 is attributedto it. The period of sleeping has a PAR of 1.0; itis assumed that during this period there is noincrement above BMR. Various occupationalactivities may also be grouped together, basedon the usual and average amount of physicalactivity involved. In addition, the PAR valuesmake no judgement about the intensity withwhich the work is carried out and, if it continuesfor a period of time, whether rest periods aretaken. Some examples are shown in Table 7.5.

Calculation of energyexpenditure

In order to calculate total energy expenditure, itis necessary to obtain a figure for the BMR.

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Various equations, such as the du Bois andHarris–Benedict equations, have been derived tofacilitate this, based on experimental measure-ments of BMR in subjects. Most widely used atpresent are those derived by Schofield, based onmeasurements made on over 10 000 subjects,and derived as regression equations from theplots of results. These, together with some morerecent data on elderly subjects, are used in thedietary reference values report (DoH, 1991), andwere the basis of the FAO/WHO/UNU (1985)recommendations on energy intake.

The equations for adults are given below(DoH, 1991).

Example of calculation of energyexpenditure

Bill is aged 40, and weighs 70 kg. His BMR iscalculated as follows: (0.048 � 70) � 3.653 �

7.01 MJ/day. Therefore, his hourly BMR � 7.01/24 � 292 kJ/hour.

He recorded his daily activity pattern andthe summary is shown in Figure 7.4. Energyexpenditure is, therefore, calculated as follows,with the appropriate PAR values, and using hishourly BMR.

PARs for calculation of energy expenditureTABLE 7.5Activity PARLying at rest/sleeping 1.0Quiet sitting activities (e.g. reading, TV) 1.2 (range 1.0–1.4)Active sitting activities (e.g. driving, playing piano) 1.6 (range 1.5–1.8)Stationary standing activities (e.g. ironing, laboratory 1.6 (range 1.5–1.8)

work, washing-up)General mixed standing/sitting (e.g. personal activities, 1.4

washing, dressing, eating)Activities involving moving about (e.g. cleaning, tidying, 2.1 (range 1.9–2.4)

cooking, bowling)Walking, average speed, making beds 2.8 (range 2.5–3.3)Gardening, playing table tennis 3.7 (range 3.4–4.4)Walking quickly, dancing, swimming 4.8 (range 4.5–5.9)Jogging, football, tennis 6.0

From DoH, 1991. Crown copyright is reproduced with the permission of Her Majesty’s Stationery Office.

BMR

MJ/day Calories/dayMales18–29 0.063W � 2.896 15.1W � 69230–59 0.048W � 3.653 11.5W � 87360–74 0.0499W � 2.930 11.9W � 700Females18–29 0.062W � 2.036 14.8W � 48730–59 0.034W � 3.538 8.3W � 84660–74 0.0386W � 2.875 9.2W � 687

Figure 7.4 Summary record of daily activity.

W � body weight (kg).

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Thus, Bill expended 9.8 MJ in the course of this day.

In comparison with his BMR, which is7.01 MJ, it is possible to calculate his physicalactivity level (PAL) throughout the day. Thisrepresents the amount of extra energy that heexpended, above his BMR, and is calculated asenergy expenditure/BMR, i.e. 9.8/7.01 � 1.4.This means that, over the day, he used 40 percent more energy than that simply needed forhis BMR.

This is a very average figure for a relativelysedentary population, typical of the UK, andforms the basis for the estimated average require-ments for energy, given in the dietary referencevalues report and summarized in Table 7.6.

Duration � PAR � BMR/ Energy (hours) hour � used

(kJ)Sleeping 7 1.0 292 2044Driving 2 1.6 292 934Personal 3 1.4 292 1226

activitiesWatching 3 1.2 292 1050

TVPlaying 1 6.0 292 1752

footballSitting at 8 1.2 292 2803

work

Total 9809 �

9.8 MJ

EAR for energy for adults in megajoules per day(Calories/day)TABLE 7.6

Age (years) Males Females19–50 10.60 (2550) 8.1 (1940)51–59 10.60 (2550) 8.0 (1900)60–64 9.93 (2380) 7.99 (1900)65–74 9.71 (2330) 7.96 (1900)75� 8.77 (2100) 7.61 (1810)


Keep a record of your own activities for two peri-ods of 24 hours. They need not be consecutive,but should represent differing levels of your ownactivity. Find your body weight and use this tocalculate your BMR. Then construct a chart simi-lar to the worked example above, to allow you tocalculate your total energy expenditure over the2 days. Work out the ratio of your total energyexpenditure with respect to your BMR: this isyour physical activity level.■ Is there anything that surprises you about the

results for the 2 days you have chosen – forexample, is the difference between them moreor less than you expected?

■ Which component of your daily activity hasmade the largest contribution to the total – is it your BMR, or a particular activity?

■ If you had a period of strenuous exercise,what proportion of the total did this consti-tute? Is this more or less than you expected?For what period of time would you need tocontinue this level of exercise for it to equalhalf of your BMR expenditure?

■ Did you have different periods of sleep duringthe two recorded days? Did this make a differ-ence to your output?

■ Compare your results with those of others.What differences can you find? Can youaccount for them?

Activity 7.4

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Conway, J.M. (ed.) 1995: Advances in human energy metabolism: review of current knowledge(Symposium). American Journal of Clinical Nutrition 52(5), 1033–75.


DoH (UK Department of Health) 1991: Dietary reference values for food energy and nutrients for theUnited Kingdom. Report on Health and Social Subjects No. 41. Report of the Panel on DietaryReference Values of the Committee on Medical Aspects of Food Policy. London: HMSO.

FAO/WHO/UNU 1985: Energy and protein requirements. Report of a joint FAO/WHO/UNU ExpertConsultation. WHO Technical Report No. 724. Geneva: WHO.


edn. Cambridge: Royal Society of Chemistry.Gibney, G.R. (2000): Energy expenditure in disease: time to revisit? Proceedings of the Nutrition

Society 59, 199–207.Gregory, J., Foster, K., Tyler, H., Wiseman, M. 1990: The dietary and nutritional survey of British

adults. London: HMSO.Schofield, W.M., Schofield, C. James, W.P.T. 1985: Human nutrition. Clinical Nutrition 39C (suppl.), 1–96.Scrimshaw, N.S., Waterlow, J.C., Schurch, B. (eds) 1996: Protein and energy requirements sympo-

sium. European Journal of Clinical Nutrition 50 (suppl. 1).Westerterp, K.R. 1999: Body composition, water turnover and energy turnover assessment with

labelled water. Proceedings of the Nutrition Society 58, 945–51.

1 Energy balance represents the relationship between energy intake and energy output.2 Energy intake is the metabolizable energy of foods, generally calculated from the proximate principles.

Dietary surveys tend to underestimate energy intakes.3 Energy output comprises basal metabolic rate, thermogenesis and physical activity.4 Basal metabolic rate is influenced by a number of factors, including age, gender and body weight.5 Energy expenditure in activity is related to the basal metabolic rate and can be calculated by the use of

factors known as physical activity ratios. The overall daily energy expenditure can be compared with theBMR in the form of the physical activity level.

SUMMARY

1 Distinguish between and account for anydifferences in the yield of energy from a foodwhen:a it is combusted (burned) in a bomb

calorimeter;b its constituents become available for use at

cellular level in the body.2 Would a diet with a low fat content (e.g. 15 per

cent of energy from fat) be appropriate for:a healthy child with an average (not large)

appetite;b an elderly, housebound person.

Explain your viewpoint.

3 Including the energy from alcohol in calculatingthe contribution from each macronutrient to thetotal energy intake can make importantdifferences to the results. Comment on thefollowing cases:a Harry: total energy intake � 12.8 MJ

fat 33 per cent, protein 15 per cent, carbohydrate 40 per cent, alcohol 12 per cent;

b Alex: total energy intake � 10.6 MJ fat 40 per cent, protein 12 per cent,carbohydrate 48 per cent;

c Sam: total energy intake � 15 MJfat 28 per cent, protein 13 per cent,carbohydrate 34 per cent, alcohol 25 per cent.

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energy balance


❏ discuss the concept of energy balance and review its components;❏ describe the situations where energy intake and output are not in balance;❏ study the components of body composition and the ways it is measured;❏ consider the health risks of excessive and low body weight, and how to bring about weight change.


❏ explain the changes in energy balance that contribute to weight loss or weight gain;❏ discuss the aetiology of overweight and underweight, including an understanding of some eating disorders;❏ identify appropriate ways of measuring components of body composition and explain the significance of

particular results;❏ suggest ways of increasing or reducing weight by diet and lifestyle changes.

Most people maintain their bodies in a state ofenergy balance within quite narrow limits, asevidenced by a constant body weight. Whenchanges in energy balance occur, they are rarelysudden or unexplained, but are most likely tooccur gradually and over a long period of time.This may make them difficult to correct, sincethey often go unnoticed until a marked changehas occurred.

In Chapter 7, the components of energy bal-ance are described. Energy intake derives fromthe food we eat and is regulated by a number ofdifferent factors, including physiological (suchas hunger), psychological (appetite or mood),social and environmental factors, all of whichinteract in complex ways, and are thus difficultto study and to control. Energy output representsthe energy used to maintain physiological andbiochemical activities (as basal metabolic rate), todigest and process the food we eat and to fuel allphysical activity. Normally, these two aspects arein equilibrium with the energy intake being suf-ficient to meet the energy output (see Figure 8.1).

Energy � Energy output (basal metabolic rateintake � thermogenesis

� physical activity)

However, this equilibrium is not necessarilymaintained on a day-to-day basis; some daysour intake is greater than our output, and onother days the opposite applies. When this hap-pens, some of the surplus energy is stored as fatin the adipose tissue. At other times, these storeshave to be drawn on to provide energy neededat a particular moment. Evidence suggests thatoverall, there is a stability of body weight, anddata from a long-term study of the populationin Framingham, Massachusetts, shows that,over a period of 18 years, most people were at a body weight within 5 kg of their originalweight. This energy imbalance represented lessthan 0.5 per cent of the total turnover in energy,implying that reasonably efficient regulationwas occurring. Subjects whose weight changedthe most were also the most likely to suffer fromdisease.

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Nevertheless, weight changes do occur; in theUK and most other Western countries, statisticsshow that incidence of overweight and obesityamong the adult population has been increasingrapidly. Trends of increased weight are also nowseen in children, often from a very young age. Inall of these cases, there is an increase in fatstores. Thus, the energy balance equation abovehas to be rewritten:

Energy intake � Energy output� energy stores

Adjusting the balance

When the energy balance is disturbed, the bodytries to restore it by making various adjustmentsto the different components of the equation.Some of these may be brought about con-sciously by our own efforts, others occur at themolecular or cellular level and are outside ourdirect control. For example, we may deliberatelyincrease or decrease our food intake, or alter ouractivity level, but the changes that occur to ourmetabolic rate and the metabolic mixture thatthe body uses cannot be consciously regulated,but may alter as a consequence of other changeswe make. The ways in which its componentsmay be adjusted to achieve energy balance areconsidered below.

Energy intake

Food is the source of energy entering the body,thus regulation of food intake will control theinput side of the balance equation. The factorsthat are involved in the control of food intake

are considered in Chapter 2. Food intake maychange or be adjusted in a number of ways:■ Deliberate reduction or increase of overall

intake, with less/more food eaten in general.This may include omitting particular meals,e.g. breakfast.

■ Limiting or increasing particular types of foodin the diet – such as high-fat foods, or thosecontaining sugar, starch or non-starch poly-saccharides (dietary fibre). For example, cakesand confectionery may be excluded, or morefruit and vegetables included in the diet.

■ Eating more of particular foods – perhapslow-energy (or ‘slimming’) foods, or foodsthat are perceived as causing weight loss.This category may also include foods thatare believed to promote development of particular aspects of body composition, suchas ‘body-building’ foods, or those with per-ceived health properties. Functional foods isa name applied to this category of foods;these are further discussed in Chapter 17.

■ Eating more snacks throughout the day,allowing greater flexibility to match appetiteand energy needs.

■ Changes in appetite, causing rejection of allor some foods, or increasing the desire forfoods (general or specific).

■ Inability to eat, for medical or psychologicalreasons, or owing to lack of availability offood. In the case of a person who is unableto eat, nutritional support in the form ofmodified, possibly liquid feed, may be pro-vided. This needs to be supplied and con-sumed in an adequate quantity to ensuresufficient energy intake.

Figure 8.1 Components of energybalance.

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In each of the above cases, energy intake islikely to change from the current one to a higheror lower level. This may be the result of a con-scious desire to change or can occur as a second-ary phenomenon, perhaps in association withillness or disease. There are also likely to bechanges to the nutritional composition of thediet in some of the cases.

In addition to changes in food intake, in somecases of disease or in eating disorders, there maybe interference with the process of digestion or absorption. Disease of the digestive tract mayprevent normal digestion, so that food is eitherlost by vomiting or passes undigested through thegut. Malabsorption may also affect the transfer ofthe digestion products into the blood. The pres-ence of stomas (where an opening to the outsideof the body has been made from the digestivetract, generally as a result of disease) or a reducedabsorptive area following partial removal of thebowel will have similar consequences.

Certain forms of eating disorders alsoinclude deliberate interference with digestionand absorption, either with the use of inducedvomiting once food has been eaten, or by usinglaxatives or purgatives to prevent the food beingabsorbed.

Finally, a drug developed for the manage-ment of obesity inhibits the enzyme responsiblefor the normal digestion of fat, so that malab-sorption occurs and undigested fat is lost in thefaeces. This has the effect of reducing the energyavailable from the food eaten.

Energy output

Basal metabolic rateChanges in basal metabolic rate (BMR) are mostlikely to occur as a result of changes in bodyweight or composition. BMR is influenced par-ticularly by lean body mass, so any alteration inthis will affect the rate of metabolism. Ageing is accompanied by a reduction in lean body massand, therefore, there is a gradual fall in BMR.Immobility as a result of illness or ageing willcause a loss of lean tissue and a consequentreduction in metabolic rate.

Conversely, training which involves exercis-ing the whole body or specific blocks of muscles

will gradually result in an increase in lean muscle mass (although this can take many weeks)and can result in an elevation of the metabolicrate. It must, however, be remembered that thesechanges in lean mass may not be immediatelyapparent by straightforward whole body weigh-ing. The changes may be accompanied by lossof adipose tissue, which may cancel out theoverall weight change. More specific measure-ments of body composition may need to bedone to identify changes in these components.

An increase in overall body weight is morecommonly associated with an increase in bodyfat. In this case, there is an increase in BMRbecause the larger tissue mass requires moreenergy to sustain it. Furthermore, an increase inthe mass of adipose tissue is associated with anincrease in the supporting cellular structure,which includes protein-containing cell wallmaterial and water. There are also increases inthe heart and skeletal muscle, digestive tract andliver to cope with the increased demands put onthem. However, the overall effect on the BMR issmaller as a result of an increase in fat ratherthan lean tissue, as the latter is more metabolic-ally active. Nevertheless, it is important toremember that a heavier person has a higherBMR than a smaller, thinner individual. This factis sometimes overlooked by people that are over-weight, who claim that their problem is theresult of ‘slow metabolism’.

When weight is lost, there is a reduction inBMR, consequent on the fall in the mass of meta-bolically active tissue to be maintained. This isone of the major problems encountered bydieters. As they lose weight, the smaller bodyactually requires less energy to sustain it and,therefore, the energy deficit becomes smaller. Theresult is that the rate of weight loss slows down.

ThermogenesisThis comprises the thermic effect of food as wellas possible ‘adaptive thermogenesis’. The thermiceffect of food is equal to approximately 10 percent of the energy consumed. It follows that anychanges in food intake will be accompanied bychanges in the amount of heat lost in processingthis food. Someone who increases their foodintake in a meal from 3.3MJ (800Calories) to

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5.0MJ (1200Calories) will use 17kJ (40Calories)more in processing this food. However, these val-ues are not consistent between individuals; someare more efficient in their energy transformationsthan others. Data suggest that the obese have asmaller thermic response to food than the non-obese, but both will exhibit an increase in ther-mic effect on overfeeding.

Adaptive thermogenesis is energy expendedas heat in response to a number of stimuli, suchas cold, infection, injury or cancer cachexia aswell as overfeeding. It is particularly importantduring hibernation in animals, and in the veryyoung mammal is a means of controlling bodytemperature, before the capacity to shiver hasdeveloped. In both cases, it is a particular typeof fat cell, known as brown adipose tissue(BAT), which is responsible for the production ofheat. The cells of BAT have a rich blood supplyand extensive sympathetic innervation, a highconcentration of mitochondria in each cell, and the presence of myoglobin for oxygentransport.

The extent of any role for BAT in the controlof energy balance in humans has not beenagreed. Its role in dissipating the energy fromoverfeeding was demonstrated initially in ratsfed on a range of ‘cafeteria foods’ typical of somehuman diets. Some of the rats remained at a nor-mal weight, whereas others gained weight andbecame obese. Those rats that were able to con-trol their weight were shown to have hypertro-phied BAT. It became clear that this had becomemore active and had dissipated the excess energyas heat, rather than trapping protons in the for-mation of usable ATP (the energy ‘currency unit’).This response of BAT is under the control of thesympathetic nervous system and several keyreceptors have been identified of which the mostimportant is the �3-adrenergic receptor. A numberof uncoupling proteins (UCP) that are involved in the production of heat in BAT have also beenidentified in the inner mitochondrial membrane.Recently, markers have been developed that allowthis protein to be located; these studies haveshown that, contrary to the earlier view that BATwas only present in infants, there is a smallamount of BAT in adults. The advances in molec-ular biology and human gene mapping have

allowed many of these features of BAT activity tobe identified in humans. A gene associated withreduced �3-receptor activity has been identifiedand linked with increased abdominal fat deposi-tion, reduced metabolism and a greater capacityfor weight gain. Genes for UCP have also beenidentified and variants discovered. Nevertheless,the importance of BAT in normal subjects is still unknown; it may possibly account for up to 10 per cent of energy balance. Certainly, theresponse of individuals to overfeeding does vary,with some gaining more weight than others.Physiologists have believed for many years thatthere might be a mechanism that allows subjectsto ‘adapt their energy expenditure to match theintake’. It is possible that BAT is one componentof this mechanism that links with other aspectsof energy balance regulation.

Physical activityThis is the aspect of our daily energy output thatis most variable, both between and within indi-viduals and, therefore, provides the greatestpotential to increase energy output.

There has been a major change in the levelof activity of people in most Western countriesin the last 30–40 years, and particularly in thelast decade. The advances in technology havereduced the need for physical effort in work,transport and leisure activities. Few people nowhave very physically demanding jobs, comparedwith 30 years ago. Many tasks related to every-day life are now less physically demanding, e.g.shopping with a supermarket trolley and car,compared to carrying shopping from the localhigh street, and making a bed with sheets andblankets, compared with straightening a duvet.Leisure activities themselves have become moresedentary, with television, video and computergames constituting a substantial proportion ofmany people’s entertainment (see Figure 8.2). In addition, children play outside much less andare generally transported to school much morewith the result that the pattern of low activitylevels is established at a young age. Schoolsport has also decreased, as pressure on the cur-riculum for academic subjects, as well as theloss of school playing fields to building anddevelopment have their effects.

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There is considerable concern about thesteady decline in activity levels and various ini-tiatives exist to raise awareness about the import-ance of activity. Current advice in the UK is that aminimum of 30 minutes of moderate activityshould be undertaken by everyone, with mostpeople aiming for at least 30 minutes moderateactivity on 5 days of the week, or 20 minutesintense activity on 3 days a week. Associated withthis there is an increasing emphasis on incorpor-ating more ‘routine’ activity into the lifestyle.This may include using the car less or walking upstairs; the intention is to include activity as partof the normal day, rather than separating it into‘exercise’, which tends to become a chore andoften stops when the initial enthusiasm wearsoff. Many schemes exist to encourage physicalactivity, including ‘the walking bus’ to take anumber of children to school, ‘exercise on pre-scription’ (Figure 8.3) to prevent or treat diseaseand many ‘get fit’ campaigns promoted in themedia and local leisure centres. There are indica-tions that a small increase in moderate to vigor-ous activity has taken place both in the UK andUSA. However, this is seen among the better-educated and better-off groups, rather than inthe more deprived areas. In addition, this smallincrease is insufficient to compensate for thedownturn in ‘lifestyle’ activity that has beenoccurring.

Many people in Britain are classed as havinglight occupational activity levels and sedentaryleisure activity; an overall physical activitylevel (PAL) of 1.4 or less is, therefore, estimated.

Studies of free-living populations in Britainconfirm these assumptions, with some findingaverage PAL as low as 1.27. This means that theamount of energy expended during 24 hours is only an additional 27 per cent of the BMR.This represents minimal physical effort. (PAL is discussed in Chapter 7.)

Changing PAL requires periods of activitythat involve movement of the body and, there-fore, muscle activity, raising cardiac output andrespiration for a reasonable period of time tomake an impact on the calculation of a 24-hourenergy output. It is for this reason that incorpor-ating several smaller increases in activity dur-ing a normal day can have more of an impacton total expenditure than one intense bout ofactivity, which lasts for perhaps only 20 min-utes. In fact, after intense exercise, there may bea period of complete inactivity, while the sub-ject recovers from the effort. The overall level ofactivity may be much less, therefore, than mightat first appear.

Spontaneous low-level activity, or fidgeting,is also of interest. It has been noted that sub-jects in overfeeding studies varied substantiallyin their levels of fat storage, which was attrib-uted to differences in ‘non-exercise activity

Figure 8.2 Using energy in everyday life.

Figure 8.3 Exercise on prescription.

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thermogenesis’, or fidgeting. This is also relatedto sympathetic nervous system activity but theexact involvement of this aspect of activity intotal energy output is as yet unclear.

How well is energy balancecontrolled?

Humans consume different amounts of food eachday, with differing proportions of macronutri-ents, and also expend different amounts ofenergy in varying activities. The preceding sec-tions have discussed the components of energybalance and shown that changes can occur ineach component, consciously or unconsciously,to bring about a restoration of energy balance.The body, therefore, strives to achieve homeo-stasis by a number of mechanisms. The regulation

of energy balance is neither perfect nor rapidand, as a consequence, changes in weight occur,reflecting these fluctuations in energy balance.

By adjusting food intakes in experimentalsubjects and concurrently measuring energyexpenditure, it can be shown that changes inweight and energy expenditure are not matchedprecisely. Both experimental and long-termobservational studies show that the body resistsan energy deficit, whether this is induced by dietor exercise, and there is a drive to compensatefor this either by increasing energy intake insubsequent days, or reducing energy expend-iture. These results confirm that maintaining aweight loss can be difficult. Strong cognitivecontrol, or will power may be needed to resistthe physiological drive to restore energy bal-ance, although exercise has been shown to help

You will need to refer to information in Chapter 7 to complete this activity.Three friends have undertaken a study of their activity. They are all male, aged 25 years, with body weights of60 kg (Tom), 70 kg (Sam) and 80 kg (Harry). The results of their activity diaries are given below

Tom Sam HarryActivity Duration (h) Activity Duration (h) Activity Duration (h)Work: sedentary 8 Work: mixed 8 Work: mainly 8

standing/sitting moving aboutOther: Other: Other:Personal activities 3 Personal 2 Personal 2

activities activitiesWatching TV 4 Watching TV 1 Watching TV 2Drive to work 1 Walk to work 1 Drive to work 1

Walking dog 1 Football 1(brisk)

Gardening 2 Swimming 1Tidying house 1 Playing 1

computer gamesSleeping 8 Sleeping 8 Sleeping 8

Total hours 24 24 24

Calculate each man’s daily energy expenditure, and express the answer as the physical activity level, to allowcomparisons to be made between them.■ What similarities and differences are there?■ What impact do their various leisure activities have on the total expenditure?■ How important is the level of work activity?■ What conclusions can you draw about the optimal way of increasing daily energy output?

Activity 8.1

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in the maintenance of weight over the long term.Restoration of energy balance during or follow-ing overfeeding is less effective, especially ifhigh-fat diets are consumed. Exercise appears tobe an important adjunct to maintaining energybalance on high-fat diets. However, there is avaried response to these disturbances of energybalance between individuals and between genders.

The relative ease of weight gain and diffi-culty of weight loss associated with physio-logical mechanisms for homeostasis means that,in some individuals, there is a fluctuation inweight over periods of time, as weight lost isregained. This has been termed ‘yo-yo dieting’.Long-term studies of population cohorts haveshown that there is an increased morbidity andmortality in people whose weight fluctuates com-pared with those who have a stable weight. It isnot, however, possible to state that weight fluctu-ation is the cause of the increase health risks, as itmay equally be true that poorer health is a causeof weight fluctuation. Nevertheless, it is likelythat weight loss followed by weight regain,repeated on many occasions, is detrimental to thepsychological well-being of the individual.

When an individual is ill, the achievement ofenergy balance may be complicated by factorssuch as the metabolic response to the illness,effects of drugs or other treatments and theaccompanying inactivity. Further, feeding or thelack of it will also have an effect on energy util-ization. Careful monitoring is required to ensurethat energy balance is maintained.

Control mechanisms

For almost 50 years, it has been suspected thatbody weight is controlled by signals that moni-tor the quantity of adipose tissue. However, thenature of the signal was not identified until1994, when a protein produced by adipose tissuewas identified and named leptin. The amounts ofleptin in the circulation are correlated withmeasures of adiposity, such as BMI and percent-age body fat. Leptin is present in the circulationin both a bound and a free form. Receptors forleptin were found originally in the hypothal-amus but many other tissues are now known to

contain leptin receptors. These include organsinvolved in energy storage, metabolism anddigestion. Other sites that contain leptin recep-tors include tissues or organs involved withimmunity, blood pressure regulation and repro-ductive organs; the role of leptin in these func-tions is still being investigated.

Leptin levels provide information to thebrain about the abundance of body fat. Energybalance is regulated by the actions of leptin inthe hypothalamus resulting in inhibition of foodintake and increase in energy expenditure. Foodintake is regulated through the release of neu-ropeptides, most notably neuropeptide Y, whichis associated with increases in food intake. Anincrease in leptin levels will inhibit neuropeptideY and, therefore, reduce food intake. The centralaction of leptin also stimulates the sympatheticnervous system, which in animals has beenlinked to thermogenesis in brown adipose tissue,allowing dissipation of energy as heat. In sub-jects with a high fat mass, evidence suggests thata failure of the leptin receptors to respond,results in a breakdown of energy balance, allow-ing fat deposition to occur (see Figure 8.4).

There are also close links between leptin andinsulin. Insulin has similar effects in the hypo-thalamus, and reduces food intake and increases

Figure 8.4 Actions of leptin. CCK, cholecystokinin.

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energy expenditure. It is now clear that insulin isinvolved in the secretion of leptin from adiposetissue, and also that leptin can inhibit insulinsecretion. Therefore, when food is eaten, polypep-tides (such as glucose-dependent insulinotropicpolypeptide; GIP) released from the intestine,together with absorbed metabolites (glucose,amino acids), stimulate insulin release. Glucosemetabolism in adipocytes eventually causes leptinrelease, which acts in the brain to cause a reduc-tion in food intake. This pathway will be mosteffective with foods that trigger insulin release,such as carbohydrate- and protein-containingfoods, and ineffective with high-fat foods. It,therefore, seems probable that the balance ofmacronutrients in the diet may influence leptinsecretion.

The feedback loop described above identifiesthe role of leptin in a medium to long-term con-trol of energy balance. Leptin is also involved inshort-term control of food intake, by increasingthe sensitivity of the response to cholecystokinin(CCK). This is one of the gut hormones associatedwith satiation, released when food enters theduodenum (see Chapter 2). Leptin levels are notconstant in an individual, as they exhibit a peakaround midnight, which for many people isapproximately 4–6 hours after an evening meal.The timing of the peak changes if meal times are altered. Levels are reduced during fasting,and cause increases in hunger even before anychange has occurred in body fat levels. This isnot helpful for weight reduction, but is a normalphysiological response to an energy deficit. Agreat deal of research effort is currently focusedon the potential use of leptin, its analogues ortriggers, in order to manipulate energy balance.In addition, investigations into the genetic codesfor various leptin receptors and intermediaries inthe pathways are ongoing, but research to datehas found very few individuals in whom muta-tions in genes for leptin production or leptinreceptors are the cause of overweight. It hasrecently been noted that pre-term babies whowere assigned to receive an enriched formularather than human milk, had higher leptin levelsrelative to fat mass, at adolescence. This suggeststhat the leptin feedback mechanism may alreadybe less sensitive at this age. This finding suggests

one possible way in which early feeding mayprogramme the later development of overweight.

Body weight andcomposition

When an individual is in energy balance, thebody weight and composition stay constant.Therefore, a growing child or an athlete intraining aiming to increase muscle bulk willneed to be in positive energy balance to accruebody mass. On the other hand, an individualwho is aiming to lose weight will need to be innegative energy balance. Measuring the bodymass and its composition is, therefore, import-ant. Most people assume that, in adults, a gainin weight is associated only with an increase inbody fat, but some increase in supporting tis-sues also occurs. Subjects who are physicallyactive and engaging in training schedules maygain weight as a result of an increase in muscle(lean) mass. Similarly, when weight is lost, therecan be a loss of lean tissue, particularly if rapidweight loss occurs. This might be the result of abadly planned slimming diet, or perhaps due toillness. It would be more accurate to describepeople as overfat rather than overweight, to dif-ferentiate between the heavy, but lean individ-ual and the person with a high percentage of fatin the body. Similarly, a light person may stillhave a relatively high percentage of fat in theirbody, but this may be not apparent if their leanmass has shrunk. This may be true of an olderadult who has perhaps become very sedentary.

Body mass index

The body mass index (BMI) is calculated as the individual’s weight (in kilograms) divided by height (in metres) squared: W/H2, in kg/m2.Indices can range from less than 20 to above 40.The World Health Organisation (WHO) has rec-ommended that the following categories be used:

BMI Grade18.5 Underweight18.5–25 Normal weight25–29.9 Overweight (Grade 1 obesity)30 Obese (Grade 2 obesity)

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These data are based on the greater healthrisks associated with increasing weight, as shownby actuarial life expectancy tables, as well asinformation about morbidity. In general, risksincrease with rising BMI, even within the bandcategorized as ‘normal’. For example, for womenthe risk of coronary heart disease in an Americanstudy was shown to be twice as great at a BMIbetween 25 and 29 as at a BMI of less than 21.Above a BMI of 29, the risk was almost 3.5 timesgreater. For diabetes, the prevalence is about threetimes greater for people with a BMI above 28.5than for those whose BMI is below 24.4. Thus, theclassifications of BMI are rather arbitrary anduseful for convenience, rather than being majorboundaries between levels of risk. It should benoted also that BMI is not an ideal measurementfor everyone, and is mainly focused on those whoare overfat, rather than overweight due to otherreasons. It takes no account of the components ofthe body weight and may, therefore, classify asobese a trained athlete who has a high percentageof lean tissue and little body fat. BMI is also use-ful for classification of degrees of malnutrition inadults, as follows (Ferro-Luzzi et al., 1992):

In addition, a chart may be used to check thedegree of overweight (see Figure 8.5).

Distribution of body fat

Additional information about the health conse-quences of increasing weight can be obtainedfrom the waist-to-hip ratio, which compares thegirth of the body at these two sites, expressingthe result as a single figure. For individuals witha predominance of fat deposition in the trunk,and particularly around the abdomen (centralobesity), the ratio is higher than for those whosefat is mainly laid down in the buttocks and hips(peripheral obesity).

In general, women exhibit peripheral obesity(also described as gynoid or ‘pear-shaped’), andmen tend towards central obesity (android or‘apple-shaped’). Ratios of more than 0.95 in

BMI Grade of malnutrition16 316–16.9 217–18.4 1

Figure 8.5 Weight assessmentchart for adults. Take a straightline across the chart from yourheight and a straight line up fromyour weight. Make a note ofwhere the two lines meet. Thiswill indicate if you are within thedesirable weight for your size. 1, underweight; 2, desirableweight; 3, overweight; 4, fat; 5, obese.

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men and 0.8 in women are taken as indicatingincreased risk. After the menopause, womenbecome more android in their shape, and this isaccompanied by greater risk of obesity-linkeddisease (see Figure 8.6).

Girth measurements of various parts of thebody including abdomen, buttocks, thigh, calf,forearm and upper arm have also been used.Age- and gender-specific equations have beenderived and cross-validated with good results.They are useful for ranking individuals within a group according to fatness, and levels of error are in the region of 2.5–4 per cent. Theadvantage of these measuring techniques is that they require only the simplest of equipment – atape measure – and can, therefore, be performedalmost anywhere. They are particularly usefulfor monitoring changes in body shape over aperiod of time. They should, however, be usedwith caution in people who are very thin, very fat or have undergone periods of physicaltraining.

Recently, good predictability has beenobtained using waist measurement only as anindicator of the need for weight managementand this is now being recommended as a verysimple public health message. Most people areable to measure their waist circumference or areaware of the measurement for clothes sizing.The measurement should be taken midwaybetween the lowest rib and the iliac crest. Levelsfor action, based on the cut-off points can bepromoted as part of the weight managementmessage. These are shown in Table 8.1.

Measuring bodycomposition

Skinfold measurements

Skinfold (or fatfold) measurements are a usefuland inexpensive way of obtaining a measure-ment of body fat content. In the hands of anexperienced operator, the specially designedcallipers can yield results within 3–5 per cent ofthose obtained by more complicated and accur-ate methods, such as hydrostatic weighting (see below). Figure 1.2 illustrates the technique.The results from skinfold measurements can beused simply to quantify the subcutaneous fat atspecific sites and monitor this in a particularindividual over a period of time. Alternatively,the results can be entered into appropriateequations to calculate the total body fat con-tent. Ideally, measurements should be taken atthe four common sites: mid-biceps, mid-triceps,subscapular and supra-iliac, and the total

Figure 8.6 Central (apple) and peripheral (pear) fatdeposition.

Action levels for weight management based on waistcircumferenceTABLE 8.1

Level of health risk Waist circumference – Waist circumference – men (cm) women (cm)

Healthy/normal 94 80Action level 1Increasing risk – no further 94–102 80–88

weight should be gainedAction level 2 102 88

High risk – medical advice shouldbe sought for weight management

Adapted from Scottish Intercollegiate Guidelines Network (1996).

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skinfold measurement used to calculate thebody fat.

A drawback of this technique is that it maynot be suitable in individuals who are very fat,elderly (fat is more compressible in older agegroups) or highly trained (muscular develop-ment makes it difficult to pinch a fatfold). Inaddition, it should be remembered that, inyoung adults, about 50 per cent of the body fatis found subcutaneously; with increasing agemore is deposited internally. Thus, a similar fat-fold reading will represent a greater total bodyfat content in an older person than a youngerone. Tables of typical skinfold results in popula-tion groups are available as standards.

Underwater weighing

This method is based on Archimedes’ principle,which states that an object’s loss of weight inwater is equal to the weight of the volume ofwater it displaces, because the object in the wateris buoyed up by a counterforce, which equalsthe mass of water it displaces. In applying this to human body composition measurements, thebody’s volume is determined by the differencebetween body weight measured in air and meas-ured when submerged in water. The density ofthe body can, therefore, be calculated using thefollowing equation.

Density of the body � Weight in air� Weight in water

The body density is composed of fat and fat-freetissue (together with a small correction for gasesin the lungs and intestinal tract, which may beadded to the calculation). It is assumed that fat hasa density of 0.9g/cm3 and fat-free tissue a densityof 1.1g/cm3. Errors may arise from assumptionsabout bone density and the water content of thebody, but these are assumed to be small.

The body density can then be used in theequation derived by Siri, to calculate percentagebody fat:

Body fat (%) � (495/body density) � 450

Clearly, this technique is not suitable for somepeople, for example, those with a fear of immer-sion, the sick and elderly people.

Other indirect methods

There are a variety of techniques that can beused to determine the internal composition ofthe body from external measurements.

Bioelectrical impedanceThis is based on the flow of electricity throughthe body, which is facilitated by the fat-free tis-sue and extracellular water because of the elec-trolyte content. The resistance (or impedance) tothe flow of current is related directly to the levelof body fat. Attaching electrodes to the hand andfoot of a subject and passing a localized electricalsignal allows impedance to be measured quicklyand painlessly. The results obtained will varywith the level of hydration of the subject and withskin temperature. However, when details aboutage, weight and height are entered, the techniquegives a quick readout of percentage body fat, andis widely used.

UltrasoundThis can be used to measure the thickness of thefat layer at various points of the body, as theultrasound beam is deflected at each interfacebetween different tissues. A similar method is theuse of near-infrared interactance, which recordsthe absorption and reflection of an infrared lightbeam, and computes fat thickness from the readings obtained.

Other techniquesOther techniques that require expensive equip-ment and are not generally available for routineuse include computerized tomography, mag-netic resonance imaging and dual-energy X-rayabsorptiometry (DEXA). The DEXA techniquehas been used particularly in the measurementof bone density.

What are the average valuesfor body composition?

Various attempts have been made to representthe ‘ideal body’, not as a goal for individuals to strive for, but to provide a reference againstwhich variations could be compared. Manyauthors use the terms ‘reference man’ and

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‘reference woman’ to describe these hypothet-ical individuals. There are clear gender differ-ences in body composition with a higher leanbody mass in males (and consequently higherbody water content) than in females. Femaleshave a greater body fat content. These genderdifferences become apparent at puberty, whengirls gain a greater proportion of fat than leantissue, whereas boys gain predominantly leantissue, and may actually lose fat during theteenage years.

Average values are as follows:

Total body fat exists as essential and storagefat. The essential fat is needed for normal physio-logical functioning, and is believed to represent3 per cent of total body mass in males, but 10–12per cent in females. Highly trained athletes ofboth genders may have fat levels approachingthese minimum values. The gender-specific fatin females is related to the reproductive role andhormone activity. At puberty, the growth spurtgenerally begins at a body weight of 30 kg, and,in addition, a minimal level of body fat must beachieved (13–17 per cent) for menstruation tobegin, and a body fat content of up to 22 percent may be needed to maintain menstrual regu-larity. If levels fall below these thresholds, men-struation will become erratic or cease. This canhappen in girls who diet excessively for psycho-logical or sporting reasons, and is discussed laterin the chapter.

Positive energy balance

Throughout Western societies, the end of thetwentieth century and the beginning of thetwenty-first century have seen a rapid rise in the prevalence of overweight and obesity, thathas been described as an ‘epidemic’. In the USA,the increase in adult obesity is progressing at 1 per cent per annum, and currently affects 20 per cent of men and 33 per cent of women.

Although the proportions affected are not yet ashigh, there are signs of increasing prevalence ofoverweight in some lower-income countries,such as Brazil and India. It is suggested that upto 10 per cent of the adult population worldwideis now obese. The WHO (1998) found that inmost countries the prevalence of obesity ishigher among women than men, with the excep-tion of Finland and the Netherlands. In the UK in1980, 6 per cent of men and 8 per cent of womenwere obese. In the Health Survey for England1991, the prevalence of obesity was 13.2 percent of men and 16 per cent of women. TheNational Audit Office in 2001 reported that 17per cent of men and 21 per cent of women areobese in England, and a further 46 per cent ofmen and 32 per cent are overweight. This repre-sents an almost three-fold increase in obesity in20 years. It is estimated that, at current rates, theaverage BMI by 2010 in Britain will be 28. Thereis great concern that obesity is increasinglyfound in children, with 13 per cent of 8 year oldsand 17 per cent of 15 year olds reported as obesein 1996.

What are the reasons?

There is an enormous amount of literature onthe complexity of the problem of obesity.Fundamentally, the problem is that at somepoint the individual has been in positive energybalance, where intake has exceeded output. Thereasons for this are considered here.

Dietary intakeData collected routinely in Britain, for example,by the National Food Survey, show that theaverage level of energy consumption has fallen.Furthermore, the interest in healthy eating hasresulted in a greater awareness about foodintake, and many ‘low-calorie’ or ‘low-fat’ prod-ucts are available in shops. Yet the weight of thepopulation is increasing, suggesting that theenergy intake is in excess of energy output.Recognition of the extent of underreporting ofdietary intakes in survey records, however, sug-gests that this fall in energy intake may not bequite as large as appears from the published figures.

Reference Reference man woman

Weight (kg) 70 60Lean body mass (kg) 60 48Body fat ( per cent) 15 25–28

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It has been proposed that one of the mainproblems with the typical Western diet is its highfat content, which is affecting the control ofenergy balance. It is clear from diet records overthe last 50 years that the percentage of fat in ourdiet has increased, at the expense of the carbo-hydrate content.

Over 50 years ago, 53 per cent of dietaryenergy was derived from carbohydrates and 35 per cent from fats. Thus, for every 1 kJ fromcarbohydrates, the UK diet provided only 0.6 kJfrom fats. By the early 1990s, carbohydrateintakes provided only 44 per cent of energy and 42 per cent came from fats, so that for each1 kJ from carbohydrates, intakes now provided0.95 kJ from fat. This represents an increase of50 per cent in the relative intake of fats. By2000, the ratio had improved a little to 0.8 kJ offat for each 1 kJ of carbohydrates. This is theresult of a fall in fat intakes. The extra carbohy-drates that are being consumed are frequentlymore refined than those eaten 50 years ago, andlack the accompanying non-starch polysacchar-ide (NSP) and micronutrients of ‘whole’ foodsthat provided additional health benefits.

Studies of dietary intakes and weight in bothmen and women also indicate that the averageBMI, and the proportion of those overweight and obese, decreases as total carbohydrate intakeincreases, largely as a result of differences inadded sugar intake. The BMI increases as the pro-portion of fat in the diet increases, regardless ofthe total level of energy intake. Figure 8.7 showsthe results of a large Scottish study that demon-strates these relationships clearly. These data sug-gest that it is, therefore, a high fat intake that ismore likely to result in overweight and that thecondition is a result of a positive fat balance,rather than positive energy balance. The results offour separate meta-analyses, reviewed by Astrupet al. (2000) consistently show that a reduction indietary fat without restriction of total energyintake, causes a reduction of energy intake andweight loss in a dose-dependent manner. This canproduce a modest but clinically important weightloss in overweight patients, with a typical weightloss of 3–4kg over 6 months.

Studies on the metabolic fate of dietarymacronutrients confirm that there is an oxidative

hierarchy, with metabolism extremely wellmatched to intake in the case of alcohol, proteinsand carbohydrates, but not for fats. Alcohol mustbe broken down and eliminated quickly from thebody because of its toxic nature and absence ofstorage site. Therefore, it dominates metabolicpathways and suppresses metabolism of othersubstrates. Amino acid oxidation matches pro-tein intake effectively. Glycogen levels have tobe regulated in the body to maintain blood glu-cose levels, particularly for the brain and ner-vous system. Thus, if carbohydrate intake falls,glucose oxidation is reduced to maintain circu-lating levels and satisfy the obligatory use ofglucose. Conversely, a high carbohydrate intakewill trigger storage and inhibit fat oxidation. In addition, carbohydrate intake induces satietythrough the release of several satiating hormones,including insulin, noradrenaline and gastric-inhibitory polypeptide. There is, therefore, veryprecise autoregulation of carbohydrate metab-olism. These adjustments made to the metabolic

Figure 8.7 The relationships between fat and sugarintakes and body weight. From Bolton-Smith andWoodward (1994). Reproduced with kind permissionof Nature Publishing.

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mixture being used are reflected in changes inthe RQ, which rises as more carbohydrate is usedin metabolism.

However, there appears to be almost noautoregulation of fat metabolism to matchintake, probably because the capacity for storageof fat is so large. Thus, an increase in fat intakedoes not trigger an increase in fat oxidation;instead, any fat that is in excess of immediateneeds is stored. Thus, fat metabolism ‘fills thegap’ between the amount of energy availablefrom the other macronutrients and the totalrequired to meet energy output needs.

This is not a problem if the total intake ofenergy from the macronutrients equals the out-put. In this situation, the metabolic mixturereflects the proportions of macronutrients in thediet. When intakes are in excess of needs, fatoxidation is inhibited and it is stored in prefer-ence to the other metabolic products. In add-ition, fat is stored very efficiently, with only 4 per cent of its energy content being wasted inthe process. If carbohydrate was stored, the ini-tial conversion into fat would waste up to 25 percent of the potential energy, making this a muchless energy-efficient process. Hence, storing fatwastes less energy than storing carbohydrate asfat; this implies that dietary fats are potentiallymore ‘fattening’. In humans, there is effectivelyno new synthesis of fats (de novo lipogenesis)by conversion of other nutrients to fat in thebody, although the biochemical capacity to dothis exists. Only in circumstances where experi-mental diets have contained very large quanti-ties of carbohydrates (in excess of 600–800g/day)for several consecutive days has there been somelipogenesis.

Dietary fat is likely to contribute to over-eating. The satiating effect of carbohydrates isgreater than that of fats. This, therefore, makes it easier for individuals to overconsume fat-containing diets without reaching satiety. Havingconsumed excess fat, subsequent food intake isnot reduced, so continued overconsumption canoccur, almost without the subject being aware of it. In addition, a fat-rich diet has a highenergy content per gram and consequently is ofa small bulk.

When the fat stores have increased, there isan increase in fat oxidation, which is reflected

in a fall in RQ towards 0.7, indicating that fatoxidation is providing the major metabolic fuel.If fat stores are reduced by weight loss, morecarbohydrate is used in metabolism and the RQincreases. It is still not clear, however, whysome individuals respond in this way to fatintakes, and others apparently do not.

Physical activityMaintaining adequate levels of physical activityhas been shown to help in achieving energy balance. Societies in the West have becomeincreasingly sedentary in the last decades of thetwentieth century. A study across Europe by theInstitute of European Food Studies (1999) hasshown that an average of 32 per cent of adultswere having no leisure time physical activityduring a typical week. Work-related physicalactivity was also low, with almost half the population studied spending 2–6 hours sittingdown at work and 20 per cent spending 6 ormore hours sitting down. Across the age range,physical activity falls sharply after the mid-30s,contributing further to increasing levels ofoverweight.

Genetic predispositionMuch work has been carried out on identical andnon-identical twins, and adoptive and naturalparents to quantify the genetic component inweight. It is clear that there is a relationshipbetween parents’ weights and those of children,some of which is inherited. The patterns of fatdistribution in individuals also show familialcharacteristics. Nevertheless, it is also evidentthat obesity is not only the result of a simplegenetic defect, but is determined by an interplaybetween factors that include genetic, environ-mental, nutritional, psychological and socialvariables. From the research base, it has beenestimated that between 40 and 70 per cent ofoverweight may be heritable. The contributionof environmental factors may account for a fur-ther 30 per cent of the cases of obesity. Theimportance of the role of the environment hasbecome clearer in the last decades, as prevalenceof obesity has increased rapidly, from a constantgene pool in the population. Advances in humangenome research will in the future be able toidentify candidate genes contributing to human

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obesity. There are a small number of single genedisorders, such as Prader–Willi syndrome, whereobesity is part of the clinical picture. However,these aside, it is likely that overweight and obes-ity occur as a result of an interplay of factorsand that, with suitable targeting and appropriatelifestyle adjustments, even subjects with agenetic predisposition to overweight should beable to maintain their weight within a reason-ably normal range.

Age and genderScientific evidence proposes several criticalperiods in obesity development that includepregnancy, early infancy, 5–7 years and adoles-cence. These are believed to be associated withbiological functions and regulated by hormonalaction. Fat cell volume and numbers may changeat these times. There is debate about the track-ing of obesity from childhood into adulthood.Certainly an overweight child has a greater riskof becoming an overweight adult. However,most overweight adults were not overweight aschildren, and have experienced positive energybalance in adulthood, as a result of factorsoperating later in life.

Weight gain tends to occur with increasingage in Western societies, with particular increasesin fat occurring between the ages of 25 and 45.For example, in England overweight or obesityis reported in 28 per cent of men and 27 percent of women aged 16–24, 65 per cent (men)and 51 per cent (women) aged 35–44, and 76per cent (men) and 70 per cent (women) aged55–64. In women, increases in body weight mayfollow pregnancy, when weight gained is notlost. Peak prevalence among men is up to theage of 50; in women increases in body weighttend to continue until the mid-sixties. Bothgenders exhibit weight loss in older ages. It ispossible that the trend in weight gain through-out the middle years of life is simply a reflectionof reduced activity levels. However, it shouldalso be remembered that basal metabolic ratedeclines with age and a failure to adjust foodintake to compensate for this will contribute toa positive energy balance. In women, the loss ofoestrogen activity after the menopause resultsin an increased central deposition of fat and anincreased waist to hip ratio.

Socio-economic statusIn Britain, there is an increased prevalence of obesity and overweight with low socio-economicstatus. In cross-sectional studies, this is seen con-sistently for women but less strongly for men.However, longitudinal studies demonstrate a con-sistent relationship between socio-economic sta-tus of origin and adult obesity. This finding awaitsexplanation but suggested reasons include: apoorer intrauterine or early life environment,increased likelihood of bottle feeding rather thanbreastfeeding and psychological/behavioural fac-tors relating to social norms. These may includepoorer self-esteem and attitudes to weight trans-mitted by parents. In addition, environmental fac-tors such as food availability and selection areimportant, with evidence consistently showingthat low income creates barriers to obtaining ahealthy diet. Lifestyle may include low activitylevels, where the environment precludes outdoorexercise, and costs prevent the use of leisure centres or gym facilities. Culturally acceptablebody size will determine how much an individual may want to change their weight and, therefore,their acceptance of current weight or success inweight loss.

Many of the factors described above applyto people from the ethnic minority groupswithin British society, who are disproportion-ately represented among lower income groups.The National Audit Office report (2001) identi-fied women of Black Caribbean and Pakistaniorigin as groups in whom there is a high rate ofobesity. Asian men and women also have agreater prevalence of central adiposity that car-ries greater health risks.

Psychological factorsIt has been suggested that some individualsovereat and become obese for psychological reasons. Both emotional disturbances and per-sonality disorders have been proposed as a causeof obesity, although in both cases there is littlegood scientific evidence to support the theory.Depression and anxiety may occur among someobese individuals, especially those who binge eat.In addition, emotional distress and low self-esteem appear to be higher among the obese. It isdifficult to separate cause and effect in thesecases, as there can be improvement on weight

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loss. Stress has been linked to weight gain, boththrough a consumption of higher fat foods, butalso raised levels of cortisol that is involved inregulation of abdominal fat stores. Those subjectswho give up smoking are particularly vulnerableto an increase in weight, and the effects may beboth psychological and physical in this case. Anaddiction to carbohydrate has been proposed,with the addict craving carbohydrates (chocolate,for example) in the way others crave alcohol ordrugs. There is little sound scientific evidence tosupport this.

Overweight may also be the result of abnor-mal dietary restraint and disordered eating, as isalso seen in anorexia or bulimia nervosa. Thesemay be associated with poor or distorted bodyimage, and greater sensitivity to external eatingcues. In women, an inability or reluctance toachieve the ideal female stereotypical body shapecreated by society is believed to play a part in theaetiology of these disorders. It is widely believedthat the current media preoccupation with ideal-ized, thin and successful women, in film, fashionor music industries is driving greater body dissat-isfaction among young women in the West. Thisalso impacts on the willingness of some youngwomen in particular to engage in physical activ-ity owing to reluctance to expose their bodies in

sports settings. This demonstrates an interactionbetween social and psychological factors result-ing in poor control of energy balance.

If psychological factors are contributing toenergy imbalance, it must be remembered thatthey are likely to play a major role in anyattempts to normalize weight and should, there-fore, be addressed in any weight loss programme.

These contributory factors are summarizedin Figure 8.8.

Health risks of overweightand obesity

Many people have the impression that beingoverweight or obese is only an aesthetic issue,linked simply to the appearance of the individ-ual. As such, then, it is considered to be up tothe individual to determine if they are contentwith their appearance. However, this is not thewhole picture – overweight and obesity bringwith them major health risks that can becomelife threatening. Health risk increases with BMIin a J-shaped relationship. Below a BMI of 20,there is increased mortality, linked to diseasesthat may cause loss of weight, such as cancersand the consequences of smoking. However, asBMI rises above 25 and especially above 30,

Figure 8.8 A summary of factorscontributing to positive energybalance.

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there is a progressive and accelerating increasedrisk of mortality. This has been recognized foralmost a century when life insurance companiesused body weight as a predictor of the ‘risk’ thata particular client might represent.

In addition to a greater risk of death, over-weight and obesity carries increased morbidity,often starting at lower levels of BMI than for mortality. Obesity itself has been classified by the WHO as a disease, but also brings a host ofmedical consequences. Those that have receivedparticular attention are cardiovascular disease,diabetes and cancers. Cardiovascular disease has

received particular attention, as there is strikinginteraction between obesity and the known riskfactors, such as smoking, hypertension and raisedblood lipids. In addition, Type 2 diabetes is also arisk factor and is, in turn, strongly associated withobesity. In fact, the risk of Type 2 diabetes is 12.7times greater in an obese woman and 5.2 timesgreater in a man than in non-obese individuals.This potentiating effect between risk factorsmakes it particularly difficult to separate the manyaspects of metabolic consequences of obesity.

There are, however, also many other effects,some of which are listed in Table 8.2.

Medical and other consequences of obesity (adapted fromLean 2000)TABLE 8.2

Type of consequence Specific examplesMetabolic effects Hyperlipidaemia

HypertensionCardiovascular disease (coronary heart disease and stroke)Type 2 diabetes mellitusAbnormality of blood clottingRisk of gallstones

Endocrine effects Oestrogen-dependent cancers (including breast, endometrium and prostate)

InfertilityMenstrual dysfunctionIncreased risk in pregnancy

Physical effects Joint disorders, arthritis, back painVaricose veinsOedemaBreathlessnessPhysical inactivity (possibly linked to bowel cancer)Stress incontinenceExcessive sweating

Psychological effects TirednessLow self-esteemDepressionAgoraphobia

Social effects IsolationUnemploymentFamily problems/marital stressDiscrimination

Surgical risk Poor wound healingChest infectionsAnaesthetic riskVenous thrombosisSleep apnoea

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Many of the consequences listed abovedevelop slowly and insidiously, and are rela-tively uncommon in people below the age of 40.However, with the increased prevalence of obes-ity in younger adults and children, it is likelythat the age of first presentation will fall.

The physical consequences of obesity increasewith its duration, as organs and systems fail tocope with the increased demand put on them.

The National Audit Office report (2001)attempted to quantify the economic costs ofobesity in England. It was estimated that obesitycosts £ 2 billion from the national economy,including at least £ 0.5 billion in treatment coststo the NHS. Life expectancy is shortened by anaverage of 9 years, there are 18 million sick daystaken each year from work and the overall mor-tality related to obesity accounts for 6 per centof all deaths annually. Recent policy documentsissued within the UK have included strategies toreduce the burden of ill health associated withobesity, both by helping overweight and obesepeople to lose weight as well as by preventingweight gain.

Treatment ofobesity/overweight

Whatever the reasons for weight gain, it is onlyby reverting to a negative energy balance thatexcess weight can be lost. Studies performed incarefully controlled metabolic ward environ-ments have shown that even subjects who claimthat they cannot lose weight on very smallenergy intakes when at home will start to loseweight when their food intake is monitored andregulated. Unfortunately, there is a tendencyamong a large proportion of the population tomislead both themselves and researchers abouttheir food intakes. Some studies have shown thatoverweight subjects are particularly likely to dothis, with some underreporting food intakes byup to 3.3 MJ (800 Calories) per day. There maynot be a deliberate intention to deceive; indeed,foods are forgotten about as they are consumedwithout thought, or considered ‘not to count’.

The common objective of these treatments is to reduce the amount of energy taken as food and/or to increase the amount of energy

expended by the body. More specifically thisshould have as its aims:■ to provide a diet that meets all the nutri-

tional requirements to maintain health, withthe exception of total energy;

■ to satisfy the individual subjects dietarypreferences, as well as any financial andlifestyle constraints;

■ to have a realistic goal for weight loss,within a specific time scale;

■ to aim for a long-term strategy to maintainthe target weight through appropriatelychosen diet, behaviour and physical activity.The major factor that will determine success

is the motivation of the individual; hence, it isvitally important to assess the expectations aswell as the willingness to adopt change. Targetscan be modest, as a success in a small weightloss can be more satisfying than a failure in alarge one. Even maintaining weight stabilityafter a period of weight gain can be seen as asuccessful outcome. Dietary intervention needsto be accompanied by practical advice on eatingpatterns, exercise or other physical activity andlong-term planning (see Figure 8.9).

Energy-controlled diets

These may be exactly specified or more flexible,and can be constructed in many different ways.They generally exclude those items in the regulardiet that provide mostly energy (such as sugarand alcohol) and are also likely to restrict fatintakes. The most successful will be those thattake into account the individual’s personal prefer-ences and circumstances. In general, these shouldcontain be set at up to 2.5MJ (1000Calories) lessthan the subjects habitual intake, depending onthe size of the individual. Some very low caloriediets have been developed, which provide evenless energy than this. They are attractive to people wishing to achieve rapid weight loss, butare unlikely to lead to better eating habits andmaintenance of the lower weight. In addition, asmany of these are commercially promoted, theiruse may be less carefully regulated. Some subjectsrespond to a variety of energy-restricted diets,changed over time, to limit boredom. A novelapproach may also be to eat more frequently,

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using carbohydrate-rich snacks and cutting downon fat-rich foods. Eating small amounts fre-quently allows better matching of intake to needs.It also avoids the ‘one large meal a day’ pattern offood intake that some people have. This is gener-ally in the evening when there is a higher level ofinsulin released that may more readily promote

fat storage. Furthermore, a large intake of food, atwhatever time of day, induces lethargy so that nophysical activity is taken afterwards. Small mealstaken at intervals throughout the day allow activ-ity levels to be maintained better. This pattern ofeating may suit some individuals, and as withother weight loss advice, needs to be negotiatedwith the subject.

Pharmacological agents

Two types of drugs are currently used. The firstare drugs acting on the digestive tract, of whichOrlistat is a major example. This is a pancreaticlipase inhibitor that decreases fat digestion andabsorption. The drug, therefore, causes steator-rhoea, with undigested fat appearing in the fae-ces, often as loose and oily stools. Some initialweight loss needs to have been achieved by nor-mal dieting before the drug is prescribed. Mostsubjects do achieve some weight loss with thedrug, although this may in part be as a result ofchanges made spontaneously to the diet, to limitsome of the unpleasant consequences when fathas been eaten.

A new generation of centrally acting drugsthat act to block serotonin and noradrenalinereuptake, and, therefore, promote satiety, hasbeen developed. An example of this class is sibutramine. Earlier examples of centrally actingdrugs, such as fenfluramine and dexfenflu-ramine, have been withdrawn owing to concernsabout their safety. It is likely that more drugs willbe developed in the near future to act on otheraspects of energy balance, such as thermogenesis,or parts of the leptin-controlled pathways. Inaddition to drugs that have been tested throughproper scientific procedures, there are a largenumber of other weight loss agents on the marketthat claim to be the ‘new answer’ to weight loss.These have often not been properly tested and do not come under the auspices of any legal pro-tection as drugs. Unfortunately, people spendmoney on these, with little chance of obtainingthe promised results. If weight loss does occur, itis likely to be as a result of better attention to dietthan to the ‘therapy’ being taken. In some cases,the treatments may actually be harmful. For allpharmacological treatment, there remains the

Figure 8.9 Some possible interventions for weight loss:slimming group, surgical intervention and exercise.

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challenge to re-educate the subject to better eating habits, for long-term maintenance.

Surgical intervention

Various approaches may be used, all of themdesigned to assist in a weight loss plan, ratherthan to be the only means of weight loss. Theseprocedures may attempt to restrict feeding (jawwiring), mimic satiety (stomach stapling, gastricbanding or balloons) or reduce absorption (bypassoperations). These surgical procedures are seen asa first step in a long-term weight loss plan forobese patients. Fatty tissue may also be surgicallyremoved, for example, in morbidly obese patientsin whom large amounts of fat hang down fromthe abdomen. This is done to relieve breathingproblems, and does not make an important differ-ence to total fat mass. Liposuction is offered as apart of cosmetic surgery, to draw subcutaneousfat deposits, often from the buttocks or thighs.However, the amount of fat removed this way isminimal and makes little difference to overallbody fat content.

Behaviour therapy

This may be formal or informal. The use of apsychologist together with a dietitian may helpto uncover some of the reasons for the initial eat-ing disorder, and perhaps address the causes.Much informal behaviour therapy occurs in slim-ming groups, where peer pressure and encour-agement from the group leader may achievebetter results than those seen in individualdieters. Motivation is a key aspect of group set-tings and may help the subject to continue withthe process rather than relapsing. A group settingalso provides the societal support that may beabsent in the subject’s home environment, andcan make them feel more ‘normal’.

Exercise

This is often perceived as a useful method ofweight loss. However, the energy deficit that canbe achieved by exercise alone would not bringabout significant loss of weight. For example,jogging for 45–60 minutes, three times a week,

would use up 4.2 MJ (1000 Calories) in a weekand it would, therefore, take up to 2 months tolose 1 kg of body fat. This can be contrasted withthe possible loss of 1 kg within 1 week by adietary intake deficit of 6.3 MJ (1500 Calories)per day.

However, exercise can be beneficial inachieving energy balance. It has been reportedthat exercise enhances fat rather than carbohy-drate oxidation and can, therefore, promotegreater fat utilization, allowing energy balanceto be maintained at higher percentage fatintakes in the diet.

In addition, regular exercise has been shownto increase insulin sensitivity, reduce plasmatriglyceride and very low density lipoprotein(VLDL) levels, raise high-density lipoprotein(HDL) levels and lower mildly elevated bloodpressure in overweight people. It is also sug-gested that exercise prior to a meal enhances thethermic effect of eating in overweight people.There are also reports that exercise induces anelevation of the resting energy expenditure,even after the activity itself has stopped. This,however, depends on the severity of the exerciseand is most likely to occur in highly trained ath-letes who incur an ‘oxygen debt’ during exer-cise; it may be less effective in people whoexercise less vigorously.

Overall, the effect of exercise on changes intotal body weight may be small. However, exer-cise may make it easier to achieve energy bal-ance and, once weight is lost, it may also help inthe maintenance of the new weight. There mayalso be protection of lean tissue during theperiod of weight loss, if the energy restriction isaccompanied by exercise. Finally, exercise pro-duces feelings of well-being, as a result of therelease of opiates in the brain. This effect maybe particularly beneficial to a subject attempt-ing to lose weight. A restricted food intake mayinduce feelings of dissatisfaction, possibly evendepression, which could be counteracted by thestimulation produced by exercise.

Unsafe methods of weight loss

There are very many dietary regimes that offerrapid weight loss, often linked to the consumption

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of particular ‘wonder remedies’. They may require the dieter to eat more of a particular food(grapefruit is a classic example), or a specificproduct, which has to be bought from the ‘counsellor’. Almost without exception, these areunproven and possibly unsafe, and should beavoided.

At present, there is no ‘magic wand’ remedyfor overweight, but weight loss is possible byreversing the energy balance to a negative bal-ance, and making the body use up some of itsstores of energy. The more slowly this weight islost, the better the chances of maintaining theloss. For most people, weight gain has occurredover a period of months and years; it is reason-able to expect the body to adapt better to a sim-ilar gradual reduction, than to a sudden crashdiet. However, the best remedy remains to avoidbecoming overweight in the first place.

Negative energy balance

Why does weight loss happen?

Weight loss can occur for a number of reasons.■ It may be deliberate, as in an overweight

subject who desires to lose weight to a newtarget for health or medical reasons. (Thishas been discussed above.)

■ Some sports require a particular body size forcompetition and demand that participantsfall into the appropriate weight category.

■ It may begin as being deliberate but becomeout of control, as in the eating disorders ofanorexia and bulimia nervosa.

■ It may occur in association with an addiction,perhaps to alcohol or drugs, which replacenormal food intake, resulting in weight loss.

■ It may be the consequence of ill-health, withthe subject unable to eat or absorb adequateamounts of food and becoming malnourishedas a result.

■ It may occur in cancer, where the substancesproduced by the tumour may cause alter-ations in metabolism and severe weight loss(cancer cachexia).

Individuals may also simply have a low bodyweight, despite an apparent high energy intake.This is likely to be genetically determined.

If weight is maintained at this level, then nointervention is needed; however, if the subjecthas difficulty maintaining even the low weightfurther investigation may be necessary.

A negative energy balance may be evi-denced by a failure to grow rather than by a lossof weight; this may be particularly true duringchildhood or adolescent growth spurt, whenenergy and nutrient needs are high. If these arenot satisfied, the growth rate will falter and thiscan be demonstrated on a growth chart, whichwill show the deviation from the predicted pat-tern. This might happen in a young child whobecomes ill and consequently has a reducedfood intake, or perhaps in an adolescent who isusing a great deal of energy in physical activity,for example, training for sport, so that insuffi-cient is left for normal growth.

In all cases, the energy intake does not matchthe expenditure and, although the homeostaticresponse of the body is to try to minimize the energy deficit, weight is lost by mobilizationof fat stores and lean tissue in an attempt tomaintain the energy supplies to the tissues.Eventually, when stores become depleted, theorgans themselves may be broken down, result-ing in death. The length of time that a person canwithstand such negative energy balance dependson the initial size of the stores, and the magni-tude of the negative energy balance. Individualson hunger strike who continue to take liquidsmay survive for periods up to 100 days. If food iseaten, even in small amounts, then survival canbe for much longer. After the first few days,when weight loss can be quite rapid, fastingresults in a loss of about 0.5 kg/day in the obesesubject and 0.35kg/day in a non-obese subject.A smaller energy deficit results in slower weightloss; for example, diets providing 5.9–7.9MJ(1400–1900 Calories) may result in a weight lossup to 0.20kg/day in obese males and up to0.12kg/day in obese females.

Underweight generally is associated with ahigher mortality rate, so excessive weight loss isundesirable and should be avoided. Those whohave a tendency to gain weight often yearn tobe underweight, yet this is also not a healthystate! Subjects who appear to be geneticallythin may wish to increase their body weight but

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may find this difficult. To avoid simply gainingfat, exercise to build lean tissue may need to beincluded, in association with increased dietaryintake. It is also important that healthy eatingprinciples are not ignored, and that adequateintakes of both macronutrients and micronu-trients are included in the diet.

Eating disordersThe eating disorders anorexia and bulimia ner-vosa cause particular concern. Despite consider-able research on both of these disorders, noeffective way of preventing them has been dis-covered. The conditions are much more preva-lent among females than males, although recentwork suggests that 5 per cent of anorexia suffer-ers may be males. The key element of both dis-orders is a distorted body image, which perceivesthe body weight to be greater than it is in reality.Consequently, attempts are made to reduce it. Inanorexic patients, these attempts may involveeating very little, with foods chosen carefully toinclude only those with very low energy content.In addition, the sufferer may exercise frequentlyand compulsively. There may be mood swingsand a denial of the problem, with baggy clothingbeing worn to disguise thinness. In girls, a diag-nostic sign is amenorrhoea and fine hair maygrow on the face and body. In the case ofbulimia nervosa, body weight may be in the nor-mal range. The pattern of eating involves binges,during which abnormally large amounts of foodare consumed. These are then almost immedi-ately followed by deliberately induced vomiting.In both cases, laxatives and diuretics may beused in an attempt to reduce weight.

There are medical consequences of both con-ditions: anorexic patients may lose so muchweight that they die. If weight loss is not quite sodrastic, other changes will still be present, whichinclude loss of muscle and bone mass, dry anditchy skin, hair loss, digestive tract irregularities(including constipation or diarrhoea), loss oftooth enamel due to vomiting, fainting and car-diac arrhythmias. Knowledge about both con-ditions is widespread among young people;websites occur on the World Wide Web that are perceived as encouraging eating disorders,with examples of how to avoid eating, how to

prevent feelings of hunger and personal stories.It is unlikely that such a site would cause an eating disorder in a healthy individual but thereis potential for someone who is experiencingbody dissatisfaction to be influenced by suchinformation.

Treatment requires both clinical and psychi-atric intervention, but often takes a long timeand may not be successful. There has to be awish on the part of the sufferer to get better;this is sometimes easier to achieve in the case ofbulimic patients than in those with anorexia.

Weight loss due to illnessThis requires careful examination and manage-ment. The aim is to increase energy intake and, therefore, obstacles to this should be minim-ized. It may also be useful to assess energyexpenditure and thereby obtain an indication ofenergy needs. A record of food intake for sev-eral days should normally be kept to establishwhere changes could be made. If poor appetiteis a problem, it is important to identify foodsthat are liked. Other possible courses of actioninclude:■ adding energy supplements to these foods

if possible;■ reducing low-energy and low-fat foods in

the diet and replacing them with high-energy snacks and meals containing somefat (preferably of vegetable origin);

■ avoiding drinking with meals, as fluids caninduce earlier satiety;

■ reducing the amount of dietary fibre (orNSP) in the diet, as this has a satiating effectand will reduce total energy intake;

Figure 8.10 The relationship between changes in leanbody mass and in fat.


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■ reducing physical activity (if appropriate)and perhaps including some muscle buildingactivity, such as work with weights.Changes in nutrition cause changes in body

composition. Generally, these move in the same

direction for the major constituents – lean bodymass and fat. However, changes in lean bodymass and fat can oppose one another, with theresult that total body weight shows little overallchange (Figure 8.10).

1 Energy balance can be affected by changes in energy intake, energy output, or both of these.2 Changes in energy intake may be the result of deliberate manipulation or secondary to changes in

appetite perhaps related to disease.3 Energy output is affected predominantly by basal metabolic rate and physical activity.4 Changes in body composition occur as a result of alterations in energy balance as the body tries to re-

establish homeostasis.5 There is an increased prevalence of overweight in the UK, which may be linked to a high-fat diet. Low

levels of activity may also play a part. Weight loss can only be achieved by measures that cause anegative energy balance.

6 Underweight may also be a problem and may occur by deliberate food restriction, or as a result ofillness and disease. There may also be some individuals who are genetically thin.

SUMMARY

1 Use your knowledge of the components ofenergy balance to analyse this case fully. Ann isa reasonably fit 40-year-old woman, weighing58 kg. She takes regular exercise. This includesswimming for 1 hour three times each week,walking her dog for 1 hour each day andspending about 1 hour each day gardening.Recently, Ann broke her leg in a skiing accidentand has been immobile for 6 weeks. She findsthat her body weight is now 64 kg, althoughshe has not increased her food intake.a Explain what has happened, in terms of the

energy balance process.b Once her leg has healed and she starts to

walk again, what could she do to return toher previous weight as quickly as possible?

2 How has your level of physical activity changed:a in the last year;b in the previous 5 years?

Can you suggest reasons for any change andpossible consequences for your diet?

3 a It is suggested that people in the Westshould become more physically active. Whatactivities do you consider to be the mostappropriate, and likely to be the mosteffective in the longer term?

b In some of the developing countries, levelsof activity have also decreased. Can you offeran explanation?

4 Design some advertising material to promotephysical activity in:a children, aged 8–11 years;b older teenagers, aged 16–18 years;c middle-aged women, aged 45–55; andd retired men, aged 65–70 years.

STUDY QUESTIONS


Astrup, A., Ryan, L., Grunwald, G. et al. 2000: The role of dietary fat in body fatness: evidence from apreliminary meta-analysis of ad libitum low-fat dietary intervention studies. British Journal ofNutrition 83(Suppl. 1), S25–32.

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Bolton-Smith, C., Woodward, M. 1994: Dietary composition and fat to sugar ratios in relation toobesity. International Journal of Obesity 18, 820–8.

Bouchard, C., Perusse, L. 1993: Genetics of obesity. Annual Review of Nutrition 13, 337–54.British Nutrition Foundation 1999: Obesity. The Report of the British Nutrition Foundation Task

Force. Blackwell Science: London.Clydesdale, F.M. (ed.) 1995: Nutrition and health aspects of sugars. Proceedings of a workshop.

American Journal of Clinical Nutrition 62(1S).Davies, J. 1994: Review of fad diets. Nutrition and Food Science 5, 22–4.DoH (UK Department of Health) 1995: Obesity: reversing the increasing problem of obesity in England.

A Report from the Nutrition and Physical Activity Task Forces. Wetherby: Department of Health.Ferro-Luzzi, A., Sette, S., Franklin, M. et al. 1992: A simplified approach of assessing adult chronic

energy deficiency. European Journal of Clinical Nutrition 46, 173–86.Fruhbeck, G. 2001: A heliocentric view of leptin. Proceedings of the Nutrition Society 60, 301–18.Havel, P.J. 2000: Role of adipose tissue in body-weight regulation: mechanisms regulating energy

production and energy balance. Proceedings of the Nutrition Society 59, 359–71.Hellerstein, M.K. 1999: De novo lipogenesis in humans: metabolic and regulatory aspects. European

Journal of Clinical Nutrition 53(Suppl.1), 553–65.Institute of European Food Studies 1999: A Pan-EU survey on consumer attitudes to physical activ-

ity, body weight and health. IEFS: Dublin.Jebb, S.A., Elia, M. 1993: Techniques for the measurement of body composition. International Journal

of Obesity 17(11), 611–21.Kirk, T.R. 2000: Role of dietary carbohydrate and frequent eating in body weight control. Proceedings

of the Nutrition Society 59, 349–58.Lean, M.E.J. 2000: Pathophysiology of obesity. Proceedings of the Nutrition Society 59, 331–6.Lean, M.E.J., Han, T.S., Morrison, C.E. 1995: Waist circumference as a measure for indicating need

for weight management. British Medical Journal 311, 158–61.Lissner, L., Heitmann, B.L. 1995: Dietary fat and obesity: evidence from epidemiology. European

Journal of Clinical Nutrition 49(2), 79–90.Moloney, M. 2000: Dietary treatment of obesity. Proceedings of the Nutrition Society 59, 601–8.Moore, M.S. 2000: Interactions between physical activity and diet in the regulation of body weight.

Proceedings of the Nutrition Society 53, 193–8.Murgatroyd, P.R., Shetty, P.S., Prentice, A.M. 1993: Techniques for the measurement of human

energy expenditure. International Journal of Obesity 17(10), 549–68.National Audit Office 2001: Tackling obesity in England – a report by the Comptroller and Auditor

General. London: The Stationery Office.Parsons, T., Power, C., Logan, S. et al. 1999: Childhood predictors of adult obesity: a systematic

review. International Journal of Obesity 23(Suppl. 8), 1–107.Prentice, A.M., Jebb, S.A. 1995: Obesity in Britain: gluttony or sloth? British Medical Journal 311,

437–9.Scottish Intercollegiate Guidelines Network (SIGN) 1996: Obesity in Scotland: integrating prevention

with weight measurement. Edinburgh: Royal College of Physicians.Singhal, A., Farooqi, I.S., O’Rahilly, S. et al. 2002: Early nutrition and leptin concentration in later

life. American Journal of Clinical Nutrition 75, 993–9.White, A., Nicolaas, G., Foster, K. et al. 1993: Health Survey for England 1991. Office of Population

Censuses and Surveys. London: HMSO.World Health Organisation 1998: Obesity: Preventing and managing the global epidemic. Geneva:

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Vitamins


❏ describe the role of water-soluble and fat-soluble vitamins in the body;❏ show the importance of the vitamins to health;❏ demonstrate the interactions between vitamins.


❏ explain the role of vitamins in metabolism;❏ account for the problems that arise if vitamins are not supplied;❏ identify the groups in the population who may be at risk of an inadequate intake, and the reasons for this;❏ discuss when supplements may be needed.

Throughout the body there are catalysts acting ona host of chemical reactions within living cells.Most of these are proteins acting as enzymes;some of these require additional ‘cofactors’ tocomplete their function. Some of these cofactorsare minerals, such as magnesium, calcium andcopper. There are also organic cofactors thatmust be consumed in the diet because the body(in general) is unable to synthesize them foritself. These are the vitamins.

Vitamins possess a number of specific char-acteristic features.■ They are organic and, unlike the minerals,

can be readily destroyed.■ They are essential and, in their absence, par-

ticular functions of the body fail and maycease. Ultimately, deficiency of a vitamin canbe fatal.

■ They generally work individually in a particu-lar aspect of metabolism. However, some vita-mins work in cooperation with one another.They may have similar effects and can thusreplace one another (up to a point). They maybe involved at different stages of the samepathway and a lack of one member may pre-vent the others being used.

■ They are present in food in small amounts,usually in both plant and animal foods. They vary in their chemical composition.Vitamins can be synthesized in the labora-tory and can be taken as supplements, which will function in a similar way to thosefound in foods, since they are chemicallyidentical.

■ They are needed by the body in smallamounts, measured in milligram or micro-gram quantities. In some cases, excessiveamounts of a vitamin are harmful. The bodyhas varying capacity to store the vitamins;thus, for some, a regular intake is needed.As vitamins occur in such small quantities

in foods, their discovery was a slow process.Traditional cultures had many practices incorp-orated into their food habits, which ensured thatvitamins were adequately supplied, although theywould not have been able to offer an explana-tion. These include the making of drinks frompine-needle infusions to supply vitamin C, andsoaking maize in lime water to liberate niacin.Limes were included in the cargo on long seavoyages in the eighteenth century in responseto a perceived lack of ‘a nutritional factor’ in the

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remaining provisions, which had traditionallyresulted in death among sailors.

Identification of the vitamins in the earlytwentieth century came from studies observingpeople and animals eating poor or restricted diets.Some of the substances that cured the signs andsymptoms were found to be fat soluble, otherswere water soluble. In the beginning, these vita-mines, as they were initially known, were allot-ted names according to the letters of the alphabet:A, B, C, etc. As the knowledge of the vitaminsexpanded, and they were chemically isolatedand identified, it became more sensible to callthem by their proper names. Nevertheless, thealphabetic naming is still used, particularly whenthere are several members of the group havingsimilar properties, where using individual nameswould be cumbersome.

There have continued to be new findingsabout the functions of the vitamins ever sincetheir original discovery. Clearly, our understand-ing of the vitamins is still incomplete and newfindings will continue to be made. In addition,some of the vitamins have been found to havepharmacological properties when present inamounts much greater than those required fortheir metabolic function, and have, therefore,been used as medication, both therapeuticallyand prophylactically. Further understanding ofthis role is also needed.

Fat-soluble vitamins

As a group, these vitamins share several prop-erties.■ They are found in the fat or oily parts of

foods, and are, therefore, absent from foodsthat are devoid of fat.

■ Their absorption and transport from thedigestive tract requires the secretion of bileand normal fat absorption mechanisms. Onthe whole, they are absorbed with the digestedfats into chylomicrons and transported in thelymph ultimately to reach the blood.

■ Their transport in the blood requires carriersthat are lipid soluble.

■ They are stored in lipid fractions of the body,for example, in the adipose tissue, or in asso-ciation with lipid components of cells.

■ Because of their insolubility in water, theyare not excreted in the urine and accumulatein the body, especially in the liver and adi-pose tissue. Large stored amounts, particu-larly of vitamin A and D, may be harmfuland, therefore, care must be taken to avoidhigh intake levels.

Vitamin A

The deficiency associated with inadequate levelsof vitamin A in the body, night blindness, hasbeen recognized for many centuries. Vitamin Awas the first fat-soluble vitamin to be identi-fied; it is now known that there are severalrelated compounds that have vitamin A activity,hence the name vitamin A will be used.

Three forms possess vitamin A activity inthe body: retinol, retinal and retinoic acid; col-lectively they are called the retinoids. There isinterconversion between the first two forms, butonce the acid has been formed it cannot bereconverted. In addition, there are provitamin Acompounds, the carotenoids, which can be con-verted, with varying degrees of efficiency intoretinol (Figure 9.1). The most important of theseis beta-carotene.

Vitamin A in foodsFoods derived from animals mostly contain pre-formed vitamin A, usually in the form of retinylpalmitate, which is easily hydrolysed in theintestine. Good sources are eggs, butter, milkand milk products, liver and fish or fish oils.Margarines contain vitamin A added as a legalrequirement to domestic size packs in the UK.

Plant foods contain carotenoids, which arered or yellow pigments found in many fruit andvegetables. In the UK, most of the provitamin isin the form of beta-carotene, although in otherparts of the world, alpha- and gamma-carotenesmay be important. Red palm oil used in parts ofAfrica is rich in alpha-carotenes. Rich sourcesof carotenoids in the West include carrots, darkgreen leafy vegetables, broccoli, red peppersand tomatoes; in addition, apricots, peaches andmango are good sources.

Ordinary cooking processes do not harmretinol or the carotenoids. Cooking of carrots,

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for example, enhances their digestibility and so makes more of the carotene available forabsorption.

In order to obtain an estimate of the totalamount of vitamin A activity consumed fromboth preformed retinol and carotenoids, it isnecessary to devise a combined unit. This is theretinol equivalent, which represents the amountof retinol consumed � (the amount of beta-carotene � 6). This accounts for losses in bothabsorption and conversion to the active vitamin.

In the UK mean total retinol intakes havebeen found (DEFRA, 2001) to be 780 �g retinolequivalents/day, which represents 126 per centof the mean reference nutrient intake (RNI).Intakes have fallen quite sharply in the last 10years as a result of lower fat intakes (e.g. fromwhole milk and spreads) and, in several groupswithin the population, particularly householdswith three or more children, the mean intake isless than 100 per cent of the RNI.

The major contributors overall are:

Vegetables (mostly carrots) 29%Meat (mostly liver) 20%Fats 22%Milk and cheese 19%

The contribution of pre-formed vitamin A isapproximately 64 per cent of the total intake,the remainder being provided by carotenoids.

In many parts of the world, the carotenoidsare the more important source as few animalfoods are consumed. Because the conversion of carotenoids to retinol is inefficient and theirabsorption is low, vitamin A status is poor inmany countries. This has implications for health,as discussed later in this section.

Absorption of vitamin ABoth forms of vitamin A in the diet have to bereleased from complexes for absorption acrossthe intestinal membrane, but the retinol is quicklyre-esterified once inside the mucosal cell, andthen incorporated into chylomicrons for trans-port. Carotenes are broken down to yield retinol.Although this conversion should theoreticallyyield two molecules of retinol from each beta-carotene, only one is thought to be produced nor-mally. Some carotenoids remain unconvertedand are absorbed as such. These include somehydroxy-carotenoids, such as lutein, alpha- and beta-cryptoxanthin. Absorption of retinolfrom pre-formed sources has an overall effi-ciency of 70–90 per cent if fat intakes are

Figure 9.1 Conversion of beta-carotene to retinol.

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adequate, but only 15–50 per cent of carotenesare absorbed.

Protein deficiency, fat malabsorption, intes-tinal infections and diarrhoea will all reduce theefficiency of absorption.

Functions of vitamin A in the bodyThe majority of vitamin A is stored in the liverand the size of the stores can be used to assessvitamin status. It is transported to its target sitesattached to a specific retinol-binding protein(RBP), and a pre-albumin in the plasma. This double carrier molecule is too large to be excretedthrough the kidneys, which protects the bodyfrom loss of vitamin A, and is received on targettissues by specific receptors.

Retinol levels in the plasma do not reflectintake and are not a good indicator of vitaminstatus because of the normal size of liver stores.However, a normal status is indicated when levels are in the range of 20–50 mg/dL. Plasmaretinol levels are generally tightly controlled.

Carotenoids also occur in the plasma andtend to reflect dietary intake; lutein comprises10–40 per cent of plasma carotenoids and maybe a useful marker of green vegetable intakes.

The different forms of vitamin A appear tohave differing functions in the body.

VisionThe retina is the light-sensitive cellular layer atthe back of the eyes. It contains two types ofcells: the rods (sensitive to dim light) and cones(sensitive to daylight and colour). In both types,the opsin proteins are associated with 11-cis-retinal, derived from retinol. Rhodopsin, foundin rods, is much more sensitive to a lack of vita-min A than is the pigment in the cones.

When light strikes rhodopsin, the 11-cis-retinal changes to the all-trans configuration,triggering a series of complex changes resultingin the initiation and propagation of a nerveimpulse, which is detected by the visual cortex.This occurs continuously in daylight so thatrhodopsin is constantly being broken down. Mostof our daylight vision is the result of changesoccurring to the pigment in the cones.

Before it can be useful in dim light, rhodopsinneeds to be resynthesized by conversion of the

all-trans retinal back to the 11-cis isomer, forfurther visual signals to be detected. This canonly occur in the dark, and in daylight occursonly when we blink. However, on entering a darkroom, rhodopsin resynthesis occurs quickly,provided that there is a supply of retinol/retinalavailable, and we quickly become ‘accustomedto the dark’, and can see again. If there is insuffi-cient supply of retinol to restore the rhodopsin,our dim light vision fails, and we suffer from‘night blindness’ (see Figure 9.2).

The speed with which we can become accus-tomed to see in the dark is a measure of ourvitamin A status. This is the basis of the darkadaptation test used to assess vitamin A status.

Cellular differentiationRetinoic acid appears to be the major form ofthe vitamin involved in gene expression andcontrol of cellular differentiation. In particular,the differentiation of epithelial cells is under the control of vitamin A, which determines theirmucus-secreting properties. There are specificbinding sites on cellular nuclei, from whichretinoic acid interacts with DNA and controlssynthesis of proteins and gene expression.

Epithelia constitute most of the body’s sur-faces and linings, and the ability to secrete mucusand keep these surfaces lubricated and washedis essential in the body’s defence. Thus, sites asvaried as the conjunctiva of the eye, the tracheaand lungs, the digestive tract linings, and theurethra and bladder are all dependent on ade-quate vitamin A to maintain their integrity andfunction.

A failure to maintain this epithelial integrityand mucus secretion results in one of the classicsigns of vitamin A deficiency: xerophthalmia,or dry eye. In this condition, there is a failure of tear production and the eye lacks lysozymeto keep it clean. It becomes susceptible to bacte-rial infections, resulting in conjunctivitis and,ultimately, damaged patches develop, known asBitot’s spots. If left untreated, the xerophthalmiaprogresses to a full breakdown of the eyeball,known as keratomalacia and accompanyingloss of sight.

Vitamin A has a key role as an anti-infectivevitamin, this is now believed to be closely linked


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to its role in the maintenance of epithelialintegrity. For example, impaired gastrointestinalepithelial integrity may allow the translocationof bacteria across the mucosa. Infection reducesthe levels of circulating acute phase proteins thattransport vitamin A, further exacerbating theproblem of epithelial integrity. Children withvitamin A deficiency are also more susceptibleto respiratory infections and measles. Supple-mentation of sick children with vitamin A hasbeen shown to improve recovery rates.

GrowthVitamin A is required for normal growth. Inaddition to the role described above in epithelialdifferentiation, vitamin A regulates bone remod-elling, involving resorption and deposition ofbone, required for linear growth. In deficiencythere is a thickening of bones resulting from arelative lack of resorbing cells. Thickening ofthe bones of the skull can cause pressure on thebrain and cranial nerves.

Antioxidant roleIn recent years, the carotenoids have beenfound to have an important antioxidant role inquenching free radical reactions, particularlythose involving singlet oxygen. This preventsdamaging chain reactions, which could result inlipid peroxidation or damage to DNA, both ofwhich have been postulated as being precursorsof disease processes, leading to coronary heartdisease and cancer, respectively. These proper-ties have been attributed both to beta-caroteneand lycopene (found especially in tomatoes).Antioxidant nutrients are discussed further inChapter 14.

Other functionsA number of other functions have been attributedto vitamin A, although the exact mechanisms arenot fully elucidated. The vitamin plays a key rolein immunity, especially for T-lymphocyte func-tion and the antibody response to infections. Itappears to have a role as an anti-inflammatory

Figure 9.2 Role of vitamin A in vision.

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agent. In addition, severe infections are associ-ated with loss of the vitamin in urine.

There is a link between vitamin A and redblood cell formation, possibly involving the util-ization or transport of iron; anaemia is a fre-quent finding in vitamin A deficiency, despiteapparently adequate iron status.

Vitamin A deficiencyAspects of vitamin A deficiency have alreadybeen referred to. A summary is provided hereand is shown in Figure 9.3.■ Vitamin A deficiency is one of the top three

major public health problems in the world,with 500 000 new cases each year, of whom250 000 become blind. It is responsible for70 per cent of cases of childhood blindness.Prevention with adequate vitamin A supple-mentation is possible.

■ Early signs of deficiency include mild anaemia, impaired dark adaptation, abnor-malities of smell, taste and balance, androughened skin (follicular hyperkeratosis). Inchildren, night blindness may be the first sign.

■ Xerophthalmia, with Bitot’s spots, mayremain as a chronic condition.

■ Keratomalacia, with involvement of the whole cornea, is often linked to more acutedeficiency, accompanied by an increased riskof infection and mortality.

■ In adults, vitamin A deficiency may takemany years to develop.

Toxic effects of excess vitamin AAcute poisoning can be induced by eating polarbear liver, but a more common risk of poisoningoccurs when supplements are taken in excessiveamounts. In the last 20 years, the levels of retinolin animal livers have increased dramatically andwere recently reported to be 19 000 �g/100 gand 25 200 �g/100 g in lamb and calf liver,respectively, as a result of the use of feed supplements. This is of concern, especially forwomen, in whom high doses of vitamin A maybe harmful to the embryo in early pregnancy.Intakes in excess of 3000 mg/day have beenassociated with birth defects (teratogenic effect).Clearly, a very small amount of liver wouldexceed this intake level.

Vitamin A derivatives are also used in treat-ment for acne and as an aid to tanning. Bothshould be used with care.

Requirement for vitamin AReport 41 (DoH, 1991) based its reference valueson the amounts needed to maintain an adequatepool of the vitamin in the liver at a concen-tration of 20 �g/g wet weight. On this basis, the RNI for men and women was set at 700 and 600 �g/day, respectively. Upper limits for

Figure 9.3 Summary of the signs ofvitamin A deficiency.


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regular intakes are also given, at 9000 �g/day inmen and 7500 �g/day in women.

Vitamin D

The principal physiological role of vitamin D is tomaintain serum calcium and phosphorus con-centrations at a level appropriate for the forma-tion of bone, support of cellular processes, andfunctioning of nerves and muscles.

Considering vitamin D amongst the vitaminscreates a problem. The definition of vitaminsstates that they are substances that (generally)cannot be synthesized in the body and that adietary intake is required. However, vitamin Dcan be made in the skin from a provitaminunder the influence of ultraviolet (UV-B) lightof wavelength between 290 and 320 nm. Therehas been considerable debate, therefore, whethervitamin D should continue to be considered as avitamin. However, there are circumstances whenindividuals may not be able to synthesize thevitamin, for example, owing to insufficient expos-ure to UV light and most nutritionists agree thata dietary source is required. In the UK, no syn-thesis occurs in the skin between October andMarch because light of the correct wavelengthdoes not reach the earth’s surface. Consequently,synthesis that has taken place during the sum-mer months has to provide the body’s vitamin Dneeds during the winter. In addition, those who are housebound or those living in an envi-ronment with high levels of air pollution mayhave to depend on a dietary source all yearround.

There are two potential provitamins for vitamin D: 7-dehydrocholesterol (vitamin D3)and ergosterol (vitamin D2). The former is present in animal fats, including the skin ofhumans, having been made in the body fromcholesterol. Ergosterol is found in yeast andfungi, and is used as a source of commercialvitamin production.

Vitamin D in the dietThere are few sources of vitamin D that are consumed on a regular basis. Butter, spreadingfats (including margarine, low-fat spreads),eggs and milk are the most regularly consumed

sources. Levels in the dairy products vary withthe seasons and are higher in the summermonths. Where vitamin D is added by law asfortification, for example, to margarine, levelsare constant throughout the year. In the UK,7.05–8.82 �g/100 g margarine is the prescribedlevel added to margarine. Low-fat spreads maybe fortified at the manufacturers discretion.Meat has relatively recently found to be a usefulsource of the vitamin. Other sources include oilyfish and liver, although these may occur rarelyin the diet. A number of manufactured foodsmay also be fortified with vitamin D, e.g. break-fast cereals, evaporated milk, bedtime drinks,yoghurts and infant foods. It is important tocheck on the label to discover which have addedvitamin D. Fish oil supplements are a richsource of vitamin D, and may be taken by indi-viduals as a prophylactic treatment for rheuma-tism and joint pains.

Recorded intake levels of vitamin D are3.3 �g/day; there is no RNI figure for the major-ity of the population. The main food groupscontributing to dietary vitamin D are reportedby DEFRA (2001) to be:

Fats and oils 31%Meat and meat products 19%Fish 16%Fortified breakfast cereals 14%Milk and cheese 8%

Most people in the UK obtain vitamin D byskin synthesis during the summer months onexposure to UV light from the sun. The day doesnot have to be sunny nor the skin completelyuncovered for synthesis to occur, the light canpenetrate thin cloud and light clothing. There isnow greater awareness of the dangers of expos-ure to solar radiation with respect to skin can-cer, with recommendations to cover the skinwith sun-screening creams or clothing. It islikely that this reduces the potential synthesis ofvitamin D. A balance between the harmful (can-cer risk) and beneficial outcomes (vitamin Dsynthesis) is required; it has been suggested thatabout half an hour per day of exposure to sun-light (avoiding the hottest part of the day) canachieve the beneficial synthesis, without riskingharmful consequences.

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Absorption of vitamin DAbout 50 per cent of the dietary vitamin is foundin the chylomicrons leaving the digestive tractin the lymph; most of this vitamin finds its wayto the liver with the remnants of the chylomi-crons. Vitamin D synthesized in the skin diffusesinto the blood and is picked up by a specificvitamin-D-binding protein (DBP), which trans-ports it to the liver, although some may remainfree and be deposited in fat and muscle.

Before the vitamin D can perform its functionsin the body, two activation stages occur. In theliver, an –OH group is added at position 25 on theside-chain (see Figure 9.4), to form 25 hydroxy-cholecalciferol (25-OH D3), which is secreted intothe blood and circulates attached to the carrierprotein. This first activation is controlled by levelsof the biologically active product of the secondactivation in a feedback mechanism.

The next stage occurs in the kidneys, wherea second hydroxyl group is added at position 1,to yield 1,25-dihydroxy vitamin D (1,25-(OH)2D3, or calcitriol). This is the biologically activeform of the vitamin, and its levels are tightlycontrolled to maintain calcium homeostasis.The activity of the enzyme 1-alpha-hydroxylase,which catalyses this reaction, is determined byparathyroid hormone and low blood calciumlevels, which increase its activity. High levels ofphosphate inhibit calcitriol production. Whenthe body does not require calcitriol to be pro-duced, the kidneys perform an alternativehydroxylation at position 24, producing 24,25-dihydroxy vitamin D. The role of this metaboliteis unclear, but it may be a way of ‘switching off’production of the active hormone.

Action of vitamin DCalcitriol, the biologically active form, has anumber of target tissues containing specificreceptors for the vitamin, the most notable ofwhich are the intestine, bone and kidney. In eachcase, the function of the vitamin is to cause anincrease in the plasma level of calcium.■ In the intestines, this is achieved by the

vitamin-stimulated synthesis of calcium-binding protein, required for absorption ofcalcium.

■ In the bone, calcium can be mobilized by theaction of the osteoclasts and also made avail-able for the osteoblasts to resynthesize bone.Thus, calcitriol enables appropriate amountsof calcium (and phosphorus) to be availablein the bones for synthesis, while at the sametime facilitating their release to maintainplasma levels.

■ In the kidneys, calcium reabsorption is pro-moted by the action of vitamin D.In summary, when plasma calcium levels fall,

parathyroid hormone is released. This causes syn-thesis of calcitriol in the kidneys. In response,more calcium is absorbed by the gut, some cal-cium is mobilized by the bone and less calciumis lost at the kidneys. Overall, these changesraise plasma calcium levels, thus cancelling outthe original stimulus.

If, however, the kidney is unable to respond tothe original stimulus in this way (because there isinsufficient 25-OH vitamin D being brought to thekidney, or the kidneys themselves are diseased),more parathyroid hormone will continue to besecreted. This can create a state of hyperparathy-roidism, which may be a feature of vitamin D defi-ciency. Before the role of the kidneys in vitamin Dand bone metabolism was fully understood,patients with kidney disease developed unex-plained bone diseases. Treatment with active vita-min D can now prevent these problems arising.

In addition, recent work has discovered calcitriol receptors in other tissues, including pla-centa, gonads, skin and cells of the immune sys-tem, suggesting roles that are not directly linkedto calcium homeostasis. Potent effects on cellproliferation and cell differentiation both in nor-mal and malignant cells have been described. Thevitamin may also be involved in downregulating

Figure 9.4 The formation of biologically active vitamin D occurs in two stages. First, in the liver, an –OH group is added at position 25. Then, in thekidneys, a second –OH group is added at position 1.


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the immune response, and vitamin D defects maybe involved in autoimmune reactions.

Vitamin D deficiencyThe lower cut off for adequate vitamin D statusis taken as a plasma 25-OH vitamin D level of10 �g/L (25 nmol/L). Elevated parathyroid hor-mone levels may be an alternative indicator ofpoor vitamin D status, but at present accuratelimits have not been published. Furthermore,there is a diurnal variation in levels of parathy-roid hormone, with a nocturnal rise. Parathyroidhormones tend to rise in the winter months inBritain, reflecting poorer vitamin D status, andthis can be reversed with supplementation.

The consequence of deficiency in growingchildren is a condition known as rickets. Thechild is miserable and in pain. The bones arepoorly mineralized and soft, so that limb bonesbend under the body weight, the spine becomescurved and the pelvis and thorax may becomedeformed. The gait becomes waddling, with bow-legs or knock knees. The cartilage at the ends ofthe bones continues to grow and enlarge withoutbecoming mineralized. Plasma 25-OH vitamin Dconcentrations may be below 8 �g/L (20 nmol/L;see Figure 9.5).

In adults, the comparable condition is calledosteomalacia. The clinical picture is of bone grad-ually becoming demineralized and soft, withunmineralized areas and loss of bone detail,although total amount of bone remains normal.There is likely to be bowing of the spine and difficulty in walking. Depression, neuromuscularchanges and generalized pain of uncertain originmay also be present. Plasma 25-OH D3 levels arelikely to be as low as 4 �g/L (10 nmol/L).

In both cases, there is muscular weaknessand bone pain; plasma calcium, and phosphorus levels may be low and plasma alkaline phos-phatase is raised.

Vitamin D deficiency was prevalent in Europein the nineteenth century, especially in urbanslum areas, where children had little exposureto sunlight. Improved environmental conditionssaw the disappearance of rickets as a majorproblem. There is an increased awareness thatrickets may be returning in various parts of theworld for a number of reasons. These can beattributed to:■ reduced sunshine exposure, for example,

owing to increased pollution, less playingoutdoors, increased use of sun creams andhighly covering clothing;

■ reduced vitamin D intakes, as a result oflonger breastfeeding (beyond 6 months),vegan/vegetarian diets, decreased use ofmilk and replacement with non-vitamin Dcontaining drinks.In the UK, there are a number of groups who

are vulnerable. In particular, this includes:■ Asian immigrants, especially living in the

northern regions;■ elderly people who are housebound;■ premature infants;■ individuals with malabsorption conditions;■ those with disease of the parathyroid, liver

or kidneys;■ those treated with anticonvulsants.

Vitamin D deficiency had largely been eradicated by the use of fortified infant milksand supplementation with cod liver oil, but reappeared in the UK in the early 1960s amongstthe new Asian immigrant communities. A num-ber of factors are believed to interplay in its aetiology in this group.Figure 9.5 Vitamin D deficiency in children – rickets.

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■ The darker skin pigmentation, more con-cealing clothing and a tendency to spendless time outdoors may limit the amount ofskin synthesis (especially among women).

■ Calcium intakes are low, as many groups usefew dairy products.

■ The high incidence of strict vegetarianism,including large amounts of non-starch poly-saccharides and phytate, may reduce absorp-tion of calcium, and possibly remove somevitamin D from the digestive tract. Possibleintake of vitamin D from meat is excluded.

■ Few sources of vitamin D are consumed.Programmes aimed at increasing supplement

use among the Asian population have been successful in reducing rickets among children,although poor vitamin D status continues to befound across all age groups. It has now beenrecognized that people within a household arelikely to exhibit similar plasma levels of vitaminD, suggesting a common, probably dietary aeti-ology. Diagnosis of deficiency in one membershould be followed by investigations of vitaminD status in other members of the householdgroup, and appropriate intervention.

Older adults who are housebound or institu-tionalized may not be getting sufficient dietaryvitamin D to compensate for lack of outdoorexposure. A significant proportion of thoseexperiencing a bone fracture due to osteopor-osis may have concurrent osteomalacia. Oftenplasma vitamin D levels are very low, withreports suggesting that 30–40 per cent of theover-75 age group have levels below 5 �g/L.Even when the individual is not totally house-bound, exposure to sunlight may be brief andinadequate to raise plasma vitamin D levels. Theefficiency of vitamin D synthesis in skin maydecline with age, as the skin becomes thinnerand contains less of the vitamin D precursor.Supplementation with 10 �g vitamin D/day seemsto be an appropriate prophylactic measure inthis group, recommended by the Department ofHealth.

Vitamin D deficiency in pre-term infants maybe linked to inadequate phosphorus supplies inthe milk and resultant undermineralization ofbone. There are high requirements for vitamin Dand feeds should provide 20–25 �g/day.

Various malabsorption conditions interferewith both calcium and vitamin D absorptionand may deprive the body of both. This is mostlikely to occur in coeliac disease, but can also be a consequence of gastrectomy and intestinalbypass surgery. Failure of the various stages inthe activation of the vitamin associated withliver or renal disease, or its excessive breakdownmay also result in deficiency. Anticonvulsantsand alcohol both induce the enzymes thatincrease the loss of vitamin D in bile and maydeplete the body.

Vitamin D toxicityExcess cholecalciferol can be toxic. This is mostlikely to occur in children by accidental inges-tion of vitamin supplements. It causes a loss ofappetite, thirst and increased urine output. Theblood calcium may rise and calcium depositsmay be laid down in soft tissues.

The margin of safety with vitamin D is notgreat and raised blood calcium may occur withregular intake of 50 �g/day.

Dietary reference valueThis is difficult to establish for vitamin D because,for the majority of the population with a normallifestyle who are able to synthesize the vitaminin the skin, a dietary source is unnecessary.However, children under the age of 3 years havehigh needs to sustain rapid growth, which maynot be met readily from the diet or by exposureto sunlight and, therefore, an RNI value of8.5 �g/day up to 6 months and 7 �g/day from 6 months to 3 years is given. Pregnant or lactat-ing women may also benefit from a regularintake of vitamin D to sustain calcium metab-olism. Older adults, who may have a reducedability to synthesize the vitamin, or who are lesslikely to spend time outside may also benefitfrom a dietary source of the vitamin. For both ofthese groups, the RNI is given as 10 �g/day(DoH, 1991). People of Asian origin, for whomvitamin D status may be marginal for culturalor dietary reasons, may also benefit from add-itional vitamin D, but no RNI has been specif-ically given. It should be noted that an intake of10 �g/day is difficult to achieve through dietarymeans, and a supplement may be needed.


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Vitamin E

Vitamin E was first identified as an antisterilitysubstance necessary for normal reproductive per-formance in rats. The rats could be successfullytreated with whole wheat. This role has, how-ever, been difficult to identify in humans. Inrecent years, it has become clear that vitamin Eis possibly the most important antioxidant vita-min in the body, playing an essential protectiverole against free radical damage.

It is now known that vitamin E consists of a group of substances belonging to two closelyrelated families: tocopherols and tocotrienols(Figure 9.6), with each existing in a number ofisomeric forms, alpha, beta, gamma and delta,making a total of eight different members of the group. The most important member, with thegreatest biological potency and accounting for90 per cent of the vitamin activity in the tissues,is alpha-tocopherol. It is this form that is oftentaken as the representative of the whole group.

Vitamin E in foodAnimal foods provide only alpha-tocopherol,whereas plant foods may contain the other iso-meric forms of tocopherol and the tocotrienolsas well. Among plant foods, vegetable oils arethe most important sources. The germ of wholecereal grains contains vitamin E (a rich sourceof tocotrienols). In addition, some is found ingreen leafy vegetables, and some fruits andnuts. Margarines manufactured from vegetableand seed oils contain some vitamin E, although

amounts vary. Breakfast cereals may be fortifiedwith the vitamin, but specific information shouldbe sought on the label.

Animal foods generally are not rich sourcesof vitamin E, although small amounts occur inpoultry, fish and eggs.

In the National Food Survey (DEFRA, 2001),the mean intakes are shown to be 9.9 mg/day.Most important contributors are:

Fats 46%Cereals and cereal products 14%Potatoes and potato products 11%Vegetables 9%

Absorption of vitamin ETocopherols generally occur free in foods;tocotrienols are esterified and must be splitfrom these before absorption. In the presence offats, absorption rates of the vitamin are 20–50per cent, with lower rates of absorption occur-ring as dosage increases. Thus, absorption fromsupplements may be as little as 10 per cent.

In the plasma, the vitamin is transported inthe low-density lipoprotein (LDL) fraction andconcentrates in the cell membranes. Highestconcentrations are found in the adipose tissue;levels increase here with increasing intakes.Other organs and tissues that contain the vita-min include liver, heart, skeletal muscle andadrenal glands. Levels in the plasma and liverare the first to decrease when intakes are inad-equate to meet requirements.

Functions of vitamin EThe chemical structure of tocopherols andtocotrienols, with an –OH group on the ring struc-ture, makes them very effective hydrogen donors.Therefore, vitamin E is a potent antioxidant and,as it is fat soluble, this activity is expressed partic-ularly in lipid environments. In donating hydro-gen the vitamin E becomes oxidized itself, whilepreventing the oxidation of something moremetabolically important, for example, polyunsat-urated fatty acids in cell membranes. This isimportant when free radicals are present, as thesehighly reactive substances can attack doublebonds, setting up chain reactions, with more freeradicals being produced. In the case of damage to

Figure 9.6 Structures of tocopherols and tocotrienols.

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fatty acids, lipid peroxides are produced that alterthe function of the cell membrane and cause pos-sibly irreversible damage to metabolic pathways.

There is interaction between vitamin E andother nutrients, particularly selenium and vitaminC in the antioxidant role. Vitamin C is involved inthe regeneration of vitamin E.

Vitamin E is particularly important in thoseparts of the body where large amounts of oxy-gen are present, including the lungs and the red blood cells. In addition, the lungs are alsoexposed to environmental pollutants, which con-tain free radicals and, therefore, protection hereis essential.

In summary, vitamin E is essential in main-taining cell membranes, contributing to theirintegrity, stability and function. Cell membranefunction is closely related to their structure and,for this reason, vitamin E has been consideredan important protective factor in the preventionof degenerative diseases, such as cardiovasculardisease and cancer. There is some evidence thatvitamin E plays a role in the prevention of car-diovascular disease but the results of interven-tion trials have not been conclusive. It has alsobeen proposed that vitamin E is essential for themaintenance of vascular integrity in the brain,where low levels may result in impairment ofcognitive function and possibly contribute todementia.

Deficiency of vitamin EDeficiency of vitamin E may occur in peoplewith fat malabsorption due to liver, pancreatic

or biliary disease, cystic fibrosis or coeliac dis-ease, and in individuals with increased or unmetneeds, such as:■ premature infants, who have received little

vitamin E via the placenta, and whose needsare high because of growth or exposure tohigh levels of oxygen in incubators;

■ adults exposed to a high free radical load,such as smokers or those working in pol-luted environments; and

■ people consuming high levels of polyunsat-urated fats in their diet, which require pro-tection by antioxidants.In all of these cases, deficiency may include

the following signs:■ red cells haemolysis;■ oedema owing to increased permeability of

membranes; or■ neurological symptoms, including loss of

muscle coordination, impaired vision andspeech, all of which may progress rapidly,and early treatment is required.Fortunately, these deficiencies are rare and,

as knowledge increases, appropriate preventivetreatment can be given.

High intakes of vitamin EMany claims have been made for potentialeffects of vitamin E megadoses. These includeimproved sports performance, slowed ageingprocesses, cure for muscular dystrophy, improvedsexual potency and improving cardiac function.Most of these are based on extrapolation fromanimals; unfortunately, evidence in humans islacking. At present, it is believed that an ade-quate level of vitamin E is important in the dietto compensate for the free radicals in our envir-onment. Research on cancer and heart diseaseprevalence suggests that fewer cases occur inthose with adequate vitamin E status (seeChapter 14). Intakes of vitamin E higher thancan be obtained from a normal diet can beachieved by supplementation. At these levels,there is evidence of reduced blood platelet sticki-ness and improved immunity. In women takingvitamin E supplements, there is evidence of alower incidence of strokes. Despite this, mostnutritionists would recommend that vitamin Eis obtained from a balanced diet, rich in grains,

Check that you understand the concept of freeradicals:■ What are they?■ How are they produced?■ What substances can promote their formation?■ What other substances can act with vitamin E

to quench them?■ What disease processes might be triggered by

free radical damage?(More information about antioxidants is given inChapter 14.)

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fruit and vegetables, rather than from vitaminsupplements.

At present, there is no evidence of harmfrom high doses of vitamin E.

Dietary reference valueThe vitamin E requirement depends on thepolyunsaturated fatty acid (PUFA) content ofthe tissues and, in turn, of the diet. On the basisof current levels of intake, it is proposed thatintakes of 4 mg and 3 mg/day for men andwomen, respectively, are adequate. An alterna-tive used in other countries relates the vitamin Eintake to the PUFA content of the diet in theratio of 0.4 mg tocopherol/g of dietary PUFA. In the UK, the average diet provides a ratio of0.6 mg tocopherol/g PUFA.

Some authors have suggested that intakesshould be considerably higher than this, up to87–100 mg/day, to protect against cardiovascu-lar disease. More work in this area is needed.

Vitamin K

This vitamin was initially isolated as a factorinvolved in blood clotting, with a haemorrhagicdisease observed in its absence. A number ofcompounds are now recognized as having vita-min K activity, all related by their structure asmembers of the naphthoquinone family. The mostimportant naturally occurring members are phyl-loquinone (K1) (Figure 9.7) and menaquinone(K2); there is also a synthetic compound, mena-dione (K3), which is water soluble and thereforehas advantages in absorption.

Sources of vitamin KThe menaquinones are synthesized by bacteria,including those which inhabit the human ter-minal ileum and colon. It is, therefore, possibleto obtain some of the vitamin requirement from

synthesis in the gastrointestinal tract. Very little isknown about the site or mechanisms of absorp-tion of this potentially large pool of vitamin K.It is unlikely that this can meet all the needs,therefore a dietary source is also required. If thecolonic bacteria are eliminated, for example, byantibiotic use, the individual is totally dependenton dietary supplies. Phylloquinones are obtainedfrom plant foods, with rich sources being thegreen leafy vegetables (such as broccoli, cabbage,spinach, Brussels sprouts) and peas. Green vege-tables supply about 50 per cent of the totaldietary intake of vitamin K1. Vegetable oils andmargarines together with foods that containthese, such as biscuits and cakes, provide a further20–25 per cent of the intake. Menaquinonesoccur in animal foods, especially liver; meatand dairy products contain smaller amounts.Generally, vitamin K is widely distributed infoods and a dietary deficiency is rare. Tea alsocontains a useful amount of vitamin K.

Intakes in the UK were found to be 72 �g/dayand 64 �g/day in men and women, respectively,averaged over the year. In a study of people agedover 65 years in the UK, the mean intake was65 �g/day. This was calculated to be below thecurrent guideline (DoH, 1991) of 1 �g/kg bodyweight, in 59 per cent of the subjects. The majordietary source in this group was vegetables,which contributed 60 per cent of the total intake.

Absorption of vitamin KBetween 40 and 80 per cent of the ingested vita-min appears in the chylomicrons entering thelymph. When fat absorption is impaired, as littleas 20 per cent may be absorbed. The water-soluble synthetic form is absorbed directly intothe hepatic portal vein and carried to the liver,where it is activated and then released alongwith the naturally occurring forms of vitamin K.These are carried in the LDL to target sites.

Figure 9.7 Phylloquinone (vitaminK1) is derived from plants and islipid soluble.

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Turnover of vitamin K is rapid and stores aresmall.

Function of vitamin KThe major role of vitamin K is to take part in thegamma-carboxylation of glutamic acid residues.This is part of a cycle in which the vitaminchanges from an oxidized form (quinone) to thereduced form (quinol). On completion of thecarboxylation, the vitamin is converted back tothe quinone form, and can be reused. The vita-min-K-dependent proteins (or gla-proteins) thatare produced participate in many reactions inthe body. The most important of these is theblood clotting cascade, in which four of the fac-tors needed contain gamma-carboxyglutamate,namely prothrombin and Factors VII, IX and X.It is thus clear why a vitamin K deficiency hasserious effects on blood clotting. Anticoagulantssuch as warfarin interfere with the regenerationof the reduced vitamin K, thus breaking the cycle.

Another gla-protein is osteocalcin, found inbone, which is needed for the normal binding ofcalcium in bone matrix. It is now recognized thatvitamin K supplementation may increase bonedensity in osteoporosis. Further evidence suggeststhat vitamin K may also inhibit bone resorptionby causing osteoclasts to undergo apoptosis.

Vitamin K appears in the brain asmenaquinone 4 where its role may be associatedwith the formation of a class of brain lipids. Othergla-proteins occur in many other organs in thebody, although at present their roles are unclear.

Deficiency of vitamin KPrimary deficiency of vitamin K due to a dietarylack is almost never seen, except in newborninfants. These are at risk because of low levelsof vitamin K in milk (especially human milk)and because the sterile gut of a young infant isincapable of contributing bacterial vitamin K. Ithas been common practice to give an intramus-cular injection of vitamin K to young infants toprevent possible deficiency. However, someconcern has been expressed in the last few yearsthat this practice may contribute to an increasedrisk of leukaemia in childhood, although theevidence is controversial. Some neonatal unitsnow give the vitamin by mouth, although it is

believed to be less effective via this route.Infants who become deficient are at risk of ahaemorrhagic disease of the newborn, withspontaneous bleeding, which can occur in thebrain, resulting in brain damage and death. Thistypically occurs in totally breastfed infantsbetween 3 and 8 weeks of life.

In adults, deficiency is most likely due tomalabsorption of fat, resulting from liver, bil-iary or pancreatic disease. Chronic use of min-eral oil laxatives and a poor intake may alsocontribute to deficiency; this may occur inanorexia nervosa. Long-term use of antibioticsmay reduce intestinal synthesis; this may be arisk after intestinal surgery, when coupled witha low dietary intake. In all cases, there is anincreased tendency to bleed.

Dietary reference valueThis is difficult to set because of an indetermin-ate amount of bacterial synthesis in the colon.The Department of Health (DoH, 1991) uses nor-mal blood clotting factor concentrations as anindicator of adequate status. This can be achievedwith an intake of 1 �g/kg per day in adults. Ithas been suggested that a higher level of vita-min K than this may be needed for optimal bonefunction, but evidence to propose a new level islacking. Prophylactic vitamin K is recommendedin all infants.

Water-soluble vitamins

With the exception of vitamin C, the water-soluble vitamins belong to the B-complex group.Many of the B vitamins share similar functionsand often work together; they can be broadlydescribed as cofactors in metabolism. They facili-tate the use of energy and are involved in theinterconversion between different groups ofmetabolites. Folate and vitamin B12 are involvedin cell division.

Owing to their chemical nature, the water-soluble vitamins have different characteristicsfrom the fat-soluble vitamins.■ They are absorbed into the portal blood after

digestion.■ When present in excess they are excreted in

the urine.

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■ The body has limited storage capacity forthese vitamins (with the exception of vitaminB12); most reserves in the body are found inassociation with enzymes where the vitaminplays a cofactor role.

■ They are more readily lost during food prep-aration processes, since they are soluble inwater (in particular, this occurs on heating,especially in water and also on exposure tolight and air).

Thiamin

The deficiency disease associated with thiamin,beriberi, has been known for 4000 years, althoughthe name was first used in the seventeenth century. The nutritional links were first recog-nized at the beginning of the twentieth century inJapan. The water-soluble agent was eventuallyisolated in 1911, and named vitamin B to differ-entiate it from the first fat-soluble vitamin – A.

The structure of thiamin is unusual in that itcontains a sulphur group in the thiazole ring(Figure 9.8).

Sources of thiamineThe most important sources of thiamin in theBritish diet are cereals, which provide 45 percent of the intake. The whole cereal grain is richin the vitamin but losses on milling are high, asmost is concentrated in the outer layers; thuswhite flour and polished rice are low in thiamin.However, thiamin is added to white flour at the rate of 2.4 mg/kg, which restores the level.Many breakfast cereals are also enriched withthiamin and, therefore, provide a useful source.Beans, seeds and nuts are also rich in thiamin,and may provide an important amount in thediet, especially in vegetarian populations. Inrice-eating countries, they are one of the mainsources of thiamin.

Meat is generally not rich in the vitamin,with the exception of pork and liver, and meatand meat products provide only 15 per cent ofdietary thiamin. Milk and related products provide 8 per cent of total intake and potatoesprovide 9 per cent. Both of these have low concentrations but, as they are consumed fre-quently, their contribution can be useful.

Mean daily intake in the UK is 1.44 mg,which represents 171 per cent of the RNI(DEFRA, 2001).

Thiamin is one of the more unstable vita-mins, especially in alkaline conditions, and attemperatures above 100°C. Estimates suggest anaverage of 20 per cent is lost in domestic foodpreparation. The presence of sulphur dioxide as a preservative accelerates destruction of thiamin.

Absorption and metabolism of thiamineThiamin is readily absorbed from the diet by bothactive and passive mechanisms. At high levelsof intake, most absorption is passive. Absorptionmay be inhibited by alcohol and by the presenceof thiaminases, which are found in some fish.However, because these are destroyed on cook-ing, the problem exists only where raw fish iseaten regularly, as in Japan and Scandinavia.

On absorption, thiamin is phosphorylated tothiamin pyrophosphate (TPP) (also called thi-amine diphosphate), especially in the liver. Themajor tissues that contain thiamin are the skel-etal muscle (about 50 per cent of all thiamin),heart, liver, kidneys and brain.

The major role of TPP is as a cofactor in a number of metabolic reactions, especiallyinvolved with carbohydrate utilisation. The mostimportant of these is as a coenzyme for pyru-vate dehydrogenase in the production of acetylcoenzyme A from pyruvate at the start of theKrebs cycle, through which 90 per cent of theenergy from glucose is released as ATP. Acetylcoenzyme A is also needed for the synthesis oflipids and acetylcholine (a neurotransmitter),and this demonstrates how thiamin is linked tonervous system function.

TPP is also required to complete the metab-olism of branched-chain amino acids (large doses of thiamin may help in maple-syrup urine Figure 9.8 Structure of thiamin.

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disease, which is caused by a genetic defect inthis pathway). Interconversions between sugarsof different carbon chain length also requireTPP, acting as a cofactor for the enzyme trans-ketolase.

Recently, thiamin triphosphate has been foundto control a chloride ion channel in nerves andmay be a further link to neurological functionsof thiamin.

Thiamin status can be assessed by meas-uring the activity in the red blood cell of theenzyme transketolase, which is TPP dependent.

Thiamin deficiencyIt is not surprising that thiamin deficiency affectsthe nervous system, as this requires carbohydratealmost exclusively as its source of energy. Lackof thiamin prevents pyruvic acid metabolism,and this accumulates in the blood, with somebeing converted to lactate. The onset of thedeficiency is slow, since most diets will containa trace of the vitamin. However, on a totally thiamin-free diet, symptoms may begin within10 days, reflecting the absence of stores.

Two separate clinical pictures may exist, andthese have been termed ‘dry’ and ‘wet’ beriberi.In the ‘dry’ form, there is excessive fatigue, heav-iness and stiffness in leg muscles, inability towalk far and abnormal breathlessness on exer-cise. Sufferers may also complain of mental andmood changes, and later of sensory loss andabnormal sensations from the skin. The paraly-sis may become so severe that the patient isunable to stand and walk, and may becomebedridden. This picture is more commonly seen inolder adults who have consumed an inadequatediet for many years. There may be anaemia andthe heart rate is abnormally fast on exercise. In‘wet’ beriberi, excessive fluid collects in the legs indicating cardiac involvement. Respirationmay be compromised because of oedema in thelungs. In addition, there may be serious damageto the brain, which can cause neurologicalchanges affecting the cerebellum, and eventu-ally a confusional state leading to psychosis;this is the Wernicke–Korsakoff syndrome.

Classically, thiamin deficiency occurred inpoor, rice-eating communities. It can still befound in undernourished communities in Asia.

In the West it is associated particularly withalcoholism, which results in a poor dietaryintake and interference by the alcohol with thi-amin absorption and metabolism. The clinicalpicture in chronic alcoholics often presents asWernicke–Korsakoff syndrome. People with lowthiamin intakes, perhaps exacerbated by vomit-ing, and those with malabsorption, for example,with biliary or inflammatory bowel disease, areat risk. Increased needs, such as in pregnancy,lactation, strenuous exercise and in cancer, alsocreate a risk.

Consumption of a diet rich in carbohydrateincreases the demand for thiamin; this may notbe met if the foods consumed are highly refined.It has been proposed that there may be a geneticvariant of transketolase that may predispose toWernicke–Korsakoff syndrome. Thiamin defi-ciency has also been proposed as a factor inAlzheimer’s disease, although this may be aconsequence of the condition rather than anaetiological factor.

Thiamin has also been proposed as anergogenic (i.e. energy releasing) factor in sportsperformance, to enhance aerobic capacity andlimit lactic acid production, but results of trialshave not supported a beneficial effect.

Dietary reference valueThiamin requirements are related to energymetabolism and, therefore, to energy intake.Deficiency occurs when intakes fall below0.2mg/1000Calories. The dietary reference valuereport (DoH, 1991), therefore, based its RNI at0.4 mg/1000 Calories to allow for variance andprovide a margin of safety.

Excessive intakes above 3 g/day are reportedto be toxic and should be avoided.

Riboflavin (vitamin B2)

Riboflavin (Figure 9.9) was originally identifiedas a growth-promoting substance, rather than a factor to cure a specific deficiency disease. Itwas isolated from a number of food substances,including milk, eggs and yeast, and for a timewas known as ‘vitamin G’. One of its most char-acteristic features is that the crystalline sub-stance has a yellow–orange colour.


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Riboflavin in foodsThe diet contains both free riboflavin as well asits two phosphorylated forms, flavin adeninedinucleotide (FAD) and flavin mononucleotide(FMN). Foods rich in riboflavin include milk andmilk products, meat (especially liver) and eggs.The major sources in the British diet derive frommilk and dairy products (43 per cent of totalintake), cereal products that contain milk andeggs (27 per cent of total) and meat (14 per centof total). Cereals alone are not a good source ofthe vitamin, unless enriched. A small amount of riboflavin is supplied by tea. Fruits and mostvegetables are not important sources of thevitamin, although the dark green leafy vegeta-bles may be important contributors, if eatenregularly.

Mean intakes of riboflavin in Britain are1.75mg/day; this represents 154 per cent of RNI.

Riboflavin is more stable to heat and lesssoluble than many of the B vitamins, but maybe lost in cooking water. It is also destroyed byexposure to sunlight. Leaving milk exposed tosunlight in glass bottles will result in the loss of10 per cent of the vitamin per hour. Paper andplastic cartons are better for protecting the vita-min content of milk.

Absorption and metabolism of riboflavinAbsorption occurs readily from the small intes-tine as riboflavin. It is believed that absorptionis better from animal than plant sources. In theplasma it is carried in association with albumin,which carries both the free vitamin and coen-zyme forms. In the tissues, riboflavin is convertedinto the coenzymes FMN and FAD, which con-stitute the active groups in a number of flavo-proteins. Greatest concentrations are found inthe liver, kidney and heart.

Both FMN and FAD act as electron and hydro-gen donors and acceptors, which allows them toplay a critical role in many oxidation–reductionreactions of metabolic pathways, passing elec-trons to the electron transport chain. Examplesinclude the following.■ FAD is used in the Krebs cycle and in beta-

oxidation of fatty acids, forming FADH2.■ FAD also functions in conjunction with a

number of oxidase and dehydrogenaseenzymes, including xanthine oxidase (usedin purine catabolism), aldehyde oxidase(needed in the metabolism of pyridoxineand vitamin A), glutathione reductase (sele-nium-requiring enzyme, used to quench freeradicals), monoamine oxidase (for neuro-transmitter metabolism) and mixed functionoxidases (used in drug metabolism).

■ FADH2 is needed in folate metabolism.The examples listed above show not only thecrucial role that riboflavin has in macronutrientmetabolism and energy release, but also theinterrelationships that exist with other nutrientsin the body.

Assessment of riboflavin status is mostaccurately performed using the activation ofglutathione reductase (a riboflavin-dependentenzyme) in red blood cells.

Deficiency of riboflavinMild cases of riboflavin deficiency occur aroundthe world, often seen in conjunction with other Bvitamin deficiencies. This is in part due to thecoexistence of many of the B vitamins in similarfoods, as well as the interaction between them atthe metabolic level. Signs of deficiency are gener-ally non-specific, but may involve the following.■ The mouth – with cracks and inflammation at

the corners of the mouth (angular stomatitis),sore, burning lips, which may become ulcer-ated (cheilosis), and a purple–red (or magenta)coloured tongue, with flattened papillae anda pebbled appearance (glossitis).

■ The eyes – with burning and itching, sensi-tivity to light, loss of visual acuity and agritty sensation under the eyelids. Capillaryblood vessels may also invade the cornea,and there may be a sticky secretion, whichmakes the eyelids stick together.

Figure 9.9 Structure of riboflavin.

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■ The skin – with an oily dermatitis, particularlyaffecting the nose, cheeks and forehead.Occasionally, the reproductive organs mayalso be affected.

■ Anaemia – may be seen in long-standingriboflavin deficiency.Some of these signs are also found in defi-

ciencies of niacin and vitamin B6, which maycoexist.

Deficiency, which includes inadequateriboflavin status, may arise from an inadequateintake, particularly when this is associated withincreased needs for growth. Cases have beenreported in adolescents consuming no milk ordairy products. Poor intakes may also be foundin the elderly and in alcoholics. There has been areported association between ocular lens opacityin the elderly and riboflavin status, but moreresearch is needed.

Pathological states, which include negativenitrogen balance, such as cancers, trauma andburns, may increase the turnover and thusincrease requirements. Increased excretion inthe urine has been reported in diabetics.

Dietary reference valueIntakes of 0.55mg/day over a period of 4 monthshave been reported to result in riboflavin defi-ciency. Earlier recommendations had been basedon levels producing tissue saturation. The upperrange of glutathione reductase activity is nowconsidered a more sensitive indicator of satur-ation. Surveys have shown that intakes in theUK achieve this level. The RNI was set at1.3mg/day for men and 1.1 mg/day for women.

Excessive intakes of riboflavin are poorlyabsorbed and, therefore, no evidence exists ofpotential harmful effects.

Nicotinic acid (niacin)

The deficiency disease associated with niacin ispellagra, named from the Italian for ‘rough skin’.The disease was recognized as endemic amongmaize-eating populations, and its occurrencespread with the introduction of maize through-out Europe and into Africa. In the early twenti-eth century, it reached epidemic proportions inthe southern states of America. A dietary cause

was suspected in the 1920s, and a protein-freeextract of meat or yeast was found to preventthe deficiency. The association with maize wasnot explained for a further 20 years. The pella-gra-preventing factor in yeast and meat extract,nicotinic acid, can be made in the human bodyfrom the amino acid tryptophan. The conver-sion is very inefficient, with only 1 mg of vitamin produced from 60 mg of tryptophan.However, tryptophan is the limiting amino acidin maize protein, so none is available for vita-min synthesis. In addition, the nicotinic acid inmaize is present in a bound and unabsorbableform. These two factors make a deficiency of thevitamin likely when the diet is poor and mainlycomposed of maize.

Nicotinic acid and its amide nicotinamide(Figure 9.10) are nutritionally important, andare collectively termed niacin.

Sources of niacinIn addition to niacin provided as pre-formedvitamin, the body makes a certain amount ofniacin by conversion from tryptophan. In theWest, the large amount of protein in the dietprobably supplies enough tryptophan to meetthe whole of the need for niacin and a dietaryintake of pre-formed niacin may not be needed.However, if protein intakes are low, insufficienttryptophan may be available to meet the needfor niacin.

Food composition tables provide an estimateof the amount of niacin supplied from trypto-phan, given as ‘nicotinic acid equivalents’. (This is calculated as 1/60th of the tryptophan content.)Adequate amounts of vitamin B6 and riboflavinare required for this conversion. An overall figurefor total niacin equivalents can then be obtained

Figure 9.10 Structures of nicotinic acid andnicotinamide, collectively known as niacin.


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by adding preformed niacin � nicotinic acid (orniacin) equivalents from tryptophan.

Rich sources of niacin equivalents are meat(especially liver), fish, peanuts and cereals (espe-cially if fortified). In the British diet, meat is themain source (38 per cent of total intake), followedby cereals (25 per cent of total), milk and dairyproducts (13 per cent of total) and vegetables(including potatoes) (11 per cent of total). It isalso worth noting that coffee and cocoa providesome niacin. The total amount of niacin equi-valents in the UK diet is reported as 27.8 mg(DEFRA, 2001), which represents 200 per cent ofthe RNI.

In some foods, niacin is bound to complexcarbohydrates or peptides, which makes it largelyunavailable. This is particularly a problem withmaize, but to a lesser extent applies to other cerealgrains. However, soaking of maize in lime waterreleases the bound niacin, making it available.This is a traditional practice in Mexico and,consequently, although maize is the staple foodin this country, pellagra does not occur.

Since most of the niacin in the diet is in theform of its coenzymes, it is relatively stable tolight, heat and air, and losses on cooking occuronly by leaching into water.

Absorption and metabolism of niacinThere is rapid absorption of dietary niacin, bothby active and passive mechanisms. The mainrole of niacin in the body is in the formation ofnicotinamide adenine dinucleotide (NAD) andNAD phosphate (NADP), which can be made inall cells. Once the niacin has been converted toNAD or NADP, it is trapped within cells andcannot diffuse out.

Excess free niacin may be methylated andexcreted in the urine. A low level of this metabo-lite in the urine (3 mg/day) is indicative of adeficiency state, and may be used as an assaymethod.

NAD and NADP act as hydrogen acceptors inoxidative reactions, forming NADH and NADPH.These, in turn, can act as hydrogen donors. Onthe whole, NAD is used in energy-yielding reac-tions, for example, glycolysis, the Krebs cycleand the oxidation of alcohol. The hydrogen theyaccept is eventually passed through the electron

transfer chain, to yield water. NADPH is mostlyused in energy-requiring, biosynthetic reac-tions, most importantly, for fatty acid synthesis.Overall, NAD and NADP play a part in themetabolism of carbohydrates, fats and proteinsand are, therefore, central to cellular processes.In addition, they are involved in vitamin C andfolate metabolism, and are required by glu-tathione reductase.

Niacin has been described as a componentof the glucose tolerance factor, which also con-tains chromium and which facilitates the actionof insulin. This role is separate from its functionin NAD.

Niacin deficiencyPellagra has been described as having three mainfeatures: dermatitis, diarrhoea and dementia.

Dermatitis affects particularly those parts ofthe body exposed to sunlight, and may have theappearance of sunburn. In chronic cases, itbecomes worse in sunny weather, and improvesin the winter months, forming patches of thick-ened rough skin. The dermatitis is almost alwayssymmetrical. The skin may become cracked andinfected in more acute cases. The inside of themouth is also affected, resulting in a ‘raw beef’tongue, which is sore and swollen. (There mayalso be concurrent riboflavin deficiency con-tributing to this sign.) The mouth may be sopainful that even taking liquids is impossible.

The whole lining of the gastrointestinal tractmay be affected by mucosal inflammation, result-ing in heartburn, indigestion, abdominal pain,diarrhoea and soreness of the rectum.

Dementia tends to occur only in advancedpellagra, and may range from headache, vertigoand disturbed sleep, through anxiety and depres-sion to hallucinations, confusion and severedementia with convulsions. If untreated, thecondition results in death.

Niacin deficiency is still found in parts ofthe world where the diet is poor and based onmaize, such as among poor communities in SouthAfrica. In India, millet diets, which are high inlysine and inhibit the use of tryptophan forniacin formation, may lead to pellagra. In theWest, low intake, as in alcoholics, or increasedneeds due to cancer, may result in deficiency.

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In addition, altered metabolism caused byisoniazid (an antituberculosis drug) or Hartnupdisease (inability to absorb tryptophan) may alsoresult in pellagra, if the problem is not anticipated.

Dietary reference valueThe level of niacin needed to prevent or curedeficiency is 5.5 mg/1000 Calories. On this basis,the RNI has been set at 6.6 mg/1000 Calories foradult men and women. High doses of nicotinicacid (in excess of 200mg/day) may cause vaso-dilatation, flushing and a fall in blood pressure.

Large doses (1 g/day) have been used in thetreatment of hypercholesterolaemia; however,side-effects, which include flushing, gastrointesti-nal discomfort and possible damage to the liver,mean that this is not a treatment of choice. Atother times, niacin has been used as a treatmentfor chilblains and schizophrenia, although thebenefits are uncertain.

Vitamin B6

This vitamin was isolated as a cure for a scalydermatitis seen in rats fed on purified diets. It isnow clear that there are three closely relatedcompounds that have biological activity. Theseare pyridoxine (found predominantly in plantfoods), pyridoxal and pyridoxamine (both ofwhich are present in animal foods, generally inthe phosphorylated form) (Figure 9.11).

Sources of vitamin B6Vitamin B6 is widely distributed in small quan-tities in all animal and plant tissues. Rich sourcesare liver, whole cereals, meat (including poultry),peanuts, walnuts, bananas and salmon. Moderate

amounts are found in vegetables, such as broccoli, spinach and potatoes. The availabilityfrom animal sources of the vitamin may begreater than that from plant sources, because ofbinding to glucoside.

Vitamin B6 is also susceptible to processinglosses in heating, canning and freezing. It isestimated that between 10 and 50 per cent maybe lost in this way.

Mean daily intakes in the UK are 2.0 mg(DEFRA, 2001). Main contributors in the totaldiet are vegetables (32 per cent of total), meat(30 per cent of total) and cereals (25 per cent oftotal). In men, beer may make a useful contribu-tion to the total intake of the vitamin.

Absorption and metabolism of vitamin B6The vitamin has to be released from its phos-phorylated forms prior to absorption; once in itsfree form, absorption is rapid. The liver and muscles are the main sites for pyridoxal phos-phate in the body; once it is phosphorylated, thevitamin is trapped in the cell.

Pyridoxal phosphate is involved in manybiological reactions, particularly those associ-ated with amino acid metabolism. Some examples are:■ decarboxylation, e.g. production of hista-

mine from histidine, production of dopamineand serotonin (important neurotransmitters);

■ transamination – for the synthesis of non-essential amino acids; synthesis of porphyrin(for haem), nicotinic acid from tryptophanand cysteine from methionine.The formation of cysteine from methionine

has homocysteine as an intermediate product,and there has been a great deal of interest in thepossible role of vitamin B6 as a factor for reduc-ing homocysteine levels. At present, the evi-dence on its usefulness as a protective factoragainst hyperhomocysteinaemia is equivocal.

Vitamin B6 also plays a role in:■ fat metabolism in the conversion of linoleic

acid to arachidonic acid, and in synthesis ofsphingolipids in the nervous system;

■ glycogen metabolism, particularly in muscle.Some recent work has shown that vitamin B6 mayalso have a role in modulating the action ofsteroid and other hormones at the cell nucleus.

Figure 9.11 Structures of the three closely relatedcompounds known as vitamin B6: pyridoxine,pyridoxal and pyridoxamine.


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Deficiency of vitamin B6There is no clear clinical deficiency syndrome,as a lack of this vitamin often coexists withinadequate intakes of some of the other water-soluble vitamins. Signs of deficiency mayinclude:■ anaemia (due to reduced synthesis of haem);■ smooth tongue, cracks at corners of mouth

(may be linked to riboflavin deficiency);■ dermatitis (as above, and niacin deficiency);■ nervous/muscular system signs – irritability,

headaches, fatigue, muscle twitching, numb-ness, difficulty walking, convulsions (espe-cially in infants).Deficiency may occur because of reduced

availability of the vitamin. This may be the resultof a poor dietary intake (due to ageing, alco-holism or abnormal eating patterns), in whichcase the deficiency is likely to involve severalvitamins and be multifactorial in origin. Alter-natively, it may be caused by increased demand,for example, during periods of growth (espe-cially in young infants born with low levels ofthe vitamin), during pregnancy and in womentaking the contraceptive pill.

Abnormal vitamin B6 metabolism leading todeficiency may occur as a result of some drugs,particularly isoniazid (used in tuberculosis), anti-convulsants and steroids, or due to liver disease,which sometimes reduces activation of the vita-min. Dialysis for renal disease causes increasedlosses of vitamin B6.

Vitamin B6 therapy has been recommendedfor the relief of symptoms associated with thepre-menstrual syndrome. Although there is noevidence of a deficiency, supplementation maybe of benefit to some women.

Dietary reference valueDepletion studies have shown that deficiencydevelops faster on high protein intakes. The RNIhas been set in relation to protein intake at15 mg/g protein for both men and women. Theelderly may have poorer rates of absorption andmetabolism, but currently there is insufficientevidence to set a higher RNI.

Care should be taken with supplement use,as some cases of sensory neuropathy have beenreported with chronic intakes of 100–200mg/day.

Folate

This vitamin was originally identified as a fac-tor present in yeast extract, which could cure atype of anaemia that had been described inpregnant women. This anaemia was similar topernicious anaemia, with large macrocytic cells,but the lesions of the central nervous systemwere absent. The active agent was found incrude liver extract and in spinach, and was thusnamed folate (from foliage).

Folate is now used as the generic name forthe group of substances with related vitaminactivity; this includes the synthetic form of thevitamin folic acid (or pteroyl glutamic acid)(Figure 9.12) and various polyglutamate forms(containing several glutamic acid residues) thatare commonly present in foods, including the 5-methyl- and 10-methyltetrahydrofolates, whichare the coenzyme forms of the vitamin.

Folate in foodsFood is analysed for folate content using amicrobiological growth assay with Lactobacillusrhamnosus (formerly Lactobacillus casei). This

Figure 9.12 Structure of folic acid.

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may not always give an accurate measurementof the amount of folate obtainable by humanson ingestion of the food. New methods continueto be developed, for example, high-performanceliquid chromatography and antibody-based tech-niques. Reference standards have also beendeveloped, which should contribute to morereliable assays. However, at present there is stilluncertainty about the validity of figures forfolate contents. The majority of food sourcescontain polyglutamates, with probably less than25 per cent being present as monoglutamate.Folic acid itself does not occur in nature, and isused only in supplements and fortification.

Richest dietary sources are green leafy vege-tables (spinach, Brussels sprouts) and liver, withlower but useful amounts in broccoli, cabbage,cauliflower, parsnips, fortified cereals andbread, oranges and whole wheat. Folate intakesare, in general, correlated with income; familieson a high income may have substantially morefolate in their diet than those on a low income.Folate intake also correlates with vitamin Cintakes, as many of the sources provide both ofthese vitamins. The main foods contributing tototal intakes include cereals and cereal prod-ucts, mainly as a result of fortification (34 percent of total intake) and vegetables, includingpotatoes (31 per cent of total). Milk and fruitboth provide small amounts. Beer intake cancontribute important amounts of folate, as aresult of its yeast content. Mean intakes in stud-ies in the UK were found to be 248 �g/day(DEFRA, 2001). Levels have increased since themid-1980s with the gradual introduction of for-tified products, especially breakfast cereals, andthe increased consumption of fruit juices. Themean intake achieves 132 per cent of the meanRNI, but there are groups identified by theNational Food Survey, in whom the mean intakeis just 100 per cent of RNI. These are particu-larly found in large households and those withthree or more children.

Folate in foods is susceptible to cookinglosses; it is less soluble in water than many of the B vitamins, but is sensitive to heat and,therefore, most cooking procedures will cause aloss of some of the vitamin. Keeping food hotfor periods of time or reheating are particularly

damaging, and can destroy all of the folate ori-ginally present. The extent of loss will dependon the particular form of the folate in food.Folic acid itself is more stable chemically thannatural folates in foods.

Absorption and metabolism of folateMost folate in the diet is in the bound form and, for optimal absorption, glutamates have to be removed to produce the monoglutamate,5-methyl tetrahydrofolate (5-methyl THF); thisis achieved with conjugase enzymes found in thebrush border and lysosomes of the duodenumand jejunum. These enzymes are zinc dependentand can also be inhibited by alcohol. There mayalso be conjugase inhibitors in some foods, suchas beans, which prevent the freeing of folate.Overall, 50 per cent of dietary folate is believedto be absorbed. The absorption of folic acid ismore efficient, with up to 85 per cent of intakebeing bioavailable (i.e. well absorbed or assimi-lated). In the USA, a Dietary Folate Equivalenthas been introduced to allow an overall folateprovision to be estimated from a variety ofsources with varying bioavailabilities.

Most folate is stored in the liver, which is,therefore, also a good dietary source of folate.Once taken up by target cells, folates are conju-gated to produce polyglutamates. Intracellularfolate, as tetrahydrofolate (THF) is used to carryone-carbon units from one molecule to another.Thus, it can accept such single-carbon groupsfrom donors in degradative reactions and thenact as the donor of such a unit in a subsequentsynthetic reaction. Such transfers are importantin a number of steps during amino acid metab-olism, for example:■ synthesis of serine from glycine (and vice

versa);■ synthesis of homocysteine from methionine

(and vice versa);■ conversion of histidine to glutamic acid; and■ synthesis of purine and pyrimidine bases, for

DNA and RNA synthesis. This explains thecrucial role of folate in cell division.The removal of the methyl group from

5-methyl THF is a particularly important step,which is catalysed by the vitamin B12-dependentenzyme methionine synthase. Without the


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presence of vitamin B12, the THF is ‘trapped’ inits methyl form and can no longer carry single-carbon units. This reaction is an essential linkbetween the two vitamins and explains some ofthe common features of their deficiency states(see Figure 9.13).

Furthermore, the methyl group removed dur-ing this reaction is used to generate methioninefrom homocysteine. Evidence suggests that ele-vated homocysteine levels may be associatedwith an increased risk of some diseases, andthus metabolic pathways that serve to reducehomocysteine levels have been extensivelystudied. The 5-methyl THF needed for methion-ine synthesis is formed from 5,10-methylenetetrahydrofolate, by the action of methylenetetrahydrofolate reductase (MTHFR). A recessivegenetic mutation in the coding for this enzymehas been found, with 5–18 per cent of individualsestimated to be homozygous for this mutation.This results in a lower level of enzyme activityand, consequently, higher homocysteine levels

when folate status is low. These findings mayoffer some explanation for the benefits of folatesupplementation in certain circumstances, forexample, the prevention of neural tube defects.Other roles for folate supplementation are dis-cussed below.

Folate deficiencyDeficiency of folate will affect rapidly dividingcells, which have a high requirement for purineand pyrimidine bases. The cells particularlyaffected are those making blood cells (in thebone marrow) and those lining the gastro-intestinal tract.

The effect on red cell formation results in amegaloblastic anaemia, in which the cells areimmature, larger than normal and released intothe blood as macrocytes. These cells are fewer innumber, affecting the oxygen-carrying capacityof the blood and producing the signs and symp-toms of anaemia. There may also be loss ofappetite, nausea and diarrhoea or constipation;

Figure 9.13 The metabolic role of folate homocysteine metabolism.

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the mouth may be sore with a smooth red tongue.White blood cell division is also affected andthere may be depression of the immune system.

Folate deficiency is most likely to occur inpregnancy in Britain. This is because the needsfor folate are increased and the mother’s storesmay be inadequate to supply the extra amountneeded. In general 20–25 per cent of pregnantwomen in Britain may exhibit signs of mega-loblastic changes in their bone marrow.

Alcoholics are also at risk, in part because ofa reduced intake, as well as due to the negativeeffects that alcohol exerts on the absorption offolate. Folate deficiency may be an indication ofan alcohol problem.

Folate deficiency may arise for a number ofother reasons, such as inadequate intake, ineffi-cient absorption or altered metabolism.

Inadequate intake may be linked to poverty,poor food choices, careless cooking techniquesor a small appetite. Particularly vulnerable arethe elderly, in whom low red blood cell folatelevels have been reported. Infants have rela-tively high needs for folate; premature babiesmay have low blood levels, and this may hindertheir growth and development. Heating of milkmay lower its folate content. Infants who arefed on goats’ milk are also at risk, as this has avery low content of folate.

Inefficient digestion and absorption may occurin a number of malabsorption conditions, forexample, in inflammatory bowel disease, coeliacdisease or tropical sprue and in protein–energymalnutrition. Folate deficiency itself also affectsthe gut’s absorptive capacity.

Altered metabolism may be largely due tointeractions with drugs, such as anticonvulsants.Some commonly used drugs, such as aspirin,indigestion remedies and the contraceptive pill,may interfere with folate metabolism; smokersmay also need more folate. In addition, somedrugs used in chemotherapy for cancer are specific folate antagonists, and will cause adeficiency during treatment.

Folate supplementsIn general, low dietary intakes of folate lead toraised plasma homocysteine levels and thesecan be reduced by giving folic acid, with the

greatest effects seen in those with the highestinitial levels of homocysteine.

Folate has been shown to be a particularlyimportant nutrient at the time of conception. A number of UK and international studies haveshown that supplementing women who havepreviously given birth to a child with a neuraltube defect (affecting either the brain or spinalcord) can reduce the risk of a further suchaffected pregnancy by almost 75 per cent. Thereis no indication that the mothers had been defi-cient in folate, although recent work has shownthat plasma levels of folate and B12 were signif-icantly lower (but still within the ‘normal’range) than in control subjects. Evidence nowsuggests that a genetic mutation increases theneed for folate in some women. However, as it isnot feasible to screen all women to identify thoseat risk, many countries now advise all womenwho are planning to or may become pregnant toensure they have adequate folate intakes. Somefoods, such as breads and most breakfast cere-als, are now fortified with folate to facilitate this.Bioavailability of folate from foods is relativelypoor, and thus a folate supplement of 0.4 mg/dayis recommended to ensure an adequate folatestatus. This should be taken ideally from at least12 weeks before conception and continued untilthe 12th week of pregnancy. Health promotioncampaigns have been used to increase aware-ness of the need for folate supplementation inthis group.

Elevated plasma homocysteine levels mayhave both atherogenic and thrombogenic actions,and these have been implicated in cardiovascu-lar disease. Homocysteine is reported to promoteoxidation of LDL cholesterol, to stimulate pro-liferation of vascular smooth muscle cells andto reduce the endothelial production of nitricoxide, an important vasodilator. Across popula-tions from Europe, Japan and Israel, a positiverelationship has been shown between totalplasma homocysteine level and cardiovascularmortality. Although increasing the intake offolate has been shown to reduce homocysteinelevels, at present, there is no strong evidencethat there is a parallel reduction in cardiovas-cular disease and further work in this excitingarea is required. Nevertheless, folate supplements


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may in future be shown to be of benefit in car-diovascular disease prevention.

Low folate status has been reported in bothpsychiatric and psychogeriatric patients. In manycases this may be due to poor dietary intake.Response to drug treatment is enhanced if folatestatus is improved. Dementia states have beenlinked to elevated homocysteine levels in somepatients and supplementation with folate maybe a preventive measure in the future.

In view of potential benefits of an adequateintake of folate, there has been debate in a num-ber of countries, including the US and UK, aboutthe introduction of fortification with folic acidof a staple foodstuff. The debate resulted in theintroduction of fortification in the USA fromJanuary 1999, where folic acid is added at alevel of 140 �g/100 g of grain. This aims toachieve an additional mean intake between 100and 1000 �g/day. A recent review (Honein et al.,2001) in the USA found that the incidence ofneural tube defects had fallen by almost 20 percent since the introduction of folate fortifica-tion. In the UK, the debate continues, despite arecommendation by the Committee on MedicalAspects of Food Policy (DoH, 2000) that univer-sal fortification of flour at 240 �g/100 g shouldbe introduced. Concerns related to fortificationwith folic acid are that increased intakes maymask vitamin B12 deficiency, and result indevelopment of neuropathy in vulnerable indi-viduals. Some drugs, especially those used inepilepsy, may also be less effective with a higherfolate intake. Further consideration is requiredof this issue (see Gibson, 2002).

Dietary reference valuesOn the basis of surveys of habitual intakes offolate, liver and blood levels of folate andamounts that prevent deficiency, the RNI (DoH,1991) is 200 �g/day for both men and women.A folate supplement of 400 �g is now recom-mended prior to and for the first 12 weeks ofpregnancy.

Vitamin B12

The existence of vitamin B12 had been acceptedsince the 1920s, when it was found that a

protein- and iron-free extract of liver given by injection could cure pernicious anaemia.However, the biologically active agent was notisolated and identified until 1948. An additionalfinding was the requirement for a factor in gas-tric juice, which would enable the vitamin B12

to be absorbed when it was given by mouth. Forthis reason, dietary treatment with liver previ-ously had to use very large amounts (of rawliver) on a daily basis to provide any improve-ment. Even at this stage, there was some confu-sion with folate, as some of the signs ofdeficiency are similar for both the vitamins. It isnow recognized that vitamin B12 is needed torelease folate from its methyl form so that it canfunction as a carrier of single-carbon units.However, not all of the functions of vitamin B12

are associated with folate.Vitamin B12 is the name given to a group of

compounds called the corrinoids; their charac-teristic feature is the presence of an atom ofcobalt in the centre of four reduced pyrrolerings. Four important forms are recognized:■ hydroxycobalamin;■ cyanocobalamin (synthetic form found in

supplements and fortified foods);■ adenosylcobalamin – active coenzyme;■ methylcobalamin – active coenzyme.

Vitamin B12 in foodsFor humans, the only dietary sources of vitaminB12 are animal foods; none is obtained from plantfoods. Ruminant animals, such as cows andsheep, synthesize the vitamin in the stomach bythe actions of the bacterial flora found there.Humans benefit from this by consuming theproducts from these animals.

Trace amounts of the vitamin may occur in aplant-only diet, resulting from contaminatingyeasts, bacteria or faecal contamination of watersources. Richest sources are animal livers, wherethe vitamin is stored in life. Meat, eggs, milk anddairy products contain smaller concentrations.

Mean intakes in the UK are 5.8 �g/day. Thisis predominantly derived from meat and fish (38 per cent of total intake) and milk and cheese(45 per cent of intake).

It is essential that vegans, who exclude allanimal foods from their diet, should have an

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alternative source of vitamin B12. Most vegansare aware of this, and supplement their dieteither with a specific vitamin supplement orvitamin-enriched products.

Excess amounts of vitamin C can interferewith vitamin B12 availability, converting it to aninactive form; care needs to be taken with highlevels of intake.

Absorption and metabolism of vitamin B12Ingested vitamin B12 has to be combined withintrinsic factor produced by the stomach beforeit can be absorbed. The binding occurs in theduodenum where the pH is less acid than in thestomach. The vitamin–intrinsic factor complexis then carried down to the terminal ileum (thelast part of the small intestine), from where thevitamin is absorbed, leaving the intrinsic factorbehind. The process is slow, although at lowlevels of intake, 80 per cent of dietary vitaminmay be absorbed. Absorption rates fall as intakeincreases. In the absence of intrinsic factor,there is only minimal absorption of the vitaminby passive diffusion and eventually a deficiencystate will develop. Although some of the vitaminmay be synthesized by bacteria in the bowel, itis not absorbed from here and does not form auseful source.

The metabolic role of vitamin B12 is associ-ated with two enzyme systems, one involved in the availability of THF and the other in themetabolism of some fatty acids.

Vitamin B12 acts as a cofactor for methyl-transferase, the enzyme needed to remove amethyl group from methyltetrahydrofolate,making THF available. Therefore, if vitamin B12

levels are low, this effectively also causes folatedeficiency. A further consequence is that aninadequate amount of methionine is produced.It is believed that this eventually results in dam-age to the myelin coating of nerve fibres.

Vitamin B12 is needed for the metabolism offatty acids with an odd number of carbons intheir chains.

Vitamin B12 deficiencyThis deficiency takes many years to develop,unless the inadequate intake starts in infancy.Most people have adequate reserves of the

vitamin, and with the body’s careful conserva-tion of the vitamin, these can be made to last for up to 30 years. However, if the reserves werenever accumulated, a deficiency can developwithin 3–4 years.

There are two aspects to a vitamin B12

deficiency.■ There is a failure of cell division, which is

similar to that described for folate deficiency,as the ultimate cause is the same, i.e. a failureto provide sufficient purines and pyrimidinesfor DNA and RNA synthesis. The main signof this deficiency is megaloblastic anaemia.Treatment with folate can reverse the signsof this aspect of the deficiency. However,this is potentially dangerous, as the under-lying deficiency of vitamin B12 will still leadto the second, neurological manifestation.

■ There is a neurological element, whichinvolves progressive damage to the myelinsheaths of the nerve fibres, with loss of con-duction velocity and gradual loss of sensoryand motor function in the periphery. If thishas been masked by folate treatment, progres-sion may have occurred beyond a reversiblestage.Although masking of B12 deficiency by folate

is unlikely to happen at normal levels of folateintake, there is a theoretical risk that supplemen-tation at high doses with folate (1000 �g/day)or high levels of fortification may lead to thisproblem, particularly among the older population.

It should also be noted that even a modestreduction in vitamin B12 status will cause anelevation of plasma homocysteine levels. Thereis growing evidence that this may be a risk fac-tor in coronary heart disease and dementia.

Deficiency of vitamin B12 arises most com-monly due to a failure of intrinsic factor pro-duction, resulting in an inability to absorb thevitamin. This form of the deficiency is known aspernicious anaemia, and occurs most commonlyin middle-aged or elderly individuals. It isbelieved that the body destroys the cells pro-ducing its own intrinsic factor, possibly as partof an autoimmune response. The production ofhydrochloric acid in the stomach is also affected.This is needed to release vitamin B12 from boundsources in food. In addition, the recycling of the


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body’s store of the vitamin travelling throughthe enterohepatic circulation is also affected.The consequence is that deficiency develops rel-atively quickly. Injections of vitamin B12 aregiven to restore levels of the vitamin in thebody; oral intakes would not be absorbed.

Deficiency may sometimes develop for otherreasons, such as:■ inadequate intake over many years (occa-

sionally occurs in strict vegetarians) andmay lead to raised homocysteine levels;

■ failure to absorb the vitamin due to malab-sorption conditions following removal ofthe ileum, excessive bacterial flora in the gutconsuming the vitamin, or interference fromdrugs (including alcohol, potassium supple-ments, biguanides);

■ repeated exposure to nitrous oxide anaes-thetics, which may inactivate the vitamin inthe body and lead to signs of deficiency.

Overall, it can be seen that dietary lack of vita-min B12 is not a common cause of deficiency,largely because, if the diet contains any animalproducts, then the very small requirement forthe vitamin will be met.

Dietary reference valueTurnover of the vitamin is very slow and con-servation very efficient, thus it is difficult toinduce deficiency. Evidence for the level ofrequirement is based on habitual intakes andresponses to treatment in pernicious anaemia.The RNI has, therefore, been set at 1.5 mg/dayfor adult men and women; this is believed to besufficient to produce stores that would allow thesubject to withstand a period of low intake.

Pantothenic acid

The name for this member of the B group of vitamins derives from the Greek word foreverywhere, suggesting that it is widespread.Biochemically, it is part of the coenzyme A mol-ecule, which plays a role in the metabolic path-ways for all the macronutrients. It is, therefore,central to energy transformations in the cell.

Deficiency has only been studied wheninduced experimentally. It includes a diverse andunspecific number of symptoms. An abnormal

sensation in the feet and lower legs, termed‘burning foot syndrome’, has been attributed topantothenic acid deficiency in malnourishedpatients, as it responded to treatment with thevitamin. In rats, pantothenic acid deficiency wasassociated with loss of colour from the fur, andthe vitamin is still included in some shampoos as an anti-grey hair factor, although there is noevidence that it has this role in humans.

No dietary reference value has been set,although it has been noted that mean intakes inthe UK are 5.4 mg/day. Main sources are meat,cereals and vegetables.

Biotin

Deficiency of biotin (a member of the B group ofvitamins) can be induced experimentally by thefeeding of raw egg white. This contains avidin,which has a high binding affinity for biotin andmakes it unavailable for absorption. The clinicalsigns include loss of hair and a fine scaly dermati-tis. Biotin is needed as a cofactor for several carboxylase enzymes, which carry carbon dioxideunits in metabolic pathways. Carboxylases occurin the metabolism of all the major macronutrientsand hence biotin has a widespread role.

Biotin occurs in many foods: richest sourcesare egg yolks, liver, grains and legumes. There isalso significant synthesis of biotin by the bacter-ial flora in the colon, although whether this isavailable or not is unclear.

Occasional cases of biotin deficiency havebeen reported in subjects with unusual dietarypractices, unbalanced total parenteral nutritionor in severe malabsorption consequent on boweldisease or alcoholism. Deficiency has also beenreported in epileptics treated with some of thecommon anticonvulsant drugs.

Intakes of biotin in Britain average 26–39mg/day; in the absence of deficiency, theseappear to be adequate. Main contributors to thediet are cereals, eggs, meat and milk (togetherwith beer, usually greater in men).

Vitamin C

As early as 1601 it was known that oranges andlemons or fresh green vegetables could protect a

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person against scurvy, a disease that broke outafter several months of a diet devoid of freshvegetables or fruit. The disease was a particularproblem for sailors in the sixteenth to eighteenthcenturies, when long sea voyages of discoverywere being made. Classical experiments by JamesLind in 1747 compared the curative properties ofcider, hydrochloric acid, vinegar, seawater andoranges and lemons in sailors suffering fromscurvy. Only those eating the citrus fruits recov-ered, within 1 week. However, the inclusion ofcitrus fruits and attention to adequate fresh vege-tables was by no means routine thereafter inexpeditions, and even Scott’s expedition to theSouth Pole at the beginning of the twentieth cen-tury came to a tragic end because of scurvy.Populations in Europe throughout the MiddleAges suffered scurvy during the winter months,and it was probably the introduction and rapidrise in popularity of the potato in the sixteenthcentury that contributed most to the decline ofthis disease.

It is important to remember, however, thatscurvy is still with us: it occurs among refugeesaround the world, in relief camps where the dietdoes not provide adequate vitamin C. It has also been reported among teenagers eating highlyrefined diets, and among the homeless of Britain.

Two forms of the vitamin have biologicalactivity: these are ascorbic acid (Figure 9.14)and its oxidized derivative, dehydroascorbicacid. The two forms are interconvertible, andare collectively termed vitamin C. If further oxidation takes place, the vitamin loses itspotency.

Vitamin C is unique among the vitamins inthat it is essential as a vitamin for only a few

animal species; most members of the animalkingdom can synthesize vitamin C from glucoseand have no dietary requirement for it. Theexceptions are the primates, including humans,and the guinea pig, together with a fruit-eatingbat and a rare bird. It has been calculated that pri-mates originally had the gene to perform this syn-thesis, but the ability was lost some 70 millionyears ago.

Sources of vitamin CMost dietary vitamin C is supplied by fruit andvegetables (see Figure 9.15). Only very smallamounts come from animal sources, mostlyfrom milk, although levels here may be reducedby pasteurization and other processing.

Among the fruits, the richest sources areblackcurrants and rosehips, but for the generalpopulation, oranges (and orange juice) probablyprovide the most vitamin. Other sources aremangoes, papayas and strawberries. Vegetablesources include green peppers, broccoli, cauli-flower and Brussels sprouts. Potatoes have avarying content of vitamin C: new potatoes arerich in the vitamin, but content declines as thestorage time increases. Traditionally, potatoeshave been a very important source of the vita-min in UK diets. However, potato consumptionhas fallen markedly in Britain, and othersources of vitamin C, notably fruit juice, havebecome more common, resulting in a changingprofile of vitamin C intake. The National FoodSurvey (DEFRA, 2001) found the mean vitaminC intake to be 59 mg/day, which represents 152per cent of the mean RNI. Intakes were lowest inScotland, Northern Ireland and North WestEngland, and also in lower income households.

Figure 9.14 Structure of ascorbic acid. Figure 9.15 Some dietary sources of vitamin C.


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Contributors to vitamin C intake were:

Fruit 52% (half of this from fruit juice)Vegetables 34% (includes 9% from potatoes)Milk 7%

Vitamin C is readily lost on cooking andprocessing. It is probably the least stable of allthe vitamins, and its destruction is acceleratedby exposure to light, alkali, air as well as heat.Therefore, most parts of the food preparationprocess may cause some loss of the vitamin.Anyone who is involved in preparing fruit andvegetables should consider the following waysof conserving vitamin C:■ handle food with care, with minimum bruis-

ing when cutting, to prevent release of oxi-dizing enzymes;

■ immerse vegetables directly into boiling waterto destroy the enzymes and thus protect thevitamin; this is also true of immersion intohot fat (e.g. in the cooking of potato chips);

■ cover the saucepan with a lid to reduceexposure to air;

■ use a small volume of water, or preferablysteam to minimize the leaching of vitamininto water; if the cooking water can subse-quently be used, then the vitamin C may stillbe included in the meal;

■ avoid adding sodium bicarbonate, whichenhances the green colour of some vege-tables but destroys much of the vitamin C;

■ avoid keeping vegetables hot after cooking,as this continues the destruction of the vita-min, so that almost none may remain after 1 hour. This is a particular problem whenfood is cooked in bulk and kept hot on serv-ing counters during a service period whichmay span 1–2 hours.Vitamin C in fruit is subject to much less

destruction, as the lower pH in acidic fruits pro-tects the vitamin. However, fruit juice loses itsvitamin content if left to stand in the refrigera-tor after squeezing or after opening of a carton.The best way to maximize intake of vitamin Cfrom fruit and vegetables is to consume asmany as possible in their raw form.

Absorption and metabolism of vitamin CBoth forms of the vitamin are readily absorbedby active transport and passive diffusion

mechanisms, although dehydroascorbic acid isbelieved to be absorbed better than ascorbicacid itself. The percentage of the ingested doseabsorbed falls as the amount consumedincreases. Overall, at levels of vitamin C usuallyconsumed, absorption rates are 80–95 per cent.In the plasma, vitamin C occurs principally asfree ascorbate; plasma levels are a reflection ofthe size of the dietary intake and continue toincrease until they reach a plateau at 1.4 mg/dL(100 �mol/L) at intakes of 70–100 mg/day.

The adrenal gland, pituitary and the lens ofthe eye have high concentrations of vitamin C.Among other tissues that have a significantcontent of the vitamin are the liver, lungs andwhite blood cells. The content of vitamin C inthe white blood cells is used as an indicator oftissue levels of the vitamin.

The total content of vitamin C in the body isknown as the body pool. Normal values for thisare 2–3 g in the adult; when this falls to lessthan 300mg, clinical signs of scurvy may appear.Vitamin C status, in other words the amount ofvitamin C within body tissues and fluids, isdependent on many factors (see Figure 9.16).These include the following.■ Intake: this depends on the composition of

the food, its length of storage, processing andcooking methods.

■ Absorption: this is affected by the total doseof vitamin ingested, the speed of travelthrough the digestive tract and the presenceof other factors in the tract, such as glucoselevels, trace elements and nitrosamines.

■ Metabolism: rates of usage will vary withmetabolic demand and the ability to recyclethe vitamin; demand may be higher insmokers, pregnancy, exercise, inflammation,diabetes and in polluted environments.Plasma levels are lower with increasing age.

■ Excretion in urine: this depends on the levelsin the plasma, glomerular filtration rate andthe renal threshold.

Roles of vitamin CMost of the roles of vitamin C in the body are related to its being a reducing agent, as the ascorbate is readily oxidized to dehydro-ascorbate. In this way, vitamin C can act as a

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hydrogen donor to reverse oxidation and, there-fore, may be termed an antioxidant. As an anti-oxidant, vitamin C can react with free radicalsand inactivate them before they cause damageto proteins or lipids. Once vitamin C has acted inthis way, it must be regenerated. This is achievedby a number of reductase enzymes, whichrestore the ascorbate from dehydroascorbate,

making it available for further reactions. Reduc-tases that are used in this way include reducedglutathione and NADH and NADPH.

The other major role of vitamin C is as acofactor for a number of hydroxylation reactions.This too may be an antioxidant role, whereby thevitamin is protecting metal ions, which act asprosthetic groups for these enzymes. Examples of hydroxylation reactions requiring vitamin Cinclude:■ formation of hydroxyproline and hydroxy-

lysine, for collagen synthesis;■ synthesis of carnitine, needed for release of

energy from fatty acids, especially in muscle;■ synthesis of noradrenaline;■ synthesis of brain peptides, including a num-

ber of hormone-releasing factors found inthe brain.Vitamin C is closely linked to iron metabolism.

It enhances iron absorption from food by reduc-ing ferric iron to ferrous iron to facilitate absorp-tion. It may also be involved in the incorporationof iron into ferritin. This may become a problemin individuals with excessive amounts of iron inthe body. As always, caution should be exercisedif large amounts of any single nutrient are taken.

Other roles have been proposed for vitamin C,including detoxification of foreign substances inthe liver and the promotion of immune function.The latter has received a great deal of publicityand many people believe that consumption oflarge amounts (often several grams) of vitamin Cwill help to prevent the occurrence of the com-mon cold. Evidence has been reviewed and has failed to show a consistent effect on preven-tion of the cold. However, moderate doses (up to250mg/day) may reduce the severity of the symp-toms of a cold. It should also be remembered thatvery high intakes of the vitamin are poorlyabsorbed (absorption may be 10 per cent or less),may cause intestinal irritation and diarrhoea, andchronic ingestion may result in kidney stones.

Overall, there is a great deal of evidence frommany studies that a higher intake of vitamin Cis associated with a lower disease risk.

Vitamin C deficiencyGeneral features of scurvy include progressiveweakness and fatigue, muscular and bone pains,

Figure 9.16 Summary of factors influencing vitamin Cstatus.


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oedema and depression. As the deficiency pro-gresses, there may be delayed wound healing andsubcutaneous bleeding, appearing as bruising andbleeding gums. Enlargement of the hair folliclescauses roughness of the skin. There may beanaemia and possible pathological bone fracturesdue to failure of normal bone formation. Deathresults from pneumonia and cardiac failure.

Many of the signs of scurvy can be linked tothe known functions of vitamin C, as describedabove. Thus, the failure of collagen synthesismay account for the bleeding from capillaries,failure of wounds to heal and bone fractures.Lack of carnitine synthesis may contribute tothe feelings of tiredness. Depression may belinked to poor neurotransmitter synthesis.

Although scurvy is relatively rare in theWest at the present time, sporadic cases are stillreported. Generally, these arise from an inad-equate intake of the vitamin, associated eitherwith poor food choices or insufficient income.There is a positive association between incomeand vitamin C intake. Disease states that affectthe appetite, such as anorexia or cancers, mayalso reduce intakes to deficiency levels.

Subclinical scurvy with low blood levels ofvitamin C and possible biochemical changes isfound in some elderly people and alcoholics.Elderly residents of institutions may be particu-larly vulnerable if large-scale catering practicesare wasteful of vitamin C. On the whole, elderlywomen tend to have better vitamin C statusthan men. Recent findings suggest that vitaminC may protect blood vessel integrity, and in theelderly may prevent cognitive impairment andpossibly stroke. There is also a possible role inthe prevention of cataract formation by normal-izing metabolism in the lens of the eye.

Smokers also have poorer vitamin C status.The explanation for this is not clear, but mayinclude a lower intake, poorer absorption andincreased turnover in combating the free rad-icals generated by the smoking.

There is growing interest in optimizing vita-min C status to promote health. Chronic disease,such as coronary heart disease, cancer andcataracts have been reported to be associatedwith low intake or plasma concentration ofvitamin C. Supplementation with vitamin C isreported to decrease blood pressure and bloodlipids, improve glucose metabolism, endothelialfunction and prevent free radical damage oflipids. It is, however, very difficult to attributeall of these effects solely to vitamin C intakes, asthese often vary in line with other nutrients in ahealthy diet.

Dietary reference valueThe requirement for vitamin C may be definedin terms of the amount needed to prevent scurvy:the majority of studies agree that an intake of10 mg/day will be preventive. Further increasesin intake do not increase plasma levels until theintake reaches 40 mg/day, when measurableamounts start to appear in the plasma. This levelof intake has, therefore, been set as the RNI bythe Department of Health (DoH, 1991), as indica-tive of sufficient supply of the vitamin to dis-tribute to the tissues.

There is a recommendation that smokersshould consume up to 80 mg/day more than theRNI, to allow for the increased needs. In termsof optimal intakes, 200 mg/day has been sug-gested, which will achieve a saturation level ofthe vitamin in the plasma. More work is neededto support this proposal.

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1 A 25-year-old mother with three youngchildren, aged 2, 4 and 6 years, is concernedthat she is not giving them a balanced diet, asmost of what they eat is made up of simpleconvenience foods. She herself tends to eatwith the children and often finishes theirleftovers. She feels tired and depressed. Sheasks if the whole family should takesupplements of vitamins and/or minerals. Whatdo you think?

2 a Why might an individual who has had asubstantial part of their intestines removed(for medical reasons) be at risk of vitamindeficiencies?

b Explain which vitamins in particular may beat risk.

3 Consider the various reasons why the following may not meet their vitaminrequirements:a a college student, living in self-catering

accommodation;b a middle-aged man, working long hours and

living alone;c a recently bereaved, elderly woman.

4 Construct tables to compare common features(e.g. functions, sources, signs of deficiency) ofthe following pairs of vitamins:a riboflavin and niacin;b vitamin B12 and folate;c vitamins C and E.

5 Can you identify any other vitamins that mightshare features in common with any of the pairsin Q.4, above?

STUDY QUESTIONS

1 The fat-soluble vitamins perform diverse functions, acting as regulators of metabolic reactions (vitaminD and K), protective agents (vitamin E), or constituents of essential chemicals in the body (vitamin A).

2 New roles are emerging for these vitamins as metabolic regulators at the nuclear level, perhaps involvedin gene expression.

3 Adequate levels of these vitamins are required, although excessive amounts are stored in the body andmay be toxic.

4 The water-soluble vitamins perform many key functions in the body; without them there is aconsiderable risk of failure of specific metabolic functions. Several of the vitamins act cooperatively, for example, folate and vitamin B12, riboflavin and niacin, and vitamin B6 and niacin.

5 The deficiency syndromes associated with some of these vitamins sometimes overlap, with similarpictures, particularly involving the skin, mouth and tongue, occurring with several vitamins, forexample, niacin, riboflavin and vitamin B6. This is also the case with folate and vitamin B12, with asimilar blood picture.

6 Many of the water-soluble vitamins are sensitive to cooking procedures and may be lost in substantialamounts. Care should be exercised when preparing foods that are important sources of these vitamins.

7 Several of the vitamins occur in similar foods:■ meats provide thiamin, niacin, riboflavin and vitamin B12;■ milk and dairy products are important sources of riboflavin and vitamin B12

■ cereals provide thiamin, niacin and folate and vitamin E■ fruits and vegetables are important sources of vitamin C and folate, as well as carotenes and vitamin K.Thus, omitting one of these groups of foods can have implications for more than one nutrient. Abalanced diet, prepared with care, will ensure that all of these vitamins are supplied.

8 Care should be taken not to consume too much of any of the vitamins. Some harmful effects have beenrecorded with excessive intakes of niacin, vitamin C and vitamin B6. Even though these vitamins arewater soluble and, therefore, any excess is excreted in the urine, large concentrations in the bodyobtained from megadoses of supplements should be avoided.

9 Supplementation with some vitamins, for example, folate or vitamin E may have positive health benefitsand more research is ongoing in this area.

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Abrams, S.A. 2002: Nutritional rickets: an old disease returns. Nutrition Reviews 60(4), 11–115.Bates, C.J. 1995: Vitamin A. Lancet 345, 31–5.Bender, D.A. 1994: Novel functions of vitamin B6. Proceedings of the Nutrition Society 53, 625–30.Boushey, C.J. 1995: A quantitative assessment of plasma homocysteine as a risk factor for vascular

disease: probable benefits of increasing folic acid intakes. Journal of the American MedicalAssociation 274, 1049–57.

Bower, C., Wald, N.J. 1995: Vitamin B12 deficiency and the fortification of food with folic acid.European Journal of Clinical Nutrition 49(11), 787–93.

Buttriss, J., Bundy, R., Hughes, J. 2000: An update on vitamin K: contribution of MAFF-fundedresearch. British Nutrition Foundation Nutrition Bulletin 25, 125–34.

DEFRA 2001: National Food Survey 2000 Annual Report on food expenditure, consumption andnutrient intakes. London: The Stationery Office.

DoH (UK Department of Health) 1991: Dietary reference values for food energy and nutrients for theUnited Kingdom. Report on Health and Social Subjects No. 41. Report on the Panel on DietaryReference Values of the Committee on Medical Aspects of Food Policy. London: HMSO.

DoH (Department of Health) 2000: Folic acid and the prevention of disease. Report on Health andSocial Subjects 50. London: The Stationery Office.

Fraser, J.D. 1995: Vitamin D. Lancet 345, 104–7.Gale, C.R., Martyn, C.N., Winter, P.D. et al. 1995: Vitamin C and risk of death from stroke and cor-

onary heart disease in cohort of elderly people. British Medical Journal 310, 1563–6.Gibson, S. 2002: Report from the folic acid public stakeholder meeting. British Nutrition Foundation

Nutrition Bulletin 27, 107–15.Honein, M.A., Paulozzi, L.J., Mathews, T.J. et al. 2001: Impact of folic acid fortification of the US

food supply on the occurrence of neural tube defects. Journal of the American MedicalAssociation 285, 2981–6.

Iqbal, S.J., Garrick, D.P., Howl, A. 1994: Evidence of continuing ‘deprivational’ vitamin D deficiencyin Asians in the UK. Journal of Human Nutrition and Dietetics 7, 47–52.

Khaw, K.T., Woodhouse, P. 1995: Interrelation of vitamin C, infection, haemostatic factors, and car-diovascular disease. British Medical Journal 310, 1559–63.

MAFF (Ministry of Agriculture, Fisheries and Food) 1994: Dietary and nutritional survey of Britishadults: further analysis. London: HMSO.

Maxwell, J.D. 1994: Seasonal variation in vitamin D. Proceedings of the Nutrition Society 53,533–43.

Meydani, M. 1995: Vitamin E. Lancet 345, 170–5.Morrissey, P.A., Quinn, P.B., Sheehy, P.J.A. 1994: Newer aspects of micronutrients in chronic dis-

ease: vitamin E. Proceedings of the Nutrition Society 53, 571–82.Scott, J.M. 1999: Folate and vitamin B12. Proceedings of the Nutrition Society 58, 441–8.Thane, C.W., Paul, A.A., Bates, C.J. et al. 2002: Intake and sources of phylloquinone (vitamin K1):

variation with socio-demographic and lifestyle factors in a national sample of British elderlypeople. British Journal of Nutrition 87, 605–13.

Vermeer, C., Jie, K-S.G., Knapen, M.H.J. 1995: Role of vitamin K in bone metabolism. AnnualReview of Nutrition 15, 1–22.

Wald, N.J. 1994: Folic acid and neural tube defects: the current evidence and implications for pre-vention. CIBA Foundation Symposium 181, 192–211.


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Minerals, electrolytesand fluid


❏ identify the major elements found in the human body;❏ describe the functions of each element;❏ consider the interactions between certain elements;❏ review the role of the different elements in the maintenance of health;❏ examine the importance of fluids.


❏ discuss the importance of the inorganic elements to health;❏ recognize the consequence for health of an inadequate or excessive intake of particular minerals;❏ identify food sources of particular minerals;❏ discuss the causes of an inadequate intake of specific minerals in certain groups of the population;❏ describe the rationale for the levels of inorganic minerals given as reference values;❏ discuss the body’s need for fluid and how this can be met.

This chapter considers those substances thatappear in food analyses as ash. These are the substances that are left behind when the carbon,hydrogen and nitrogen have all been burnt awayin the presence of oxygen as, for example, in a bomb calorimeter. Commonly called minerals,these substances occur in nature in water, the soiland in rocks, and are taken up by the roots ofplants and thereby find their way into animals.Humans, therefore, consume minerals both fromplant and animal sources, although foods of ani-mal origin generally have a higher content as theminerals have been concentrated in the tissues.

The body contains about 22 known minerals,of which the majority are believed to be essentialto life. Those that are considered to be nutrition-ally important are shown in Table 10.1. Theiramounts in the human body and in food have an extraordinarily wide range, from over 1 kg ofcalcium in an adult to 5–10 mg of chromium.Altogether they account for 4 per cent of theweight of the body.

Average amounts ofminerals found in the adulthuman body

TABLE 10.1

Minerals Total body contentMajor mineralsCalcium 1200 gPhosphorus 780 gPotassium 110–137 gSulphur 175 gSodium 92 gChloride 84 gMagnesium 25 gTrace mineralsIron 4.0 gZinc 2.0 gManganese 12–20 mgCopper 80 mgIodide 15–20 mgChromium 2.0 mgCobalt 1.5 mgSelenium 3–30 mg

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Some of the minerals are present in the bodyas contaminants from the environment and, as far as is known at present, have no essentialfunction in the body. These include vanadium,arsenic, mercury, silicon, tin, nickel, boron,lithium, cadmium and lead.

The major minerals are those present inamounts greater than 5 g; this applies to cal-cium and phosphorus. Also of great importance,although present in rather smaller quantities,are the electrolytes, namely sodium, potassiumand chlorine (as chloride ion). Although sulphuris listed, it does not occur freely in the body but is an essential component of the sulphur-containing amino acids.

In addition, there are the trace minerals thattogether amount to approximately 15g. Althoughpresent in small amounts, these trace substancesare vital for particular functions in the body.

The minerals have several features in common.■ They exist in the body in one of two forms:

– as biological components – in the skel-eton, in haemoglobin, in thyroid hor-mones and many enzymes;

– in their ionized state in the body fluids,where they serve to maintain homeostasis.

Whichever of these forms occurs, the mineralsretain their chemical identity.

■ Once in the body, it is sometimes difficult forthe mineral to be excreted. Those that dis-solve in water can be lost in the urine; othersare lost in the faeces, either by being secretedinto the digestive tract (usually in bile), or bybeing lost when cells are shed from the intes-tinal lining. Toxic minerals are harmful inthe body because they may be difficult toexcrete without the use of special drugs tochelate and remove them. In addition, thosethat are similar in size and properties to theessential minerals may displace them. This iswhat happens when strontium and caesiumfind their way into bones and milk in placeof calcium.

■ Minerals are generally resistant to heat, airand acid, which is why they remain when afood has been burned in a bomb calorimeter.This also means that they are rarely lost during food preparation procedures, although

the ones that are water soluble can be lostinto cooking water.

■ A problem with some minerals is that they arefound in food as large complexes attached toa number of different compounds. Probablythe most prevalent is inositol hexaphosphate(phytate), which is found in cereals, legumesand nuts, and which binds calcium, iron andzinc. This interferes with their absorption inthe digestive tract, reducing their bioavailabil-ity. A similar problem can occur where min-erals are present in foods containing largeamounts of dietary fibre (non-starch polysac-charides; NSPs).

■ Some minerals interfere with the absorptionof other minerals, competing for the samecarrier mechanism in the digestive tract. Forexample, large amounts of calcium mayinterfere with the absorption of iron andmagnesium, and zinc can reduce absorptionof iron and copper. For these reasons, takingsupplements of one mineral may cause animbalance of other minerals in the body.

Major minerals

Calcium

Calcium is the most abundant mineral present in the body, amounting to almost 40 per cent of the total mineral mass. The majority is pre-sent in bone where, together with phosphorus(as hydroxyapatite Ca10(PO4)6(OH)2), it plays anessential part in hardening the skeleton andteeth. In addition, this calcium is a reserve ofthe mineral for its role in body fluids as ioniccalcium, which is essential for nerve impulsetransmission, muscle contraction and bloodclotting.

Sources of calciumThe main dietary sources of calcium are milkand dairy products. For vegetarians who do notuse dairy products, tofu set with calcium salts orcalcium-enriched soya milk may be importantsources of calcium. In addition, cereals andcereal products may supply a reasonable amountof calcium, although this may be less wellabsorbed from wholegrain cereals owing to the

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presence of NSP and phytate. All wheatflour inthe UK, with the exception of wholemeal has,since 1943, been fortified with calcium carbon-ate by law, and provides the equivalent of94–156 mg calcium/100 g of flour. Although anumber of expert reports have in recent yearsconsidered this addition to be no longer neces-sary, it currently remains in force. Green leafyvegetables, such as spinach, broccoli and kale,contain good amounts of calcium, but itsabsorption may be inhibited by the presence ofoxalates.

Other sources of calcium may include smallfish, such as sardines, whose bones (when eaten)supply calcium, dried figs, nuts (e.g. almonds,brazil nuts), parsley, watercress and black trea-cle. Unless these foods form a major part of thediet, their contribution to the total dietaryintake will be small.

In parts of the world where the water is hard(i.e. contains many dissolved salts), it can sup-ply a significant amount of calcium to the day’sintake.

Daily intakes in the UK, reported by the 2000 National Food Survey (DEFRA, 2001), are863 mg. This represents 125 per cent of the meanreference nutrient intake (RNI); in householdswith three or more children, the mean intakeonly just exceeds the RNI, suggesting that thereare groups that do not meet this figure. The maincontribution comes from milk and cheese (54 percent), and cereals (30 per cent).

Absorption of calciumCalcium salts are generally not highly soluble,which makes their absorption from the dietproblematic. Several factors can enhance orinhibit the absorption of calcium.

Enhancing factorsThe most important of these is vitamin D, whichcauses the synthesis of a calcium-binding pro-tein in the intestinal cells that transports cal-cium into the plasma. The ability to synthesizethis protein and the amounts made are regu-lated by homeostatic mechanisms involvingparathyroid hormone and active vitamin D, inresponse to changes in circulating levels ofplasma calcium. In this way, calcium absorption

can be increased to meet increased needs in the body.

Lactose (present in milk) also enhances cal-cium absorption by keeping it in a soluble form.The presence of lactose and the large amountsof calcium found in milk make this an excellentsource of the mineral. Other sugars and proteinalso enhance calcium absorption. The acidicenvironment of the upper digestive tract alsofacilitates the solubility of calcium. Therefore,taking large amounts of ‘indigestion prepar-ations’ that lower acidity may compromise cal-cium absorption.

Inhibitory factorsCalcium absorption is reduced by phytic acidpresent in whole cereals, owing to the formationof insoluble calcium phytate. However, yeastfermentation probably breaks some of this downin the making of bread. It is also believed thatpeople who regularly eat foods containing phy-tate develop a phytate-splitting enzyme, allow-ing them to make greater use of the calcium.

Oxalates (present in spinach, rhubarb, beetroot, chocolate, tea infusions, wheat bran,peanuts and strawberries) may also inhibit cal-cium absorption owing to the insoluble natureof the calcium oxalate salt. Non-starch polysac-charides may trap some calcium making itunabsorbable in the small intestine. However,fermentation of the soluble NSP in the largeintestine may release the calcium for absorptionhere.

Unabsorbed fats will combine with calciumto form soaps, removing the calcium from thebody. This is a particular problem in steator-rhoea, in which loss of vitamin D, a fat-solublevitamin, may aggravate the problem of calciumabsorption. However, more recently, it has beensuggested that a high calcium intake, with largeamounts lost in the faeces, may help to removesome fats from the body and be of benefit inpreventing raised blood lipid levels. This is dis-cussed further in Chapter 14.

There has been some doubt about the role ofthe calcium:phosphorus ratio in determiningthe bioavailability of calcium. At normal 1:1ratios of the two minerals, there is no adverseeffect of phosphorus on calcium absorption.

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If phosphorus intakes are very high (ratio of 1:3with calcium), calcium metabolism may bealtered, with hypocalcaemia and oversecretionof parathyroid hormone, but there is little evi-dence that absorption of calcium is affected.

Overall absorption of calcium in adultsaverages about 30 per cent at a low-moderateintake (up to 500 mg); as intakes increase, thepercentage absorption falls. Generally, as theneed for calcium increases, for example, duringgrowth and in pregnancy and lactation, the effi-ciency of absorption improves. A summary offactors involved in calcium balance is shown inFigure 10.1.

Role of calcium in the bodyIn bonesCalcium is principally located in bones, where itis found both in the dense cortical bone and in

the less dense trabecular bone. The skeleton isan active reservoir of calcium. The mineral iscontinually being laid down (by osteoblasts)and resorbed (by osteoclasts) as bone growth (in childhood and adolescence), and mainte-nance (in adults) take place.

During growth in childhood and adolescencethere is a net gain of bone and, therefore, of cal-cium. In the early adult decades, the amount ofbone remains relatively constant in health,although it is in a state of constant flux with abalance between the activities of osteoclasts and osteoblasts. However, if there is a period ofimmobility or changes in levels of some hor-mones, such as cortisol or oestrogens, then boneloss will occur. The amount of bone graduallydeclines with age. This happens earlier and morerapidly in women at the time of the menopause,particularly in the first 2–3 years. The gradual

Figure 10.1 A summary of factorsinvolved in calcium balance.NSPs, non-starch polysaccharides.


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decline then continues as the rates of bonebreakdown exceed bone repair. This may resultin the bone becoming so fragile that it is easilybroken; this condition is called osteoporosis andis discussed later in this section.

In blood and body fluidsThe calcium present in body fluids is crucial tothe normal homeostasis of the body and the levels are tightly regulated to remain within narrow limits of 2.2–2.6mmol/L. This is achievedby the regulatory hormones, namely, parathy-roid hormone, active vitamin D (1,25-dihydrox-ycholecalciferol) and calcitonin, acting on thegut, bones and kidneys in response to changes incirculating calcium levels (see Figure 10.2).

Overall, when plasma calcium levels are low(or phosphate levels are high) parathyroid hor-mone is secreted. This increases calcium levelsby promoting synthesis of active vitamin D and,thus, increasing calcium absorption from thegut, reducing calcium excretion at the kidneyand stimulating calcium release from the bone.Conversely, high calcium levels cause the releaseof calcitonin from the thyroid gland. Thisinhibits bone mobilization and promotes cal-cium uptake into bone.

Why does plasma calcium need to be closelyregulated?Calcium is essential for blood clotting; it is part of the clotting cascade by which insoluble

prothrombin is converted into the thrombin of ablood clot by the action of fibrin and severalother clotting factors. If calcium levels are insuf-ficient, blood will not clot. Muscle contractionand nerve impulse transmission at nerve endingsboth involve the movement of calcium across the cell membrane, increasing intracellular levelsand triggering contraction or depolarization.

Calcium excretionCalcium is lost from the body via the faeces andurine, with very small amounts lost in sweat.Loss in the faeces represents the calcium unab-sorbed from the diet, together with endogenouscalcium from digestive secretions, especially bileand cells shed into the digestive tract, amount-ing to approximately 100 mg/day. Total losses in the faeces, therefore, depend on the amountconsumed. Urinary calcium represents the finaladjustment of plasma calcium levels, with themajority (up to 97 per cent) of the calcium filteredbeing reabsorbed by the renal tubules.

Levels of urinary calcium are increased:■ on a high calcium intake;■ by a high protein diet;■ by high sodium intake;■ in women at the menopause.

Levels of urinary calcium are decreased:■ in old age;■ by a high potassium intake;■ by a high magnesium intake;■ by a high phosphorus intake.

Figure 10.2 The regulation ofplasma calcium.

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Health aspects of calciumBone health and osteoporosisAs the numbers of older adults increase in mostWestern societies, as a result of a number ofdemographic changes and longer life expectancy,there is growing public health concern about therising incidence of osteoporosis among this age-ing population. Bone loss is a normal componentof ageing and in many people the progressivebone loss causes no clinical problems, whereas inothers the bone is sufficiently weak to fractureeven under a minor impact. Osteoporosis is thusthe loss of bone mass and micro-architecturewith age resulting in fragile bones, which aresusceptible to fractures. The most vulnerable sitesfor fracture are the radius at the wrist, the verte-brae of the spine and the neck of the femur in thepelvis. All of these fractures cause pain and dis-ability, and represent a significant cause of mor-bidity and mortality, resulting in immense coststo the health services. In the UK alone, in 2000,there were a reported 90000 fractures associatedwith this condition; other Western countries areexperiencing a similar ‘epidemic’.

The problem is much more common, but notexclusive to, older women, in whom it is esti-mated that one in three may suffer from thecondition. This is because of the accelerated lossof bone at the time of the menopause, linked tothe withdrawal of the female hormones. In men,the loss is much slower and more consistent.

Adult bone health is determined by the ‘peakbone mass’ (PBM) achieved at the end of boneaccretion, and the later rate of bone loss. Currentevidence suggests that the most desirable methodof prevention is to achieve a high peak bone massby the age of 20–25, so that the critical point forfracture is not reached when bone is lost in laterlife. Figure 10.3 shows the average rate of boneaccretion up to peak bone mass, and the declinein bone mass with ageing. Bone mineral is lostfrom about the age of 35–40, at the rate of0.3–0.4 per cent of the bone mass per year. Boneaccretion is most efficient and rapid during theteenage years, with 90 per cent of peak bonemass achieved by a mean age of 16.9 years, and95 per cent by 19.8 years. Both endogenous andexogenous factors play a part in determiningbone mass. It has been estimated that genetic

components may account for 75 per cent of thevariation in mass. However, exogenous factorshave an important role to play. It is evident thatseveral factors needed for optimal bone forma-tion should be in place at this critical time. Theraw materials for bone formation must be supplied in sufficient amounts. This includesprincipally calcium, but also other minerals andvitamins. Rates of calcium deposition have beenreported to peak during puberty, reaching levelsup to 1960mg/day. In comparison, daily turnoverin an adult is between 300 and 600mg/day. It hasbeen proposed that intakes as high as 1300mg/day may be needed for maximum calcium reten-tion. Calcium sources need to feature at all mealsduring the day for teenagers to ensure this levelof intake. Unfortunately, data about calciumintakes in teenagers show that these are oftenbelow the reference levels of 800mg for femalesand 1000mg for males.

Other factors that may help in the develop-ment of a high peak bone mass in young adultsare the following.■ Exercise. Weight-bearing exercise in particu-

lar promotes bone metabolism. In addition,exercise promotes food intake, ensuringhigher intakes of calcium as well as helpingto maintain a normal body weight.

■ Body weight. Excessively thin females (with abody mass index (BMI) below 20) may beamenorrhoeic. The absence of normal men-strual cycles and lack of oestrogen will pre-vent normal bone accretion. This may be aproblem both in girls suffering from eatingdisorders, and those who train excessively and

Figure 10.3 Changes in bone mass with age. (FromBritish Nutrition Foundation, 1991. Reproduced withkind permission of the British Nutrition Foundation.)


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try to reduce their body weight. Body size isgenerally a good indicator of bone mass.Increased muscular development requiresstronger bones to support movement, thuspromoting greater bone density. The largerframe of the male is also associated with agreater bone mass than the smaller female.

■ Alcohol and smoking. These both reducebone accretion and are, therefore, detrimen-tal to bone health.

■ Vitamin D. Adequate exposure to sunlightfor the synthesis of vitamin D is important,because of the critical need for vitamin D incalcium absorption.

■ Vitamin K. Osteocalcin and matrix gla-protein are both vitamin K-dependent factorsinvolved in bone mineralization. An adequateintake of this vitamin is, therefore, import-ant to facilitate bone development.

■ Vitamin C. This is an essential factor for thesynthesis of collagen that forms part of thestructural framework for bones.

■ Other dietary factors. Inclusion of phytate,non-starch polysaccharides, high protein,sodium or phosphorus intakes in the diet mayplay a part. They may hinder calcium absorp-tion or promote increased urinary excretion.Once peak bone mass has been achieved,

weight-bearing exercise and a healthy dietaryintake are required to maintain it. Any period ofimmobilization will have a detrimental effect onthe bones. All of the factors listed above con-tinue to be important for bone health. The bonesare a major source of alkaline buffering capacityin the body, consequent on their content of cit-rate, carbonate and sodium ions. In general, theWestern diet is rich in foods that produce acidresidues on metabolism, which, therefore, needto be buffered, drawing ions out of the bones.Such foods include protein sources (both animaland plant) and cereals. Osteoclasts are stimulatedby a more acidic pH and thus resorb more cal-cium from the bones. This is excreted in greateramounts in an acidic urine, perhaps contributingto osteoporosis.

Some foods, such as milk, produce a rela-tively neutral residue, whereas fruit and vege-tables produce an alkaline residue. Evidence tosupport the beneficial effects of milk, fruit and

vegetables on bone was provided by the DASH(Dietary Approaches to Stopping Hypertension)study (Sacks et al., 2001), in which an increasein the number of servings of fruit and vege-tables resulted in a substantial reduction in urinary calcium excretion.

Vegetarianism and high-fluoride intakes havebeen linked to lower incidence of osteoporosis,although the mechanisms are not clear.

At the menopause, the use of hormonereplacement therapy for a period of about 5 yearsis recognized as an important means of prevent-ing bone loss. Women who are overweight atthis time of life appear to have a lower risk of thecondition; it is believed that naturally occurringoestrogens produced by metabolism in the adi-pose tissue offer some protection to the bones.Smoking accelerates the normal rate of bone lossafter the menopause. Male smokers also have anincreased risk of bone loss. Exercise can promotebone health even in the elderly, and can min-imize the progressive reduction in bone mass.Exercise is also important in helping to maintainmobility and balance, and reduce the risk of fallsthat could result in a fracture. Supplementationwith calcium and vitamin D after the menopausehas been shown to delay bone loss and reducethe risk of fractures in some studies, but there isstill debate about the general application of thismeasure and the doses needed. Soy proteinisoflavones have also been shown to reduce theloss of bone density around the time of themenopause, although more research is needed.These factors are summarized in Figure 10.4.

General screening for osteoporosis is notcurrently a public health recommendation inthe UK, although those at high risk would bene-fit from early diagnosis. Risk of osteoporosis isgreater in people with coeliac disease, inflam-matory bowel disease and on prolonged steroidtherapy. Individuals with a family history of(maternal) osteoporotic fracture may be atgreater risk. Dual x-ray adsorptiometry (DEXA)is the most widely used method, although newtechniques include biochemical markers of boneresorption, such as urinary pyridinium crosslinkexcretion and quantitative ultrasound (QUS).Overall, there are many unanswered questionson the subject of osteoporosis. It seems clear,

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however, that achieving a high peak bone massin early adulthood is probably one of the bestways of preventing the development of the condition.

Colon cancerThere is some evidence that calcium may reducethe incidence of colon cancer. It has been sug-gested that bile acids and fatty acids are bound tounabsorbed calcium, and are thus removed fromthe colon. This reduces the potential for harmfuleffects if they were to linger in the colon.

Blood pressureIndividuals who have higher intakes of calcium,especially from dairy products, have beenshown in several studies to have lower bloodpressure. In addition, calcium supplementationcan lower blood pressure.

Dietary reference valuesThese are difficult to determine, as there is nosingle satisfactory approach. The figures recom-mended in Report 41 (DoH, 1991) are, therefore,

based on the factorial approach, taking intoaccount needs for growth and maintenance. Theaverage absorption is assumed to be 30 percent; the reference nutrient intake for adults is700 mg/day. There are no specific recommenda-tions made to take into account possible healthimplications.

Phosphorus

Phosphorus is often considered together withcalcium, as both are present in bone. In blood,they have a reciprocal relationship and are con-trolled by similar mechanisms. Phosphorus iswidely available in both animal and plant foodsincluding meat, poultry, fish, eggs and dairyproducts, and in cereals, nuts and legumes.Small amounts occur in tea and coffee. It iswidely present as a food additive in bakerygoods, processed meats and soft drinks.

Absorption and metabolismThe body absorbs phosphorus more efficientlythan calcium, at rates of 60–90 per cent,

Figure 10.4 Factors influencing bone health.


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depending on body needs. An inadequate intakeis, therefore, unlikely.

Dietary phosphorus can be either organic or inorganic in origin, most absorption takingplace in the inorganic form. Phosphorus found incereals and legumes as phytate is only partly liberated during digestion, with approximately 50 per cent being absorbed. Absorption from thedigestive tract is reduced by the presence of mag-nesium and aluminium, both of which may befound in indigestion preparations. This is unlikelyto lead to phosphate deficiency, unless there isalso a metabolic problem involving the kidneys orparathyroid gland that regulate phosphate levels.Calcium also reduces phosphorus absorption.

Together with calcium, phosphorus is themajor mineral constituent of bone where itoccurs as hydroxyapatite, and 85 per cent of thebody’s phosphorus is found here. The remaining15 per cent is distributed within the soft tissues,as phospholipids in red blood cells and plasmalipoproteins, in DNA and RNA, and a smallamount as inorganic phosphate. The inorganicphosphate compartment is, however, critical, as itreceives phosphate from the diet and from boneresorption, and loses phosphate to urine andbone mineralization. It is also the primary sourcefor all of the biochemical reactions that requirephosphates as the currency for energy transform-ations. It is, therefore, central to the functioningof the metabolic machinery. Phosphates are alsocritical as buffers to maintain normal pH in thebody. Cells have limited storage capacity forphosphate and, therefore, draw on the inorganicphosphate pool for their needs.

Phosphorus levels in the body are regulatedmainly by renal excretion under the influence ofparathyroid hormone, which causes increasedurinary loss. (This allows plasma calcium levelsto rise – a major function of the hormone.)Abnormal levels of phosphate in the blood aregenerally the result of renal or parathyroid dysfunction, rather than dietary excess or defi-ciency, since there is extensive recycling of themineral. However, intakes may be low in prema-ture infants, vegans, alcoholics and people whouse aluminium-containing antacids regularly.Deficiency of phosphorus can cause bone loss,and result in rickets and osteomalacia.

A low level of extracellular inorganic phosphate (hypophosphataemia) will result incellular dysfunction. Signs and symptoms mayinclude anorexia, anaemia, muscle weakness,bone pain, parasthesia (pins and needles) and, ifacute, confusion and death.

Intakes of phosphorus in the UK average1.2–1.3 g/day; a minimum intake of 400 mg/dayhad been proposed to maintain adequate plasmaphosphate levels. The RNI (DoH, 1991) is givenas 550 mg/day for adults, based on an equimo-lar ratio with calcium intakes.

Magnesium

The human body contains approximately 25 gof magnesium, of which 60 per cent is found inthe bones, the remainder in the soft tissues and1 per cent in the extracellular fluid. It is themost abundant divalent intracellular ion.

Food sources of magnesium include wholegrain cereal, nuts, legumes, seafoods, coffee, tea,cocoa and chocolate. Chlorophyll found in greenleafy vegetables contains magnesium. Intakes inthe UK are reported to be around 227 mg/day.

Absorption and metabolismAbsorption of magnesium occurs in the smallintestine and appears to be more efficient whenintakes are low. Absorption is improved by vita-min D, and reduced by the presence of fattyacids and phytate. Plasma magnesium levels arekept constant by precise regulation of excretionvia the kidney to match amounts absorbed. Themagnesium found in bones is thought to act as areservoir to sustain plasma levels. The remainingmagnesium is largely found in muscle and othersoft tissues. It occurs as part of cell membranesbut is also an essential activator of over 300enzyme systems. Most notably it is involved inall enzyme systems utilizing ATP. In addition,magnesium is involved in protein synthesis,energy production, muscle contraction andnerve impulse transmission.

There are many situations in which magne-sium competes with or interferes with the actionof calcium in the body. For example, magnesiuminhibits the blood clotting process, it may alsoinhibit smooth muscle contraction by blocking

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the calcium binding sites. However, the actionsof vitamin D and parathyroid hormones, whichregulate calcium, both require the presence ofmagnesium.

Magnesium deficiencyIn humans this is most likely to be secondary to other disturbances in the body. These mayinclude:■ inadequate intakes in protein–energy mal-

nutrition;■ prolonged intravenous feeding;■ in alcoholics, excessive gastrointestinal tract

losses as in vomiting, diarrhoea or malab-sorption;

■ excessive excretion as in the use of certaindiuretics, or in uncontrolled diabetes involv-ing tissue catabolism.

Studies of patients in intensive care units haveshown that hypomagnesaemia may occur in upto 65 per cent of cases, often in association withlow potassium levels.

Hypocalcaemia is a major sign in magne-sium deficiency and may contribute to the clin-ical picture. Low levels of magnesium result ingradually progressive muscle weakness, neuro-muscular dysfunction, irregular heartbeat andultimately coma and death.

Health aspects of magnesiumEpidemiological evidence suggests that coronaryheart disease is more common where magnesiumlevels in the water supply are low; however, evi-dence on this is conflicting. It has been proposedthat adequate magnesium protects the cardiacmuscle against ischaemic injury. Furthermore,magnesium has been advocated as therapy inacute myocardial infarction to strengthen cardiacmuscle contraction and possibly reduce mortal-ity. Magnesium supplementation has also beenproposed as a treatment for osteoporosis butmore work is needed. Magnesium has been usedsuccessfully as a treatment in pre-eclampsia of pregnancy, to reduce the risk to both motherand infant.

Because of the absence of a clear-cut defi-ciency in healthy adults, a reference value is dif-ficult to define. The Department of Health (DoH,1991) suggests that an intake of 3.4 mg/kg per

day, equal to 270 mg in women and 300 mg inmen, is an adequate intake.

Sulphur

Sulphur enters the body as the sulphur-containingamino acids methionine and cysteine. The sulphur-containing side-chains in these aminoacids can link to each other forming disulphidebridges, which give great strength to the peptideproduced. These bonds are found in proteinsthat form the hard parts of the body, such asskin, nails and hair. Sulphur is also present inthe vitamins thiamin and biotin.

These amino acids are required for the syn-thesis of proteins and connective tissue con-stituents, such as chondroitin sulphate. Sulphuralso has an important role in the detoxifyingpathways used by the liver for removal of wasteproducts and participates in acid–base balance.

A mixed diet is unlikely to be short of sul-phur as most proteins contain over 1 per centsulphur. Egg and milk proteins are particularlyrich in methionine, which is especially impor-tant in tissue growth and regeneration after illness and injury.

Microminerals or traceelements

Iron

Iron is part of the haemoglobin molecule inblood and, as such, accounts for two-thirds ofthe body’s iron content. In this role, combinedwith the protein globin, it is the carrier of oxy-gen from the lungs to the tissues and, therefore,plays a vital role in survival. In addition, some isfound in myoglobin, which is the pigment foundin muscles that has a high affinity for oxygen.

The remainder is used in enzymes (especiallycytochromes, which are essential in oxidation–reduction reactions), stored in the body or isfound in the blood, being carried between sitesin the body.

The total amount of iron present in the bodyvaries with the body weight, gender and long-term nutrition. It is also affected by the state ofhealth, growth and pregnancy. On average, the


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body iron content averages 50 mg/kg of bodymass in men and 38 mg/kg in women.

Sources of ironIron occurs in the diet in two forms: as haemiron mainly in foods of animal origin, and non-haem, or inorganic iron, predominantly fromplant foods. The richest sources of haem ironare meat and fish (liver is one of the richestsources of iron, although many people never eatit). Cereals contain inorganic iron, which mayalso be bound to insoluble compounds such asphytate. However, fortification of white breadflour with iron does ensure that some additionaliron is available without competition from phy-tate, which is removed in the milling process.Legumes and green vegetables also provideiron, although the availability of this is muchless than from the animal sources. Other sourcesof iron include nuts and dried fruits. Milk anddairy products are very low in iron, and intakesof large amounts of milk may be linked to pooriron status.

Iron supplements are widely available. Theycontain a variety of iron salts – sulphate, succin-ate, gluconate and fumarate – and have varyinglevels of bioavailability. It is stated that in thosetaking supplements, these contribute 7.5 mg/day of iron.

Average intakes of iron in the UK are10.1 mg/day, which represents 97 per cent of theaverage RNI (DEFRA, 2001). Most of the groupsstudied in the National Food Survey had meanintakes that fell below 100 per cent of the RNI.Only households with no children achievedintakes of 100 per cent or more of the RNI. Inthe Health survey for England 1994 (Colhounand Prescott-Clarke, 1996), low iron stores werereported for 4 per cent of men and 26 per centof women. Main contributors in the UK to ironintakes are cereal products (53 per cent), meat(13 per cent) and vegetables (16 per cent).

Absorption of ironThe two forms of iron in the diet are absorbedwith different efficiency. Organic (haem) ironmust be hydrolysed from any protein to which itis attached and is then absorbed relatively eas-ily, albeit slowly; the overall absorption of iron

from meat may be 20–25 per cent. The absorp-tion takes place most effectively in the duode-num, and is inversely related to the level of ironstores.

Non-haem, inorganic iron must first be solu-bilized and hydrolysed before absorption canoccur. Hydrochloric acid in the stomach performsthis function and also converts any ferric (Fe3+)iron in food to its (absorbable) ferrous (Fe2+)state. This reaction is also facilitated by ascorbicacid (vitamin C), which can dramatically improveinorganic iron absorption. Other factors that canenhance the absorption of inorganic iron includecitric acid, lactic acid, fructose and peptidesderived from meat; all of these form ligands with the ferrous iron, maintaining its solubilityand thus facilitating absorption. Alcohol is alsobelieved to enhance iron absorption.

There are, in addition, a number of factorsthat reduce absorption of inorganic iron. Thesegenerally bind with the iron, making it unavail-able for absorption. Most notable are:■ phytate (in whole cereal grains);■ polyphenols (in tea, coffee and nuts);■ oxalic acid (in tea, chocolate, spinach);■ phosphates (in egg yolks);■ calcium and zinc.

These interactions make it extremely difficultto predict how much iron will be absorbed froma particular meal. For example, iron absorptionfrom plant foods can be as little as 2–5 per cent,but can be enhanced tenfold by the presence ofvitamin C. Tea will reduce iron absorption by asmuch as 60 per cent. Overall, iron absorptionfrom the diverse UK diet is estimated to be 15 percent. Under certain circumstances, for example,in pregnancy, absorption may be 90 per cent.However, if the diet contains little or no meat,and substantial amounts of phytate-rich foods,absorption is likely to be less than 10 per cent.Factors influencing iron absorption are summar-ized in Figure 10.5.

Advice to people who have marginal intakesof iron should, therefore, include simple guide-lines about food combinations that may be bene-ficial. However, it is clear that there is often littlerelationship between dietary iron intake andiron status, and mechanisms exist in the bodythat regulate uptake in response to physiological

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circumstances in as yet incompletely under-stood ways.

Control of absorptionOnce iron has been absorbed into the body,there is no means of eliminating a surplus,which can be toxic in excess, other than by lossof blood. In severe iron overload, the patientmay be bled to remove iron, or is prescribed achelating drug, which binds to the iron andallows it to be excreted. It is clearly preferableto have a mechanism that can prevent the entryof iron into the body when it is not needed. In ahealthy individual a ‘mucosal block’ operates,which regulates the amount of iron allowed intothe circulation according to the level of storespresent in the body. Thus, more is absorbedwhen the body stores are low or the needs areincreased, for example, in pregnancy.

As it passes through the mucosal cell, theiron is oxidized back to the ferric state andattached to the transport protein transferrin forcirculation around the body. Iron not requiredby the body is trapped within the mucosal celland is lost in the faeces when the lining cells ofthe gut are shed at the end of their life cycle.

Iron in the bodyThe main endogenous source of iron is thebreakdown of red blood cells by the reticulo-endothelial system. This is added to the iron fromthe diet (exogenous iron) for use and storage.

Iron is carried in the body fluids attached tothe protein transferrin, which takes it from sitesof absorption or release to sites of iron utiliza-tion or storage. A substantial amount of iron istransported around the body each day; normalconcentrations of transferrin are 2.2–3.5 g/L,which at any time are carrying 3 mg of iron.During the course of a day, 25–30 mg of iron aretransported around the body in a very efficient‘recycling’ mechanism.

Red blood cells have an average lifespan of120 days, which means that, each day, 1/120thof the total red cell count is broken down andhas to be replaced. The bone marrow requires24 mg of iron per day to make red blood cells.This daily need for iron demonstrates howimportant it is that recycling of iron occurs inthe body: it would be impossible to take in thesequantities of iron on a daily basis. With anabsorption rate of 10 per cent, the diet wouldhave to contain 240 mg of iron simply to meetthe needs for red cell synthesis.

Iron is used:■ predominantly by the bone marrow, for red

blood cell synthesis (between 70 and 90 percent is used here);

■ by muscle cells for myoglobin synthesis;■ in metabolically active cells for the produc-

tion of cytochromes in mitochondria;■ in synthesis of hormones and neurotrans-

mitters; and■ in immune function.

Figure 10.5 Influences on ironabsorption.


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Losses of ironSmall amounts of iron are lost daily from thedigestive tract lining, skin cells, in bile, urine andany small blood losses. Overall, this ‘obligatory’loss of iron amounts to approximately 0.9mg/day in men. In women, there is a monthly loss of iron in menstrual flow, estimated to be equi-valent to an additional 0.7mg/day on average.However, up to 10 per cent of women may have heavy menstrual losses, which may equateto an additional daily iron loss of up to 1.4 mg.Additional iron loss is generally associated withpathological changes in the digestive tract, such as ulcers or cancer causing bleeding. Somedrugs such as aspirin, taken regularly, may also cause small blood loss into the gut, which,over time, can amount to a significant loss of iron.

Ideally, the obligatory losses are compen-sated by iron absorbed from the diet, whichshould be sufficient to restore iron balance.However, if insufficient iron is ingested therewill be a gradual depletion of iron stores, even-tually resulting in iron deficiency.

Stored ironIron in excess of immediate needs is taken tostorage sites in the liver, bone marrow andspleen, where it is stored in association with aprotein called ferritin. Ferritin can accommo-date over 4000 atoms of iron in its interior andthus prevent any toxic effects. It has been sug-gested that even a moderate level of iron stor-age may be a risk factor for cardiovasculardisease and cancer. Stored iron, acting as a pro-oxidant, has the potential to cause oxidativestress through the production of free radicalsand thus dysregulate antioxidant–oxidant bal-ance. Small amounts of ferritin are present inthe circulation, and this can be measured toreflect the size of the iron stores. Plasma ferritinlevels of 12 mg/L or less are suggestive ofdepleted iron stores. If the iron stores becomevery large, ferritin molecules can clumptogether to form haemosiderin, which allowssafe storage of more iron. However, in excess,this too can be toxic and is associated with aserious condition called siderosis, in which liverfunction deteriorates.

Iron deficiencyWhen iron stores become depleted, the amountof ferritin in the blood will fall. This will be thefirst sign of iron deficiency. The daily physio-logical need for iron will still be met with recyclediron, but as this gradually becomes depleted, and the saturation of transferrin becomes less,the supply of iron for the synthesis of new red blood cells will become inadequate and thecells produced will contain less haemoglobinand be smaller and fewer in number. This is the typical blood picture of iron-deficiencyanaemia. Markers of iron status can, however, bemisleading. For example, both ferritin and trans-ferrin are affected by the acute phase responseassociated with infection, and levels fall. Thus,measurement of these indicators can give mis-leading results during periods of infection andmay lead to inappropriate treatment with iron.

When the number of red cells becomes solow that the oxygen-carrying capacity to thetissues is affected, the individual will suffer thesymptoms of anaemia, including fatigue, apa-thy, loss of appetite and poor temperature regu-lation. There may also be changes to the mouthand digestive tract symptoms, linked to reducedcell replication. The nails may become brittle.

In addition, it is now recognized that low ironstatus also affects other physiological parameters.Capacity for physical work is affected owing toinadequate oxidative mechanisms.

Deficiency of iron that occurs in the first 2 years of life can significantly impair mentaland motor development. This may result in poormemory and learning, and a low attention span.There is still ongoing debate concerning thereversibility of this effect on treatment with iron,with some studies indicating a permanent reduc-tion in mental test scores. Equally, there are con-flicting results in studies of older children, withsome aspects of learning, such as languagescores, affected more than maths scores.

Immune status is also depressed, related to a reduced bactericidal capacity of phagocytesowing to a lack of oxidative enzymes. However,iron is also needed for bacterial growth, and aniron deficiency in malnourished children mayactually protect them from bacterial infection. Astreatment starts, the increased availability of iron


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for the bacteria without an associated improve-ment in immune function can result in rapid andfatal infections. Adequate vitamin A status is alsoneeded for normal recovery to take place.

Iron deficiency is a major health problemworldwide, with anaemia affecting up to 10 percent of the world population. Evidence from sur-veys indicates that in Western countries between20 and 30 per cent of women of child-bearingage have negligible iron stores. Iron-deficiencyanaemia probably only occurs in between 2 and8 per cent of these populations.

There are certain subgroups who are atmuch greater risk of deficiency and anaemia fora number of reasons. These include people with:■ inadequate intake due to low income, poor

food choice or vegetarian diets;■ low absorption rates due to interference

from other dietary components, low stom-ach acidity or parasites;

■ increased needs or losses owing to growth,pregnancy, heavy menstrual losses or bleed-ing from other causes.

These factors tend to occur in infants, children,teenagers and women of child-bearing age, andthese constitute the main vulnerable groups.

Diagnosis of poor iron stores can be made on the basis of low ferritin levels in plasma, anda reduction in the saturation of transferrin. Low levels of haemoglobin signify advancediron deficiency. Anaemia is diagnosed when theblood haemoglobin levels falls below 13 g/L inmen and 12 g/L in women. Patients often fail torecognize the early symptoms of iron deficiency,as these develop over a long period of time.

Prevention of iron deficiency is important. It can be achieved by:■ including more sources of iron in the diet;■ using more bioavailable iron;■ reducing foods that compromise iron

absorption;■ using iron-fortified foods, especially in

infants and young children; and■ taking iron supplements when iron losses

are high (e.g. in menstruation).

Dietary reference valuesReport 41 (DoH, 1991) takes into account theobligatory losses of iron and estimates of the

average absorption rates for iron. Assuming thisto be 15 per cent from mixed diets, the RNI foradult men is 8.7 mg and for women is 14.8 mg.However, it is accepted that there will be some10 per cent of the female population whoseneeds will be greater than this, and who mayneed supplements. After the menopause, the RNIfor women falls to the same level as that of men.

No additional increment is proposed forpregnancy, although it is recognized that thereare increased iron requirements amounting to680 mg over the whole pregnancy. It is assumedthat women will have adequate stores of iron onwhich to draw and there is also a saving on dailyiron balance from the cessation of the menses.Some women with inadequate stores may, how-ever, require additional iron. Levels of haemo-globin that fall below 10 g/L in pregnancy havebeen shown to be associated with progressivelyincreasing risk to the baby, pre-term deliveryand associated complications. Iron absorptionmay increase between five- and nine-fold dur-ing pregnancy as needs increase. It is, therefore,difficult to make predictions of the exact dietaryneeds at this time, and serum ferritin or haemo-globin levels should be monitored.

Zinc

Human zinc deficiency was first reported in the1960s in the Middle East in teenage boys foundto have poor growth and delayed sexual matur-ation (hypogonadal dwarfism). It was subse-quently reported among children and amonghospitalized patients on intravenous nutritionin the USA. It is now recognized that zinc isessential for the activities of many enzymes andregulatory proteins, and plays a part in numer-ous, diverse functions of the body.

Sources of zincDietary intake of zinc is correlated with the protein content of the diet because zinc occurscomplexed with proteins and their derivatives.Particularly good sources are lean meat (espe-cially offal), seafoods and dairy products. Pulsesand whole grains are a moderate source, but areof importance in vegetarian diets. Low levels ofzinc occur in leafy vegetables, fruit, fats, alcohol


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and refined cereals. As with other divalent min-erals, bioavailability is a determinant of the use-fulness of particular dietary sources. Animalsources of zinc are generally more readily avail-able than plant sources.

The average daily intake in the UK is 8.0 mg(DEFRA, 2001). Main contributors of zinc in theBritish diet are meat and meat products (30 percent), cereal products (27 per cent) and dairyproducts (23 per cent). In many groups, espe-cially in households with three or more chil-dren, the average intake fell below 100 per centof the RNI, indicating some groups at risk of lowintakes.

Absorption of zincBoth ingested zinc as well as that secreted invarious digestive juices, such as bile and pan-creatic juice, are available for absorption. Zincis released from bound sources and attaches toamino acids, which facilitate its absorption. Theamount absorbed is regulated to match theneeds of the body, although the mechanisms areunclear. There is competition for the absorptionmechanism from other divalent ions, such ascalcium and iron, which may reduce zincuptake. Stress has been shown to increase zincuptake.

Inhibitors of zinc uptake include phytate(especially in the presence of calcium), oxalicacid, polyphenols and folic acid. Zinc taken intothe mucosal cells may be bound to metalloth-ionein and then lost from the body when thecells are shed. This is thought to provide animportant mechanism for regulating body levelsof zinc. Overall, rates of zinc absorption average30 per cent, although considerable variationmay occur with different dietary combinations.

Zinc in the bodyZinc is involved in:■ the metabolism of all the macronutrients;■ the production of energy;■ nucleic acid synthesis (and therefore cell

division);■ oxygen and carbon dioxide transport (in car-

bonic anhydrase) antioxidant mechanisms(through superoxide dismutase);

■ the immune system;

■ protein synthesis, and is especially import-ant in wound healing and growth:

■ the storage and release of insulin;■ nuclear transcription and activation of pro-

teins that regulate gene expression.With so many roles, it is not surprising that

zinc is widely distributed throughout the body.Major sites are the muscle (60 per cent), bone(30 per cent), skin (4–6 per cent), with theremainder found in liver, kidney and plasma.There is no readily identified store of zinc,although in catabolic states, zinc is releasedfrom muscle and made available to the plasma.The liver provides ‘fine tuning’ of plasma zinclevels, which are tightly controlled, by releasingzinc from metallothionein–zinc complexes in itscells. In infection, zinc is taken up by the livermetallothionein and plasma levels fall. Levels ofzinc in other tissues, such as bone, brain, lungand heart, remain relatively stable in the eventof low zinc intakes.

Excretion of zinc occurs mostly via the fae-ces through secretion into the digestive tract.Small amounts are lost in the urine and in skin cells.

Zinc deficiencyZinc status is difficult to measure becauseplasma zinc levels can be affected by a numberof situations unrelated to status. Measures thathave been used but are believed to be insuffi-ciently reliable include white blood cell zinclevels, urinary excretion and hair zinc.

Signs of mild deficiency may includedepressed appetite, poor taste acuity, delayedwound healing, immunosuppression, poor growth,skeletal abnormalities and delayed sexual mat-uration in children (see Figure 10.6). People inWestern societies are increasingly eating foodsin which the zinc content has been reduced byprocessing. It is likely that poor zinc status maybe an increasing problem. Reports from both theUSA and Europe have found that the amountsof zinc provided by typical diets are below therecommended allowances for children, adoles-cent girls, women of reproductive age and elderly men and women. There is concern thatindividuals have insufficient zinc reserve tocope with increased demand, e.g. growth and


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tissue repair. In developing countries, the oppos-ite problem exists: there may be sufficient zincin the diet, but the absorption is inhibited byother factors.

Marginal zinc deficiency may be a problem inchildren and in elderly subjects who have poorappetite and who consume little meat. It has beensuggested that poor zinc status in pregnancy,especially in the first trimester, may be linked to intrauterine growth retardation, although theevidence is conflicting. Other situations in whichzinc deficiency may occur include protein–energy malnutrition and prolonged intravenousnutrition. Alcoholics, patients with malabsorp-tion and diabetics may also exhibit abnormalzinc status.

Severe zinc deficiency is associated with an inborn error of zinc metabolism, known asacrodermatitis enteropathica, which affects theintestinal uptake of zinc. This produces a severerash, which is prone to secondary infections,growth failure and behavioural abnormalities.Maintenance on large doses of supplementalzinc is necessary.

It has been suggested that zinc deficiency maybe a component in anorexia nervosa and treat-ment with zinc sulphate has been reported to helpin restoring normal eating patterns. However,although zinc status may be poor in sufferers, it isunlikely to explain the whole syndrome.

Dietary reference valueFigures for the daily turnover of zinc are used asthe basis for setting dietary reference values. Inadults, systemic needs appear to be 2–3 mg/day,and these can be converted into RNI, using anestimate of 30 per cent for absorption of dietaryzinc. Thus, RNIs for adult men and women are9.5mg/day and 7.0mg/day, respectively. No addi-tional increment is recommended in pregnancy,since it is assumed that metabolic adjustmenttakes place to provide the extra zinc.

Excessive intakes of zinc may cause nauseaand vomiting, and at 50 mg/day may interferewith immune responses, and the metabol-ism of iron and copper. Caution should, there-fore, be exercised in taking zinc-containingsupplements.

Figure 10.6 Signs of zincdeficiency.


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Copper

There are approximately 100mg of copper in theadult human body and the amount decreaseswith age. Deficiency of copper is well known inanimals, and results in anaemia and failure tomature. In humans, deficiency has been recog-nized for many years, but the diagnosis and sig-nificance of any suboptimal status in populationsis still uncertain.

Sources of copperThe content of copper in plant foods varies withsoil conditions and food processing techniques.However liver, shellfish, nuts, seeds (includingcocoa) and legumes together with the outer parts of cereals are reported to be the richestsources (0.3–2.0 mg/100 g). Bananas, potatoes,tomatoes and mushrooms have intermediate levels (0.05–0.3 mg/100 g). Low levels are foundin milk, bread and breakfast cereals. Drinkingwater can be an important source, where copperpiping is used, and can provide up to 6 mg/day.

Estimated daily intakes of copper in the UKwere 1.8 mg/day, the range for developed coun-tries being 0.6–1.6 mg/day. Intakes among vege-tarian populations have been reported to rangefrom 2.1 to 3.9 mg/day. Analysed values arereported to be higher than those calculated fromfood composition tables, reflecting the variabil-ity in foods. Meat and meat products (27 percent), together with cereal products (27 per cent)are the main contributors of copper in the UK diet.

Absorption of copperCopper is absorbed mainly in the duodenum and jejunum, at rates of 35–70 per cent. The effi-ciency of absorption appears to vary inverselywith intake. The transfer of copper across thebaso-lateral membrane of the enterocyte isenergy dependent and carrier mediated, andthere is competition for the pathway from otherminerals, most notably zinc and iron. Otherinhibitors include an alkaline pH, molybdenum,calcium and phosphorus, and possibly the pres-ence of phytates and sulphides. Absorption isenhanced by the presence of animal protein,human milk and fructose. On absorption, copper

is bound to plasma albumin, but becomes rapidly bound to caeruloplasmin in the liver,which then forms the major circulating source ofcopper. Copper is also secreted into the digestivetract, especially in bile, and this forms the mainexcretory route and is believed to be an import-ant mechanism for maintaining a constant bodypool of copper.

Copper in the bodyCopper is found tightly bound to proteins, termedmetalloproteins, some of which are cuproen-zymes and take part in a variety of intracellularand extracellular reactions.

Of the total amount of copper in the body, 40 per cent is found in muscle; the remainder is in the liver, brain and blood (in red cells and ascaeruloplasmin in plasma). Essential for ironmetabolism, caeruloplasmin converts ferrous ironinto its ferric state. The ferric iron then binds totransferrin and enters cells. An absence of caeru-loplasmin, therefore, results in accumulation of iron in liver and brain. Caeruloplasmin is also involved in the response to infection as oneof the acute-phase proteins. Copper occurs as acomponent of several enzyme systems, includingcytochrome oxidase, superoxide dismutase andvarious amine oxidases. Cytochrome oxidase isthe essential final link of the electron transportchain for the production of energy as ATP. Copperis a component of the free-radical-quenchingenzyme superoxide dismutase, which also has animportant role in protecting the body from dam-age by products of the response to infection.Amine oxidase is used in cross-linkage formationin the connective tissue proteins collagen andelastin. Copper-containing enzymes are alsoinvolved in melanin production, formation ofmyelin, and for neurotransmitter synthesis (suchas catecholamines, dopamine and encephalins). A summary of the roles of copper in the body is in Figure 10.7.

Deficiency of copperCopper deficiency has been reported in smallpremature infants, malnourished infants and inadults fed intravenously for long periods.

Premature infants lack the copper normallytransferred from the mother in the later stages


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of pregnancy. As milk is also low in copper,these infants are particularly vulnerable toinadequate copper status. They may sufferanaemia, neutropenia, skeletal fragility and asusceptibility to infections. Similar signs maybe seen in infants being rehabilitated from mal-nutrition.

In animals, studies have shown increasedcholesterol levels and vascular weakness incopper deficiency, which may lead to cardiovas-cular disease. In vitro, copper has been shown tobe a pro-oxidant, causing oxidative damage tolipoproteins, thus implying a possible contribu-tory role in atherosclerosis. However, in thebody, it is mainly bound to caeruloplasmin,which prevents this damage occurring, andmay, therefore, act as an antioxidant. Studies in which subjects were supplemented with add-itional copper, at 6 mg/day, found no increase in susceptibility of lipoproteins to oxidation.

A rare genetic defect, Menkes’ disease hasnow been shown to be caused by a defect in acopper-transporting ATPase. In this disease, thetransport of copper across the placenta, the gas-trointestinal tract and the blood–brain barrier isdefective, and the individual suffers from acute

copper deficiency, with growth failure, mentalretardation, bone lesions and anaemia.

Copper toxicityCopper accumulates in the body in Wilson’s disease, a rare genetic disorder, now also found tobe due to a defective copper-transporting ATPase.In this case, transport into bile for excretion is affected, so that copper accumulates in thebody, and becomes deposited in soft tissues; thecondition used to be fatal. Treatment involveschelating agents, which allow the excess copperto be excreted.

Accidental ingestion of excess copper causesvomiting and diarrhoea, which may eliminatethe mineral from the body. Chronic poisoninghas been reported in patients on haemodialysis,where copper pipes were used, and in vineyardworkers using copper fungicide sprays. A max-imum safe range for adults has been set at 12 mgcopper/day by the World Health Organisation(WHO).

Copper balance is reported to be achievedwith intakes of 1.62 mg/day, and a minimumdaily requirement has been given as 0.4–0.8 mg/day, by trials on healthy young men. Report 41

Figure 10.7 The role of copper inthe body.


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(DoH, 1991) proposes an RNI of 1.2 mg/day foradults.

Selenium

The amount of selenium present in the bodyvaries with the local environment, as its contentin soil is variable. Levels are low where soils are acid, and rainfall heavy. In some countries,for example, Finland, fertilizers contain added selenium to enhance the content in the soil. Inrecent years, there has been a reduction in thedietary intake of selenium in some parts of theworld, including Britain, and epidemiologicalevidence suggests a possible link between selenium and certain diseases. As a result, moreattention has been paid to this trace element.

The selenium content of foods is related tothe protein level, since it is found as selenocys-teine (in animal products) or selenomethionine(in cereals). However, it should be rememberedthat the actual content within a particular sam-ple of food will depend on the level in the soil or in the diet of the animal, and variation maybe up to 100-fold. In addition, many Westerndiets contain foods from different parts of theworld. This makes it very difficult to calculateselenium intakes accurately using food tables.Only where there is dependence on local pro-duce can a more accurate prediction of seleniumintake be made.

In the UK, brazil nuts are the richest dietarysource, with fish (especially shellfish), and offal(kidney and liver) providing a moderate source.Meat and eggs also provide moderate amountsof the element. Cereals and cereal products canprovide a useful source, depending on their ori-gin. In the UK, bread was an important source inthe past, when flour was imported from NorthAmerica. Presently, European flour is used, andthe selenium levels in bread have fallen consid-erably. It is believed that this has had a majoreffect on average selenium intakes in the Britishdiet, which have fallen from an average of62 �g/day in the late 1980s to 39 �g/day. Fruitand vegetables are generally low in selenium. In the UK, selenium intakes derive mostly from meat and eggs (39 per cent), cereals (22 per cent), dairy products (15 per cent) and fish

(13 per cent). Intakes in vegetarians have beenfound to be lower than the average in the UK.Selenium is also consumed in the form of sup-plements (see Figure 10.8 for some sources ofselenium).

Absorption and metabolismAbsorption of selenium, especially as selenome-thionine, appears to be efficient and may be ashigh as 80 per cent. Inorganic forms are less wellabsorbed. In the body, selenium is incorporatedinto proteins (known as selenoproteins) andfound particularly in the liver, kidneys, muscle,red blood cells and plasma. The red blood celllevels remain fairly constant and can be used toassess long-term intake, whereas the plasmalevel tends to reflect recent intake. Selenium levels in toenail clippings are also used as anindicator of long-term intake. Activity of glu-tathione peroxidase in red cells is a useful indi-cator of selenium status; however, it reaches aplateau with high exposure levels.

Urinary excretion is the main means of regulating selenium levels in the body; after highintakes, some selenium may be lost in the breath.

Glutathione peroxidases are the major selenium-containing enzymes in the body. Theenzymes occur in several variants, in differentlocations to provide protection against damageby reactive oxygen species. They occur bothintracellularly and in plasma, within cell mem-branes, and have recently been found in spermand in the gastrointestinal tract. Their role is toact as a catalyst for the reactions that removehydrogen peroxide and other hydroperoxides to produce water or other harmless products.Glutathione peroxidase works in conjunctionwith other cellular enzymes, such as catalase andsuperoxide dismutase, as well as other dietary

Figure 10.8 Sources of selenium in the diet.


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antioxidants such as vitamin E and C (seeChapter 14 for more information on antioxi-dants). Selenium is also involved with iodinemetabolism in the conversion of thyroxine (T4)to its active form triiodothyronine (T3), in thethyroid gland.

Selenium has recently been shown to play arole in the normal functioning of the immunesystem. Defence against infection involves theproduction of reactive oxygen species, whichmust be removed by antioxidants to protectimmune system cells from damage. It is sug-gested that selenium plays a key part in this, byprotecting cells of the immune system in thelymph nodes, spleen and liver from damage.

The presence of a glutathione peroxidase insperm has led to research on links between malesubfertility and selenium status, with some posi-tive results indicating improvements in spermmotility following supplementation with selen-ium in men with low status of this mineral.

Deficiency of seleniumSelenium deficiency is closely related to that ofvitamin E and adequate amounts of one of thenutrients can in part compensate for a lack ofthe other. Two conditions found in China –Keshan disease and Kashin–Beck disease – havebeen linked to low selenium status.

Keshan disease, named after the regionwhere it was originally found, is an endemic car-diomyopathy, characterized by multiple necrosisthroughout the heart muscle, which becomesreplaced with fibrous tissue. It affects mainlychildren under 15 years and women of child-bearing age living in rural areas, where seleniumcontent of the soil is low. It has a seasonal pre-sentation, and other factors apart from selenium,such as a viral infection, may also be involved.Since the recognition of the involvement of sel-enium, public health measures, including a morevaried diet, have largely eliminated this disease.

Kashin–Beck disease involves degenerationof the joints and cartilage in young people upto the age of 20, leading to painful swelling of joints. Selenium deficiency appears to be acausative factor, but low iodine intake and toxinsor contaminants in food, coupled with a poorand unvaried diet probably contribute to this

disease. Neither disease is seen in other parts ofthe world, although selenium intakes may beequally low.

Patients fed intravenously are at risk of deficiency, if attention is not paid to selenium levels. Semi-purified synthetic diets may also bedevoid of selenium.

Public health roles of selenium have beenstudied particularly in relation to cancer andcoronary heart disease. Epidemiological evi-dence points to a possible inverse relationshipbetween selenium status and cancer mortality,especially for prostate, colon and rectal cancers.Prospective studies and supplementation trialsprovide further evidence that, in populationswith low selenium status, there is a possibleincreased risk of cancer and that supplementa-tion may reduce this risk. However, other evi-dence suggests that high levels of selenium maystimulate tumour development, so at present acautious approach is needed. Damage by oxygenreactive species is believed to contribute to thedevelopment of atherosclerosis, so the role ofselenium within the antioxidant defences is animportant aspect of coronary heart disease pre-vention. At present, data on the specific role ofselenium in cardiovascular disease is equivocal.

The effect of supplementation with seleniumhas also been studied in the context of immunefunction, which is shown to be impaired in selenium deficiency. Although some benefitshave been noted following supplementation withselenium, for example, in infectious disease inthe elderly and respiratory tract infection inchildren, it is too early to assume that this effectwould be replicated in everyone, regardless ofprior nutritional status. Selenium status declinesearly in HIV infection, and administration ofselenium at this time may slow replication of thevirus and progression of the disease.

On the basis of the evidence from China,Report 41 (DoH, 1991) gives the lower referencenutrient intake (LRNI) for selenium as 40 �g/day.The basis of the RNI is the level of intake thatwill sustain a blood selenium level at which glutathione peroxidase levels reach a plateau inthe red blood cell. The values are 75 �g/day formen and 60 �g/day for women. These values arehigher than current (2000) recommendations in


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the USA (55 �g/day for men and women) andfigures provided by WHO (1996) of 40 and30 �g/day for men and women, respectively.Concern has been expressed that the use of sel-enium supplements may pose a health risk fromtoxic levels. Maximum upper safe levels havebeen proposed in a number of countries, rangingfrom 200 to 450 �g/day.

Iodine

Iodine exists in the body as iodide, which is farless toxic than the iodine from which it derives.Any iodine ingested in food is rapidly convertedto iodide in the gut. Iodide is necessary for theproduction of the thyroid hormones, whichmaintain the metabolic pattern of most cells inthe living organism. In addition, the hormonesplay a key role in early growth and developmentof organs, especially that of the brain. In humans,this occurs in fetal and early post-natal life.Therefore, iodine deficiency at this time of life, ifit is severe enough to affect thyroid function, willcause hypothyroidism and brain damage, andmental retardation. In the adult, an absence ofiodide results in an enlargement of the thyroidgland, but has major consequences when itoccurs in pregnant women.

Sources of iodideMost of the iodine in the world is in the oceans,since the land masses have had the iodineleached from them by glaciation, rain andfloods. Thus, soils that are mountainous, land-locked or subject to frequent flooding, togetherwith the crops grown on them are most likely tobe devoid of iodine. This is true of many of thecentral regions of large continental landmasses.In Europe, most countries are still characterizedby mild to moderate iodine deficiency, althoughiodine is added to salt in many of these.However, low urinary excretion of iodine is stillfound in Belgium, Italy, Czech Republic,Hungary and Romania.

In the UK, iodine status is considered ade-quate. Milk is the major source of iodide, as aresult of increased use of cattle-feed supple-ments containing iodine as well as iodine inmedications and disinfectants used in animal

husbandry. In addition, seafoods are a richsource, particularly haddock, whiting and her-ring. Plaice and tuna have a lower iodine con-tent. Seaweed and products made from it may berich in iodine, although not all have a high con-tent. Vegans who rely on these sources shouldensure that the intake is adequate. In the USA,bread contains iodine from improvers used inthe baking industry. Iodized salt is an importantsource of iodine in areas where food sources arelow in the mineral.

Mean intakes of iodine in adults in the UKare 180–250 �g/day.

Absorption and metabolismIodide absorption is efficient and the free iodideis concentrated by the thyroid gland, whichtakes it up actively against a concentration gradient. The gland contains 70–80 per cent ofthe body’s iodide and uses it in the synthesis ofthyroid hormones, combining it with the aminoacid tyrosine in a stepwise process. The com-pleted hormones contain three or four atoms ofiodine. These are stored attached to a proteincolloid until required. Release is regulated bythe thyroid-stimulating hormone (TSH) producedby the anterior pituitary gland. Any iodine thatis not used in the final hormones is recycled.Most organ systems in the body are under theinfluence of thyroid hormones, which controlmetabolism.

If the intake of iodine is insufficient, thyroidhormone levels fall and the pituitary respondsby increasing secretion of TSH to accelerateuptake of iodine by the gland. Normally, theresulting hormone shuts off the release of TSH.However, in the absence of iodine, insufficienthormone is produced to cause this and TSHsecretion continues. This results in enlargementof the cells of the gland as they attempt to trapiodide from the circulation. In addition, unfin-ished thyroid hormones may accumulate in thegland, contributing to the swelling. The overallsize of the gland increases and it may becomeprominent as a swelling in the neck. This isknown as a goitre. Gross enlargement of thethyroid may compress other structures in theneck, leading to difficulties in breathing andswallowing.


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Goitres most commonly become apparent inpuberty and during pregnancy, as the needs foriodine increase. The extent of damage to theinfant depends on the severity of iodine defi-ciency but is associated with the failure of hor-mone transfer across the placenta to function infetal brain development. Figure 10.9 shows someof the causes and effects of iodine deficiency.

In mild iodine deficiency (intakes of50–99 �g/day), there is likely to be thyroidenlargement in pregnancy, but no measurableeffect on development of the neonate or child.With moderate iodine deficiency (intakes of20–49 �g/day), there is likely to be congenitalhypothyroidism in the infant, and abnormalitiesof psychoneuromotor and intellectual develop-ment in children and adults. In populations withsevere iodine deficiency (intakes below 20 �g/day), goitre occurs in 90 per cent of females ofchild-bearing age. Infants born to these mothersare likely to suffer endemic cretinism, a syn-drome of mental retardation, several neurologicalsigns including deaf mutism, spasticity andmotor rigidity as well as dwarfism. Up to 15 percent of children in these areas may be affected.

It has been estimated that this intellectualimpairment results in the loss of 10–15 IQ pointsat a population level, and can severely limitnational development.

This is a preventable disorder, since iodidesupplements can be given to women in vul-nerable areas, either in the form of salt, iodizedoil or by injection. Up to 1 billion people live in areas of the world where iodine levels areinadequate, and the use of supplements is amajor public health priority to prevent such disability.

There are some interactions between selen-ium and iodine, whereby selenium deficiencytogether with iodine deficiency may reduceneurological damage.

Goitre may also arise because of inhibitionof iodide uptake by the gland by substancesknown as goitrogens. These include goitrins,which originate in the cabbage family, and thio-glycosides, which are found in cassava, maize,bamboo shoots, sweet potato and lima beans.They are largely destroyed by cooking, but maycontribute to 4 per cent of cases of goitre in the world.

Figure 10.9 Causes and effects ofiodine deficiency.


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Excessive intakes of iodine can also causethyroid enlargement; this may occur when people consume large amounts of seaweed.

Report 41 (DoH, 1991) states that an intakeof 70 �g/day appears to protect populationsagainst the occurrence of goitre; with a marginfor safety, the RNI is stated to be 140 �g/dayfor adults. A European figure for recommendedintake is 150 �g/day for adults, with an increaseto 200 �g/day in pregnancy.

Chromium

Chromium can exist in either trivalent or hexa-valent form, with the former being more bio-logically active. Both forms appear to exist intissues and may interconvert.

The richest sources of chromium are spices,brewer’s yeast, meats (especially beef), wholegrains, legumes and nuts. However, doubts havebeen expressed about the accuracy of some of theanalytical methods used to assay chromium infoods, and values may need to be revised whenbetter techniques are developed. Refining offoods causes a significant reduction in levels ofchromium, and consuming a refined diet resultsin a very low intake of chromium. It has alsobeen suggested that sugars may stimulate loss ofchromium in the urine.

Absorption of chromium may be very poor,with less than 2 per cent of inorganic chromiumand 10–25 per cent of organic chromium beingabsorbed in animal studies.

It is postulated that chromium potentiatesthe action of insulin by combining with nico-tinic acid and amino acids to form glucose toler-ance factor (GTF). The effectiveness of insulin is, therefore, greater with chromium than in itsabsence. In addition, chromium may have rolesin lipid metabolism, specifically by affectinglipoprotein lipase activity, and in nucleic acidmetabolism, by affecting the integrity of nuclearstrands.

Chromium is excreted mainly in the urine, at levels of 1 �g/day. Chromium deficiency is not clearly defined, with many people appar-ently consuming less than the requirement for chromium. Glucose tolerance is improved by chromium supplementation at levels of

150 �g/day of chromium. In general, levels ofchromium in Western populations decline withage. There are a very small number of reportedcases of chromium deficiency in patients main-tained on intravenous nutrition for long periods.Symptoms included impaired glucose toleranceor hyperglycaemia. Chromium is available as asupplement, and suggested roles include ameli-oration of diabetes and gestational diabetes,lipid abnormalities and insulin resistance. Dosesof trivalent chromium up to 1000 �g/day appearto be safe.

Report 41 (DoH, 1991) suggests a ‘safe intake’for chromium of more than 25 �g/day, for adults.

Fluoride

Fluoride is essential for the production of hard,caries-resistant enamel in the teeth but, whenpresent in water supplies in amounts greaterthan 2–3 mg/L, it causes mottling of the dentalenamel. Even though these teeth are discoloured,they are still resistant to caries.

Fluoride intake is largely determined by thelevel in the water supply, as few foods containsignificant amounts. Tea and seafoods are themajor dietary sources. Where naturally occur-ring levels are low, fluoride has been added to the water supply of parts of the world forover 50 years as part of the effort to reduce theincidence of dental caries. In addition, fluoridetoothpastes are widely available in many coun-tries. These can provide an additional source offluoride, especially for children, who may swal-low significant amounts from the toothpaste.

Fluoride in solution is very readily absorbedfrom the digestive tract; absorption of foodsources ranges from 50 to 80 per cent. Afterabsorption, fluoride is taken up, particularly bythe bones and teeth, where it becomes incorp-orated into the calcium phosphate crystal struc-ture apatite, replacing the (–OH) group, andforming fluoroapatite. This is a harder material,and more resistant to decay than apatite. Thepresence of fluoride also accelerates the rem-ineralization process when teeth have started todemineralize in the presence of low oral pH.Finally, the presence of fluoride in saliva altersthe bacterial flora in the mouth and reduces


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acid production. Thus, the pH fall after sugarconsumption is less in the presence of fluoride.All of these mechanisms help to protect teeth.

In communities where fluoride is present inthe water supply at recommended levels of1 mg/L, there is at least a 50 per cent reductionin tooth decay when compared with areas thathave no fluoride. There has been considerablecontroversy about the desirability of addingfluoride to water supplies, and human rightscases have been heard by the courts. The safetyof the procedure has been thoroughly investi-gated and, at present, there are no scientific datato support the claim that fluoridation is harmfulto health. The widespread availability and use offluoride toothpaste has made a significant dif-ference to caries incidence in most Europeancountries. For individuals who regularly use this,there are few additional advantages from fluori-dated water. However, in every society, there aresectors for whom tooth cleaning and the use oftoothpaste is not a habit; in these cases, fluori-dated water can make an important contributionto dental health. Dental health is discussed fur-ther in Chapter 6.

There appear to be no other requirements forfluoride apart from this role in dental healthpromotion.

Sodium and chloride

These two minerals are considered together,because they occur together in foods and in thebody, as well as in seawater and the earth’s crust.Salt has been held in very high regard by peoplethroughout history, and there are many expres-sions in common speech that use the word saltto indicate worth or value. The word ‘salary’ isderived from salt, indicating the use of salt as ameans of payment, or payment as a means ofgetting salt!

Together with potassium, sodium and chlor-ide contribute in large measure to the osmolalityof the body fluids, which, in turn, determinestheir distribution and balance. Changes in osmolality may involve changes in the contentof minerals or of water. Restoration of a normalbalance activates mechanisms that regulatemineral excretion or water loss via the kidney,

by means of hormonal control, through aldos-terone, rennin–angiotensin or antidiuretic hor-mone, as appropriate.

Sodium is the major cation of extracellularfluid, comprising over 90 per cent of the cationsin the blood. Some 40 per cent of the body’ssodium is present in bone as an integral part ofthe mineral lattice, but it is not clear how read-ily this can be mobilized to maintain sodiumlevels in extracellular fluids.

Sodium plays a crucial role in:■ maintaining osmolality of body fluids;■ maintaining the extracellular fluid, and hence

the blood volume;■ acid–base balance;■ maintaining the electrochemical gradients

across cell membranes.The electrochemical gradients are especiallyimportant in nerve and muscle cells, where theyare vital for the propagation of nerve impulsesand for muscle contraction. They are also import-ant in the absorption of substances across cellmembranes against concentration gradients, for example, in the digestive tract and kidneys.The maintenance of electrochemical gradients at all times in the body consumes the greatestpart of the daily energy requirement for life, as the ATP pumps move the ions across cellularmembranes.

Since sodium is essential to homeostasis, itis clear that the levels of sodium in the bodymust be carefully regulated, regardless of levelsof intake. Further, there is no functional store ofsodium, so the daily needs must be met by con-trol of excretion when intake is variable.

Chloride occurs generally in associationwith sodium as the major anion in extracellularfluid, but it is not found in bone. It can alsoassociate with potassium in intracellular fluids,and can readily cross the cell membrane. Inaddition to its role in electrolyte balance associ-ated with sodium, it is also essential for thetransport of carbon dioxide in red blood cells,and in the formation of hydrochloric acidsecreted by the stomach. Chloride is the majorsecretory electrolyte of the whole digestivetract. Losses of digestive juices, especially invomiting, can deplete the levels of chloride inthe body.


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Sodium and chloride in foodsMost foods naturally contain a low level ofsodium: plant foods contain very little sodium,while animal foods contain low to moderate levels. The majority of sodium in the diet comesfrom foods that have undergone some processingor manufacture and to which salt has been added.In addition, salt may be added during home cooking or at the table. In general, the greater theconsumption of processed foods, the higher willbe the sodium intake. Not surprisingly, sodiumintakes are very variable, both within a popula-tion, and between people in different countries.

In the UK, average daily sodium intakes are2.6 g, although the range usually quoted is from2 to 10 g. Main food sources quoted by DEFRA(2001) contributing to the total intake in the UKare meat products (21 per cent), bread (13 percent) and other cereal products (24 per cent). If no salt is added to foods, the sodium intakefrom natural sources would be between 0.5 and1 g/day. Thus, it is evident that the greater partof our intake originates from added salt.

Sodium comprises 39 per cent by weight ofsodium chloride, which represents the majorsource of sodium in the diet. Total daily intakesof sodium chloride (salt) in the UK average 7.7 gin women and 10.1 g in men, with a range of3–14 g and 4–18 g, respectively.

Sodium (usually as chloride) is used in foodprocessing and manufacture because of itsproperties as a:■ preservative (e.g. in meats, dairy products,

preserved vegetables);■ flavouring agent (e.g. in breakfast cereals,

crisps, packet soups, bread); and■ texture enhancer (e.g. in cheese, preserved

meats).Other sodium salts are used as raising agents(see Figure 10.10).

It is not easy to measure sodium intakes, asthere is so much variability between individualsand a proportion of that used in cooking may bediscarded before consumption, e.g. in cookingwater. A more reliable approach is to measure24-hour urinary sodium excretion, which closelymirrors the intake. Lithium can be used as amarker of cooking or table salt and measured inthe urine.

Absorption of sodium and chlorideBoth sodium and chloride are readily absorbed.Sodium has been shown to be absorbed by aseries of pathways that can function in both thesmall intestine and the colon.

In the West, intakes of sodium are generallymuch greater than the requirements and, thus,the sodium taken into the body must be regu-lated by excretion.

Chloride is absorbed passively, generallyfollowing electrochemical gradients establishedby the absorption of cations. It is also exten-sively secreted into the digestive tract, althoughmost of this is subsequently reabsorbed.

The concentration of sodium in extra-cellular fluids is maintained at 3.1–3.3g/L (135–145mmol/L). If levels increase above this, water isretained to maintain osmolality and the extracel-lular fluid volume increases. This is subsequentlylost by increased sodium and water excretionover 1–2 days. Conversely, a fall in sodium levelswill result in conservation by the kidneys of bothelectrolytes and water. These mechanisms resultfrom the interplay of a number of hormonal andnervous system factors; a full explanation will befound in physiology textbooks.

Sodium excretion occurs principally via thekidneys, which filter and then reabsorb largeamounts of sodium in the course of a day. Thisprovides a great deal of flexibility to adjust theplasma levels precisely. Significant losses mayalso occur in sweat, when physical work is per-formed in hot conditions. Acclimatization resultsin a lowering of the sodium losses in sweat; inthe short term, exposure to conditions causing

Figure 10.10 Sources of sodium.


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excessive sweating may necessitate an increasedsalt intake.

Excretion of chloride is primarily throughthe kidneys, where it accompanies sodium loss.

Sodium and healthIt is estimated that approximately 30 per cent of the variance in blood pressure is attributable togenetic predisposition and 50 per cent to environ-mental influences. Genetic variants may affectthe functions of the kidney, but also interact withhormonal and metabolic alterations. Salt is one of the environmental influences, and intakes ofsodium have been shown to correlate positivelywith blood pressure, with high intakes consideredto be risk factors for stroke and cardiovasculardisease. The relationship with blood pressure hasbeen shown in cross-cultural studies and in ameta-analysis of data from a large number ofseparate studies. The relationship is, however,complicated by the influence of alcohol and BMI,which also influence blood pressure. Nevertheless,when these are taken into consideration, there is apredictable increment of blood pressure withincreasing sodium intakes. This increment alsoincreases with age, so that a small increase in saltintake has a greater impact on blood pressure atage 65 than at age 25. Conversely, reducing saltintake can lower the blood pressure, although thiseffect may take up to 5 weeks to become appar-ent. Reductions in salt intake have also beenshown to potentiate the effects of blood pressurelowering medication. The effects of salt reductionare greater in those individuals with a higherblood pressure and there is still debate as to theeffectiveness of salt reduction in normotensiveindividuals. The amount of potassium in the dietwill also modify the response.

In terms of public health measures, theINTERSALT study showed that deaths fromstroke were highly correlated with urinarysodium excretion levels in various communities.Community intervention studies, such as inPortugal and North Karelia (Finland), havedemonstrated that reducing salt intakes can havesubstantial effects on the average blood pressurein the community. In North Karelia, the meanreduction in blood pressure was 10mmHg in adults. In the Netherlands, reducing the salt

content of infant formulae resulted in lowerblood pressures in the children at follow up,aged 15 years, with no further measures in theintervening period. Results from the DASH-Sodium trial (Sacks et al., 2001) in the USA haveindicated that a highly significant reduction ofblood pressure can be achieved in normotensivesubjects with salt intakes of 3.8 g/day. Modestreductions were obtained at levels of 6.5 g/day.This confirms earlier results found in the ori-ginal DASH trial in hypertensive subjects. It isimportant to note that the DASH diet includes a combination of interventions, i.e. the diet isrich in low-fat dairy products, wholegrain cereal,vegetables and fruit as well as low salt intake.

The UK Department of Health (DoH, 1992) in its report on the nutrition of elderly peoplehas recommended that intakes of salt should not exceed 6 g/day; this implies a reduction in average salt intakes in the UK by 3 g/day.

Many people find it difficult to reduce saltintake as they have become accustomed to thetaste of their food at a particular level of saltaddition. Practical advice needs to be given tohelp people achieve a reduction; most import-antly, this should be attempted over a period oftime to allow the taste buds to adapt to lowerlevels. Depending on the original level of intake,reduction can be achieved by:■ using less or no salt at table;■ reducing amounts of salt used in cooking;■ using alternative flavouring agents, such as

herbs and spices; and■ reducing the amounts of processed and

manufactured foods in the diet, perhaps byselecting ‘lower salt’ varieties.

Dietary reference valueThe RNI for sodium is 1.6 g/day for adults, withan LRNI of 575 mg/day. The majority of peoplein the UK consume levels in excess of the RNI.There appears to be no physiological advantageto this, and in the light of evidence of the rela-tionship with blood pressure, it is suggested thatcurrent intakes are needlessly high and shouldnot rise further. A reduction in the salt contentof manufactured foods would make a signifi-cant contribution to reducing salt intakes in thepopulation.


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Special care should be taken with sodiumintakes in young infants, as their ability to regulate sodium levels in the body is not well-developed in the first weeks of life. In addition, if there is vomiting and diarrhoea, serious deple-tion can result.

Potassium

Potassium is the major intracellular cation ofthe body, with almost all of the body’s contentfound within the cells, the majority of it boundto phosphate and protein. Like sodium, potas-sium is essential for cellular integrity and themaintenance of fluid, electrolyte and acid–basebalance. It is also involved in the propagation of the nerve impulse and muscle contraction.Potassium that leaks out into the extracellularfluids is quickly pumped back to maintain thedifferential between the composition of the fluids outside and inside cells, on which muchof the cellular function depends.

Potassium in foodsDaily intakes of potassium in the UK arereported as 2.7 g. Thus, the levels are similar tothose of sodium. Main contributors of potas-sium in the British diet (DEFRA, 2001) are vege-tables and potatoes (29 per cent) and moderatelevels are obtained from cereals (15 per cent),dairy products (18 per cent), meat (13 per cent)and fruit (11 per cent). Foods that are rich in

potassium include dried fruit and nuts, choco-late, treacle, meat and raw vegetables.

Potassium absorptionThis occurs readily in the upper small intestineand colon with 90 per cent of ingested potas-sium absorbed, although the mechanisms are notfully understood. Potassium levels in the bodyare carefully regulated to maintain low levels inthe plasma (3.5–5.5 mmol/L) and much higherlevels (150 mmol/L) in the intracellular fluid. Thetotal amount of potassium in the body is relatedto the lean body mass.

Regulation occurs by means of hormonallycontrolled secretion into the glomerular filtratein the kidneys. The kidneys are very efficient atremoving surplus potassium from the body, butless precise at preventing loss when body levelsare low. Small amounts of potassium may belost in the faeces and sweat.

Potassium deficiency is unlikely to occur for dietary reasons because of the widespreadoccurrence of the mineral in foods. However,low blood potassium may result from excessivelosses of gastrointestinal fluids, for example, invomiting, diarrhoea, purgative or laxative abuse.Certain diuretic drugs may also remove exces-sive amounts of potassium from the body. Theseresult in mental confusion and muscular weak-ness. The muscular effects may affect the heart,causing sudden death, or the smooth muscle ofthe intestinal tract, resulting in paralytic ileusand abdominal distension. This may be a firstsign of low plasma potassium in children.

High levels of blood potassium are generallyassociated with tissue breakdown, in catabolicstates and starvation. More potassium is lost in the urine and the body gradually becomesdepleted of potassium with shrinkage of theintracellular fluid volume. In uncontrolled dia-betes mellitus, accelerated tissue breakdown will cause increased urinary loss of potassium.Treatment with insulin can cause plasma levelsto fall dramatically, resulting in cardiac arrhyth-mias, and care must be taken to avoid this.

Potassium and healthStudies on the relationship between blood pressure and diet have indicated that a high

If you have previously kept a record of your dailyfood intake, you can return to this for the activity.If not, first make a list of all the things you haveeaten in the last 24 hours.■ Identify the main sources of salt/sodium in this

intake (you may need to check food labels todo this accurately).

■ What sort of foods are contributing to thissalt intake? Are there lower salt alternativesavailable?

■ Plan a modified diet that contains less salt.■ What problems would you have in achieving

this? Are there some foods you could avoidstraight away?

Activity 10.1

FLUIDS – KEEPING THE BODY HYDRATED ❚

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potassium intake is beneficial in reducing bloodpressure (see Figure 10.11). In many primitivecommunities, potassium intakes are muchhigher than those of sodium. Consequently,these societies tend to have low levels of bloodpressure, possibly because of the beneficial ratioof the two minerals. In Western societies, theconsumption of fruit and vegetables has tendedto decrease, as the intake of processed and manu-factured foods has increased, thereby reversingthe Na:K ratio. Studies indicate that a higherlevel of potassium intake (3.5 g/day) facilitatesthe body’s ability to deal with sodium excess.Further, potassium intakes between 2.5 and3.9 g/day have been shown to reduce bloodpressure in both normotensive and hypertensivesubjects.

Potassium intakes may need to be restrictedin renal disease, when the kidney is not regu-lating plasma levels effectively. The roles ofsodium and potassium in blood pressure regula-tion are summarized in Figure 10.11.

Dietary reference valueThe RNI for adults has been set at 3.5 g/day,although it is recognized that intakes may bemuch higher than this. Toxicity is unlikely, how-ever, at normal dietary levels. Intakes in excess of17.6 g/day may cause harmful effects, but theseare only likely to occur with supplement use.

Fluids – keeping the bodyhydrated

Humans can survive for long periods of timewithout food; several weeks’ survival has beenreported. However, if fluids are withheld, thereis a rapid deterioration and death may resultwithin 10 days.

This is not surprising when we recognize thatwater is the single largest component of bodycomposition, comprising 50–60 per cent of thetotal body weight in an average adult. Water con-tent is somewhat higher in males than in females,as the higher percentage body fat in females isassociated with less water than is muscle.

Water is an essential component of the bodybecause:■ the process of ingestion, digestion and

absorption is facilitated by the presence of water, including the various secretionsalong the digestive tract containing digest-ive enzymes;

■ elimination of unabsorbed material via thecolon requires water to facilitate its passage;

■ metabolic reactions occur in an aqueousenvironment;

■ nutrients and metabolites are transported insolution within extracellular or intracellularfluids;

■ mucous membranes must be kept moist fornormal functioning, including the exchangeof gases during respiration in the lungs;

■ the excretion of waste products via the kidney occurs in water;

■ regulation of body temperature by transferof heat within the circulation and the pro-duction of sweat.Fluid intake is, therefore, essential for our

survival and we require a regular intake. Yet,despite these key roles, there is no recommenda-tion made on the intake of water in the DietaryReference Values Report in the UK (DoH, 1991).

Fluid balances

There is a daily turnover of body water equiva-lent to approximately 5 per cent of our bodyweight. The actual amount depends on a varietyof circumstances. The average values for a

Figure 10.11 Roles of sodium and potassium in bloodpressure.


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healthy individual who is sedentary and lives ina temperate climate are given in Table 10.2.

Water lossIt can be seen from the above that water is lostfrom the body in a variety of ways.

UrineThe amount of urine produced is under hor-monal control and is adjusted to achieve fluidbalance in the body. Therefore, the volume andconcentration of urine will reflect the state ofhydration of the individual. Following largeintakes of fluid, the urine will be dilute and paleand straw-like in colour. Pale urine is an indica-tor of a good level of hydration in the body. Asfluid intake decreases, or other losses of fluidincrease, the colour of the urine becomes darker.Thus, dark yellow or even brownish urine is asign of severe dehydration. This is a very simpleguide that anyone can follow to monitor his orher state of hydration.

The volume of urine is affected by certaindietary items. Protein and sodium contents ofthe diet can both increase the volume of urinethat needs to be excreted (known as obligatoryloss). This is associated with the need to elim-inate waste products (urea from protein metab-olism, and sodium) and maintain homeostasis.Thus, both a high-protein or a high-salt diet willincrease obligatory urine losses. In these cases,it is important to increase fluid intakes to ensureadequate levels to meet excretory needs.

Alcohol is a diuretic and, therefore, increasesthe loss of urine from the body. Whether this will have a dehydrating effect depends on thevolume of fluid ingested with the alcohol. It isestimated that a 10 mL diuresis occurs for each

gram of alcohol ingested. In practice, therefore,an 8 g intake of alcohol (equal to 1 unit), wouldcause 80 mL of diuresis. If this was taken as ahalf pint of beer, then more fluid would havebeen taken in than was being lost, and dehydra-tion would not result. However, with strongerdrinks, taken in a smaller volume, such as wineand spirits, alcohol ingestion will lead to diur-esis, causing dehydration.

Caffeine-containing drinks, such as coffee,tea, chocolate and colas, together with some ofthe ‘energy drinks’ on the market also have thepotential to act as diuretics. This also applies torelated compounds, such as theophylline andtheobromine, that are found in tea and choc-olate. There has been considerable debate aboutthis matter, and widely repeated advice that allof these drinks are of no value for hydrationbecause of their diuretic effects.

However, it has now been established thatthere is no evidence in the scientific literature toshow that at normal intakes of caffeine, that is,less than 300 mg/day, there is any diuretic effectand the beverage can contribute fully to thehydration of the body. In the UK, the daily caf-feine intake from tea and coffee has been foundto be 239 mg/day, well within the limit statedabove. Studies that have indicated a diureticeffect of caffeine have used higher doses thanthis (300–700 mg), in caffeine-depleted well-hydrated individuals. In this case, caffeine doeshave a diuretic action.

Although hot beverages, such as coffee and tea, vary in their actual caffeine content,dependent on the method of preparation, averagevalues for these drinks are shown in Table 10.3. It is, therefore, recommended that all of thesedrinks can be used to hydrate the body withoutcausing a diuretic action.

FaecesThe fluid loss here is generally small. However,amounts can increase if there is diarrhoea whenup to 2 L may be lost via this route each day.Diarrhoeal disease associated with contamin-ated water is a major cause of death in childrenin developing countries, and emphasizes theimportance of aiming to maintain hydration inthis situation.

Average values for dailyturnover of body water in a temperate climate

TABLE 10.2

Input (mL) Output (mL)Food 1000 Urine 1300Drinks 1200 Faeces 100Metabolism 350 Skin 750

Lungs 400Totals 2550 2550


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SkinLosses through the skin occur continuously and are an essential part of the body’s tempera-ture control mechanism. They will, therefore,vary with the environmental temperature andthe amount of physical activity. In a hot environment, the body loses heat by evaporationof large amounts of sweat, and the fluid balancemay become disturbed. Amounts of sweat mayincrease to 2–3 L as a result. Physical activitycompounds these losses. Any increase in phys-ical activity generates body heat, which must belost through sweating. Moderate exercise mayincrease sweat losses to 1 L/hour. If this occursalso in a warm environment, sweat losses maybe as high as 2–3 L/hour. Individuals working inhot environments, such as steel workers, minersand catering workers also have high sweat lossesthat need regular replacement.

Children exposed to heat may lose propor-tionately more sweat because of a greater surfacearea to volume, and will have a more criticalneed for water to replace this. Thirst mechanismsmay not be very sensitive, so encouragement todrink may be needed.

In a person who has a raised body tempera-ture, it is estimated that skin losses of water aspart of thermoregulation are increased by500 mL for each 1°C above normal.

LungsLosses occur here continuously, as gaseousexchange in the lungs takes place in a moistenvironment. Losses increase when there is low

humidity, for example, in dry climates or air-con-ditioned offices, as well as in aircraft and at highaltitude. Increased respiratory rates during exer-cise also increase the hourly rate of water lossfrom the lungs. Water loss also increases via thisroute in patients who are attached to ventilators.

Water gainWater is produced in the body during metabolicreactions and this contributes a small amount tothe body’s water economy. This is a continuoussource of water for cellular needs.

Water is also obtained from the food con-sumed. Almost all food contains some associatedwater. Semi-liquid foods, such as soups, yogurtsand ice cream, are obvious examples; fruit andvegetables contain a high percentage of water.Even foods that appear to be relatively ‘solid’,such as bread, cereal foods, cakes, meats anddairy products, contain some water. Some examples are shown in Table 10.4.

It follows that a person who has a smallappetite, or is unwell and, therefore, eating verylittle will gain small amounts of water by thisroute, and will need to make up for this byincreasing their fluid intake. A normal mixeddiet, however, will provide up to 1 L of waterfrom the food consumed.

Consumption of liquids is governed by thirstand habit, both of which can be overridden.When fluid volumes fall in the body, there is nor-mally a rise in osmolality of body fluids, and anincrease in sodium concentrations. These triggerthe thirst mechanism. It can be seen that thirstdoes not prevent the fall in fluid volume, but follows on from it, by which time there is alreadysome dehydration. Furthermore, the thirst mech-anism is not a very sensitive trigger for fluidintake. Other triggers might include a dry mouthand reduced saliva production. Overall, it is muchbetter to be in the habit of taking fluids regularly,without waiting to be thirsty. In people with ahigh fluid turnover, such as athletes, anticipatingthe need for fluid and keeping hydrated is a sensible precaution against dehydration. Inunusual circumstances, if large amounts of salthave been lost through profuse sweating, anintake of a large volume of water may reduceplasma osmolality further and cause continued

Average caffeine (inmilligrams per averageserving) for some beverages

TABLE 10.3

Beverage Caffeine content (range)

Tea 40 (30–55)Instant coffee 58 (42–68)Filter coffee 90 (60–120)Decaffeinated coffee 2 (1–4)Hot chocolate 5 (1–8)Cola 23 (11–70)‘Energy drinks’ 48 (1–70)


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urine loss. This situation is potentially dangerousand requires an intake of salt with water to restorenormal electrolyte balance. In the majority of cir-cumstances, adequate salt is obtained from nor-mal dietary intakes to prevent this happening.

Large intakes of fluid can also be taken vol-untarily, for example, on social occasions. Inthis situation, there is rarely any thirst for thedrinks, but the normal controlling mechanismsare overridden by conscious control.

Similarly, thirst sensations may be weak orcan be ignored. The sense of thirst decreaseswith age, so the risk of dehydration is greater in older adults. Children may also not respondadequately to the sensation of thirst and becomevulnerable to dehydration, especially if under-taking physical activity in which they becomevery involved. The urge to drink may also beignored if it is inconvenient or difficult to emptythe bladder. This may be for social reasons, orbecause of a lack of facilities, or incontinence or

impaired mobility. All of these situations maypresent a risk of dehydration.

Dehydration

Although there is no doubt about the essentialnature of water in the body, the signs and symp-toms of dehydration are less well described.

Mild dehydration (a deficit of 500mL–1L, or1–2 per cent of body weight) will cause thirst tobe triggered. There is no clear evidence whetherthis level of dehydration has a detrimental effecton cognitive function. Mild to moderate dehydra-tion (a deficit of 1–3.5L or 2–5 per cent of bodyweight) will lead to headaches, early fatigue, loss of precision in tasks, inability to concentrate,irritability and nausea. Progressively greaterdehydration will cause an elevation of body tem-perature, increased heart rate and respiration,dizziness, weakness and raised blood pressure.Ultimately, renal function will be impaired andthe person may become comatose. Death can fol-low if fluid balance is not restored.

The prevalence of mild dehydration is notknown, although it is likely that a substantial pro-portion of the population of all ages have inad-equate fluid intake. Concern has been voicedabout the need to ensure that schoolchildren haveaccess to fluids during the day to prevent loss ofconcentration owing to dehydration. Amongolder persons who are admitted to hospital, dehy-dration and confusion are common findings.

Some long-term studies have indicated thatchronic hypohydration may be associated withhigher incidence of colon and breast cancer,although further research in these areas is needed.

How much to drink?

From the above discussion it is clear that fluidintake is important, and the optimal way ofavoiding dehydration is to develop a habit of regular fluid intakes without waiting for thirstto intervene. The quantities needed will dependon the factors discussed above that affect fluidlosses and will vary between individuals. As ageneral rule, however, most sedentary adults, in atemperate environment require to drink between1.2 and 1.5 L each day. This assumes that a further 1 L of fluid is obtained from the food

The water content of somefoods (as a percentage)TABLE 10.4

Food WaterWhite flour 14White bread 37Semi-sweet biscuits 2.5Doughnut 27Ice cream 62Lentil soup 78Baked white fish 76Peas 78Boiled potatoes 80Lettuce 95Banana 75Orange 86Boiled rice 68Cornflakes 3Sponge cake 15Cheddar-type cheese 36Fruit yogurt 77Cooked meat 60Grilled oily fish 65Carrots 90Potato chips 52Tomato 93Apple 85Grape 82


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consumed. In this way, a fluid intake of 35mL/kgbody weight per day would be achieved.

What to drink?

Some guidelines suggest 6–8 glasses of waterper day, although it is not necessary to consumeonly water.

As has been discussed above, it is only alcohol that, in practice, has a diuretic effect and may not contribute to hydration. However,low alcohol beers can be used to help towardshydration. Most other commonly consumed bev-erages can be counted towards the fluid intakeallowance. However, it is important to considersome of the other attributes of common drinkswhen selecting what to consume.

WaterThis is often the easiest and cheapest fluid todrink. Consumption of water has increased inrecent years, with the popularity of bottledwaters. The habit of carrying a bottle of waterduring the day has become widespread and is auseful reminder to drink.

Soft drinksThese include carbonated drinks, dilutables(squash/cordial) and fruit juice drinks. These areof varying nutritional quality. Some may be‘low calorie’ but others may provide up to fourteaspoons of sugar per portion. Levels of phos-phoric acid are often high in the carbonateddrinks and this has cariogenic potential. Some

fruit juice drinks have added nutrients, such asvitamin C, but may also be high in sugar.

Fruit juicesThese are useful as they provide both vitamin Cand possibly phytochemicals that may haveadditional health benefits.

MilkThis is less popular than in the past, but there is a growing market in flavoured milks and probiotic products based on milk. These may,however, contain added sugar. Milk provides a useful range of nutrients, especially calciumand riboflavin. In addition, it is a useful sourceof vitamin B12, vitamin A, iodine, magnesium,phosphorus, potassium and zinc. It is a nutrient-dense food, in relation to its energy intake, espe-cially if a reduced-fat milk is drunk.

Tea and coffeeBoth of these are popular beverages. They canmake a useful contribution to hydration. Ifdrunk with milk, additional nutritional valuemay be gained.

Overall, it is sensible to consume a range ofdrinks, according to taste. Care should be takenthat drinks do not cause damage to teeth or provide unnecessary additional energy, if thereis concern about weight management. Mostimportantly, fluid intake should be frequent andadequate to maintain hydration.

1 The minerals constitute a diverse group. Their roles may be structural, protective or regulatory.2 Levels of the minerals are generally closely regulated, either by control of absorption or by control of

excretion, to prevent excessive amounts accumulating in the body.3 Some of the minerals, especially calcium, zinc, copper and iron, may compete with one another for

absorption.4 Many of the minerals function as cofactors for enzymes involved in metabolic processes. These range

from energy transformation to synthesis of essential biological materials in the body.5 Intakes of the minerals in the UK are generally adequate, with the exception of iron and zinc, where there

is evidence of inadequate intake, and absence of stores in a significant proportion of the population.6 Deficiency states for some of the minerals are more clearly defined than for others. However, in many cases,

deficiency is more likely to develop as a secondary consequence, rather than due to primary dietary lack.7 Fluid intakes may be marginal in some people and represent a significant risk of dehydration.

Developing a habit to drink regular amounts of fluids is important.

SUMMARY


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Appel, L.J., Moore, T.J., Obarzanek, E. 1997: A clinical trial of the effects of dietary patterns onblood pressure. New England Journal of Medicine 336, 1117–24.

British Nutrition Foundation 1991: Calcium. Briefing Paper No. 24. London: British NutritionFoundation.

British Nutrition Foundation 1995: Iron nutrition and physiological significance. The Report of theBritish Nutrition Foundation Task Force. London: Chapman & Hall.

British Nutrition Foundation 2001: Selenium and health. Briefing Paper. London: British NutritionFoundation.

Colhoun, H., Prescott-Clarke, P. (eds) 1996: Health survey for England 1994. London: HMSO.DEFRA 2001: National food survey 2000. Annual Report on food expenditure, consumption and

nutrient intakes. London: The Stationery Office.Delange, F. 2000: The role of iodine in brain development. Proceedings of the Nutrition Society

59, 75–9.DoH (UK Department of Health) 1991: Dietary reference values for food energy and nutrients for the

United Kingdom. Report on Health and Social Subjects No. 41. Report of the Panel on DietaryReference Values of the Committee on Medical Aspects of Food Policy. London: HMSO.

DoH (UK Department of Health) 1992: The nutrition of elderly people. Report on Health and SocialSubjects No. 43. London: HMSO.

EURODIET Working Party: Final report. 2001: European diet and public health: the continuing chal-lenge. Public Health Nutrition 4(2A), 275–92.

Hamet, P. 1995: The evaluation of the scientific evidence for a relationship between calcium andhypertension. Report of the Life Science Research Office, Federation of American Societies inExperimental Biology. Journal of Nutrition 125, 311–400.

Heaney, R.P. 2000: Calcium, dairy products and osteoporosis. Journal of the American College ofNutrition 19(2), 83S–99S.

Jeejeebhoy, K.N. 1999: The role of chromium in nutrition and therapeutics and as a potential toxin.Nutrition Reviews 57(11), 329–35.

Maughan, R., Shirreffs, S. 2002: Keeping the body hydrated: why it’s necessary and how to achieveit. Nutrition in Practice 3(1), 1–4.

National Osteoporosis Society 1999. Diet and bone health. London: National Osteoporosis Society.

1 List those groups in the population who are atrisk of poor iron status and provide a discussion of the causes for each group.

2 Construct a table to identify some commonand contrasting features of iron, calcium andzinc. You could consider the following in yourcomparison: dietary sources, influences onabsorption, functional role and how referencevalues are set.

3 a Explain why healthy eating advicerecommends a reduction in sodium intakes.

b Which foods might need to be restricted inthis case?

4 A number of minerals have a regulatory role inthe body. These include iodine and chromium(a role in the function of hormones in the body)and selenium (involved in antioxidant function).a Explain these roles.b What are the consequences of deficiencies?

5 Develop a table to distinguish those minerals inwhich a deficiency is most likely to be ofprimary (dietary) origin from those where asecondary cause is more likely.

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New, S.A, 2001: Exercise, bone and nutrition. Proceedings of the Nutrition Society 60, 265–74.Nutrition Society Symposium 1994: Newer aspects of micronutrients. Proceedings of the Nutrition

Society 53(3), 557–636.Rayman, M.P. 2002: The argument for increasing selenium intake. Proceedings of the Nutrition

Society 61, 203–15.Sacks, F.M., Svetkey, L.P., Vollmer, W.M. et al. 2001: Effects on blood pressure of reduced dietary

sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-SodiumCollaborative Research group. New England Journal of Medicine 344, 3–10.

Sojka, J.E. 1995: Magnesium supplementation and osteoporosis. Nutrition Reviews 53(3), 71–80.Strain, J.J. 1995: Micronutrients interactions (symposium). Proceedings of the Nutrition Society

54(2), 465–517.WHO, Food and Agriculture Organisation, International Atomic Energy Expert Group 1996: Trace

elements in human nutrition and health. Geneva: WHO.

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pregnancy and lactation


❏ establish the importance of nutrition in preparation for and throughout pregnancy;❏ discuss the nutritional needs during pregnancy;❏ identify specific groups in the population who may be at particular risk in pregnancy;❏ describe the possible links between pregnancy outcome and long-term health;❏ discuss the nutritional needs in lactation;❏ identify some of the influences on the mother in choice of feeding method.


❏ explain the importance of good nutritional status at conception;❏ discuss some of the metabolic changes that occur in pregnancy in the mother and how these influence her

nutritional needs;❏ explain why certain dietary patterns may be associated with increased vulnerability in pregnancy;❏ devise general dietary advice for optimal pregnancy outcome.

Based on studies of well-fed pregnant women in the 1950s in the UK, the physiological normfor weight gain in a 40-week pregnancy was set at 12.5 kg. This appeared to be associatedwith optimal outcome of pregnancy and hasbeen used as a reference since then. The 12.5 kgcomprises:

Fetus 3.5 kgIncreased maternal tissues 5.0 kg

(including uterus, mammary glands and blood volume)

Stored fat 4.0 kg

These increases were also believed to prepare themother’s body for lactation, in the form of storedenergy for milk production.

On the basis of such figures, it would seemreasonable to conclude that the mother needs toconsume a significantly greater amount of foodduring the pregnancy in order to provide suf-ficient nutrients and energy to build these extratissues. The corollary of this is that pregnancy

outcome, both in terms of the mother’s healthand the well-being of the baby, would beadversely affected if her nutritional intake werenot increased.

In recent years, a better understanding hasemerged of the relationship between nutrition ofthe mother and pregnancy outcome. This hasshown it to be very much more complex thanstated here, as well as far from fully understood.

This chapter considers the importance ofnutritional status before pregnancy, at the timeof conception, and in the presence of majorphysiological changes, which occur duringpregnancy. The indicator of outcome of preg-nancy that is widely used is the birthweight ofthe baby. A favourable outcome is the deliveryof a healthy full-term infant, weighing between3.5 and 4 kg (in the UK; some countries use4.5 kg as the upper end of the range). This isassociated with the lowest risk of infant andperinatal morbidity and mortality. Above thisbirthweight there is an increased likelihood of

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obstetric complications as well as neonatal mortality and morbidity. Babies born weighing less than 2.5 kg (termed ‘low birthweight’) havea 40-fold greater risk of neonatal mortality thanthose born at optimal weight, and the survivorshave an increased risk of neurological disordersand handicap, as well as infection. Work byBarker (1998) and others indicates that infantswho experience growth restriction in the wombor in early life may be more susceptible to laterdegenerative disease. It is, therefore, importantto minimize these risks wherever possible. It is,however, also important that the mother herselfarrives at the end of pregnancy in a healthystate and well enough to be able to care for hernewly born infant.

Nutrition before pregnancy

The nutritional status of a woman at the time ofconception reflects her diet and lifestyle over anumber of years, even perhaps going back toher own infancy and childhood. These aredependent on many environmental and socialfactors, which must be taken into account.

Several features of the pre-pregnancy dietmay affect the chances of conception or thesuccess of pregnancy. For example:■ vitamin D deficiency in adolescence may have

resulted in rickets with pelvic malformations,making a normal delivery impossible;

■ a dietary deficiency of vitamin B12 may causeinfertility; and

■ a history of dieting, or in its extreme formanorexia nervosa, can result in poor nutri-tional status, with low reserves of manynutrients.Research on underweight women has found

that low body fat stores are associated withamenorrhoea and infertility. Evidence of thisassociation comes from records obtained inwartime from places where food supplies werecritical, such as Holland and Leningrad, as wellas from more recent studies in infertility clinicsand on women with anorexia. These indicatethat a body mass index (BMI) of 20.8 appears tobe a threshold for normal pregnancy, and thatthere is a minimum ratio of fat:lean body massneeded to support pregnancy.

Women who are obese (BMI above 30) mayalso experience infertility, as the associatedchanges in insulin activity and sex hormonesmay reduce the viability of the ovum.

It would, therefore, appear to be desirable thata woman planning to become pregnant shouldaim to achieve a BMI within the range of 20–26.If this is achieved by adopting healthy nutritionalpractices, then the reserves of micronutrients willalso be maximized.

Research on primates and human volunteerssuggests that the most crucial phase is the 14days prior to conception, when the follicle in the ovary is growing rapidly before it extrudesthe ovum at ovulation. The environment for thedeveloping ovum in the ovary requires appropri-ate hormone levels. These are crucially depend-ent on the maternal state of nutrition both interms of protein as well as other nutrients. Thesemay include iodine to ensure normal thyroidhormone function, magnesium and zinc for thebinding of hormones at their receptor sites, andfolic acid for the normal growth of the follicle.

It is clear that nutrition prior to pregnancyhas long-term implications and that, for an optimum outcome, diets should be adequate andwell-balanced before conception.

Nutrition at the time ofconception

The embryo at conception and in the first weeksafterwards is extremely vulnerable. The major-ity of the organs and systems develop in thefirst 8 weeks after conception. The essentialenergy and nutrients for this are derived fromthe mother’s circulation and from the lining ofthe womb. It is, therefore, critical that these canprovide the necessary nutrients in appropriateamounts. At this stage in the pregnancy, the pla-centa has not yet formed, so there is no mecha-nism to protect the embryo from deficiencies inthe maternal circulation. It is, therefore, not sur-prising that nutritional status and nutritionalreserves at this time are vital. Studies from theDutch hunger winter (1944–45) showed that,among the women who did bear children, it wasthe ones who had experienced the full durationof hunger (8 months) prior to conception who

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had the most severely affected infants withrespect to malformations.

Trials on the prevention of neural tube defects(NTDs) have shown that supplementing the diet of ‘at risk’ women with folic acid (4mg/day) for 3 months before conception and up to the 12thweek of pregnancy significantly reduced the riskof NTD in the fetus. Since folate is needed for celldivision, it is suggested that these levels overridea metabolic abnormality linked to neural tubeclosure. In the majority of cases, it is impossible topredict which women might be at risk and onlythose who have already had one affected fetuscan be identified as requiring particular supple-mentation. As a result of these studies, womenwho might become pregnant are now advised inthe UK by the Department of Health (HEA, 1996)to increase their intake of folate by at least 400 �gdaily. This is more than the typical diet providesand, therefore, foods fortified with folic acid, orfolic acid supplements, are needed. The Folic AcidCampaign is further discussed in Chapter 18.

Foods that are a good source of folate are listed inFigure 11.1.

Retinol has also received particular attentionin recent years. Reports have suggested thatextreme intakes of retinol (doses from 8000 to10000 �g/day) are teratogenic (i.e. cause fetalmalformations). Such a level of intake is likely tobe taken regularly only in the form of supple-ments. The main dietary source of retinol thatmight contain these levels is liver. A 100g servingof liver might contain up to 10000 �g of retinol;it is unlikely, however, that this would be eaten ona daily basis. Nevertheless, women who may betrying to become pregnant are advised to avoidliver and liver products, as well as supplementsthat contain megadoses of retinol, as there is avery small risk of harm. No cases of fetal damageattributable to liver intakes have been reported inBritain.

Alcohol is also a potential teratogenic agent, particularly if taken in large amounts, forexample, in binge drinking. Women who are

Figure 11.1 Sources of dietaryfolate.


234

considering becoming pregnant should, there-fore, avoid consuming large amounts of alco-hol. This is important in view of the likelihoodthat damage may be done in the first weeksafter conception, before the woman realizes sheis pregnant. Later in pregnancy, alcohol taken inmoderate to large amounts may result in growthretardation, or more seriously in fetal alcoholsyndrome. This includes a series of characteris-tic malformations and defects affecting the face,heart, brain and nervous system, and is gener-ally associated with reduced mental capacity.For this reason, general advice in the UK is tolimit alcohol intake in pregnancy to no more thanone standard drink per day and, in any case, toavoid consuming more than 15 units per week.In men who drink heavily, there is likely to be areduced sperm count, which may be a contribu-tory factor in reproductive failure in a couple.

The weight of the woman and, in particular,her body fat content at the time of conception isalso an important determinant of the metabolicchanges that occur during pregnancy. Researchsuggests that a low fat content at conception is asignal to the body to conserve energy so that themetabolism during the pregnancy becomes veryefficient and the total energy costs of the preg-nancy are low. This is mediated by altered leptinlevels. Conversely, in women with high fat storesat conception, there is little energy conservationand the cost of pregnancy is high. Nevertheless,even with this adaptability, mothers with low fatstores give birth to lower birthweight babies thando those with higher fat stores.

Research also suggests that there are nutri-ents that may be protective at this stage of preg-nancy, having an antimutagenic effect. Theseinclude riboflavin, vitamins C and E, and mono-unsaturated and polyunsaturated fats. Foods thatare particularly rich in antimutagens are fruitand vegetables, although their activity is likelyto be destroyed by cooking.

Nutrition duringpregnancy

Considerable changes occur in the mother’sbody during pregnancy. In addition to thedeveloping fetus, there are changes in her own

tissues, with an expansion of the plasma vol-ume and red cell mass, increase in the size ofthe uterus and mammary glands and depositionof fat.

In the 1970s, incremental calculations of theamount of extra protein and fat laid down dur-ing pregnancy were performed, which gave anestimate of the energy and protein needs of these‘capital gains’. In addition, an allowance wasadded for the extra ‘running costs’ of the heaviermaternal body. Such calculations produced afigure for the total additional energy cost ofpregnancy of about 335 MJ (80 000 Calories).These figures were used in many countries as thebasis for setting recommended intake levels forpregnant women.

Recent findings have shown that energymetabolism exhibits considerable variation, withpregnancy being maintained successfully at anadditional energy cost of 523 MJ (125 000Calories) in well-nourished women in Sweden,and with an energy deficit of 30 MJ (7150Calories) in women in the Gambia not receivingnutritional supplementation. A woman’s adap-tive mechanisms to pregnancy can include:■ an increase in food intake to meet energy

needs;■ laying down of fat stores/mobilizing fat

stores;■ an increase or reduction in the basal meta-

bolic rate (including the costs of synthesisand maintenance of new tissues);

■ a reduction in physical activity costs (seeFigure 11.2).

Think about what you have just read, and answerthe following question.How would the following cases cope with themetabolic demands of pregnancy?■ A rural peasant woman in a food-deficient,

poor country.■ A normal-weight woman living in an industri-

alized Western country.■ An overweight woman, living in a Western

country.■ A 14-year-old girl, living in a Western country.

Activity 11.1

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In this way, the energy costs of supporting adeveloping fetus can be maintained at very dif-ferent levels of energy intake.

In addition to metabolic adaptations in termsof energy, the body also undergoes other physio-logical changes to increase the efficiency ofnutrient utilization and to optimize the supply to the fetus. Many of these changes commence inthe early weeks of pregnancy while the fetus isstill very small and its nutritional demands low.At this time, the mother may conserve nutrientsin her tissues. Evidence suggests that this appliesto protein in particular, with reduced amino acidoxidation occurring in the liver. In the laterstages of pregnancy, as the fetus enters a rapidgrowth phase, this protein can be made availablefrom the mother’s tissues to supplement thatconsumed in the diet. In this way, the needs can

be met without a major increase in intake beingnecessary.

The mother also makes greater use of lipids asa source of energy for her own needs, thus spar-ing glucose for the needs of the fetus. This changeis brought about by alterations in hormone levels,particularly insulin. There are adaptations also inthe muscular activity of the intestines, so thatfood spends a longer time being digested andabsorbed. This increases the efficiency of absorp-tion, particularly for minerals such as calciumand iron. In addition, both of these may be betterabsorbed in response to the physiological regula-tion, which occurs as a result of the increasedneed for the minerals.

The slowed activity of the intestines maycause heartburn and constipation. Heartburnarises because the muscles at the top of the

Figure 11.2 Adaptive mechanisms in pregnancy to conserve energy.


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stomach are more relaxed, which allows refluxof the acidic stomach contents into the lowerpart of the oesophagus, causing irritation andpain. Some practical suggestions for relievingheartburn include:■ eating small, frequent meals;■ taking liquids separately from meals;■ avoiding spicy or fatty foods;■ sitting upright while eating;■ waiting 1 hour after eating before lying down;■ not exercising for at least 2 hours after eating.

Constipation occurs because of the longertime available for absorption of water from thedigestive tract. Increasing both fluid and non-starch polysaccharide (NSP) intakes can help torelieve this problem, as will maintaining a mod-erate level of activity.

What are the dietary goalsin pregnancy?

Generally, pregnant women do not eat a diet sub-stantially different from that eaten by the rest ofthe female population. Studies around the worldof pregnant women in different cultures and atdifferent levels of income show that pregnancycan occur successfully at varying levels of nutri-tional intake, although there are limits to the protection afforded the fetus at low intake levels.Whether the baby that is born is as healthy as possible may not necessarily be apparent inthe first instance, since current research suggeststhat the intrauterine environment is crucial tolong-term health (this is discussed later in thechapter).

Birthweights are lower in babies born towomen who have lower energy and nutrientintakes, with particularly strong relationshipsseen with intakes of the minerals magnesium,iron, phosphorus, zinc and potassium, and thevitamins thiamin, niacin, pantothenic acid,riboflavin, folic acid, pyridoxine and biotin.Increasing the food intake does not result inprogressively larger and larger infants. Studiesby Doyle and colleagues (1990) show that thereis a threshold birthweight (of 3.27 kg) abovewhich extra food intake makes little difference,but below which there is a progressively lowerbirthweight as intakes are reduced.

For optimal outcome measured in terms oflowest perinatal mortality, women who areunderweight before pregnancy need to increasetheir food intake more and gain more weightthan those of normal weight. The converse is trueof overweight women. Various guidelines arenow available for the recommended weight to be gained in relation to pre-pregnancy BMI (seeTable 11.1 for figures recommended in the USA).

The diet in pregnancy

From what has already been said, it is clear thata pregnant woman does not need to ‘eat fortwo’. The mother’s appetite should be a goodguide to her overall needs for energy.

In the first three months of pregnancy, up to70 per cent of women suffer from nausea andvomiting. Although this is commonly termed‘morning sickness’, probably only 10–15 per centof women experience sickness in the morning. In the remainder, it can actually occur at any timeof day or night – and in some women occurscontinuously. Nausea and vomiting of pregnancy(NVP) is a better name for this syndrome. It mayrange from a mild nausea to quite severe, fre-quent vomiting. The condition appears to be moreprevalent in societies that consume animal prod-ucts and it has been suggested that NVP is a pro-tective mechanism against potential parasites andpathogens that may be ingested at a critical timein early pregnancy and threaten the embryo.Paradoxically, NVP appears to be associated with a favourable outcome of pregnancy, includinghigher birthweight and longer gestation. It has

Guidelines on weight gainin pregnancyTABLE 11.1

Pre-pregnancy Recommended BMI (w/h2) weight gain (kg)19.8 12.5–1819.8–26.0 11.5–1626–29.0 7–11.529.0 6 (minimum)

Institute of Medicine 1990. Part I, Weight gain. Committee onnutritional status and weight gain during pregnancy. Food andNutrition Board. Washington DC: National Academy Press.Reproduced with permission.

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been proposed that this may be the result of theadaptation of the placenta to a reduced foodintake in the first trimester, which then favoursfetal growth once NVP resolves. Frequent mealsor snacks are recommended, even if the womanhas little appetite for them. It is important that thefood eaten is as nutritious as possible and often itis high carbohydrate foods that are best tolerated.Dehydration is also a risk and salty foods thattrigger thirst mechanisms may also be useful. Animproved quality of the diet may be important tocompensate for the period when food intake is low (see Figure 11.3 for general diet tips inpregnancy).

Appetite is usually good in the middle part ofpregnancy, so that food intake is at or a littleabove normal pre-pregnant levels. This ensuresan adequate provision of energy and nutrients toform a reserve for the greater needs of the lastmonths.

In the last 3 months, the needs of the fetus arehigh and the mother’s appetite may increase. She

is limited in her capacity for food, however,because of the pressure of the enlarged womb onher stomach. The diet chosen should contain avariety of foods to supply the necessary nutrients.Report 41 (DoH, 1991) recommends a smallincrease in energy intake of 0.8MJ (200Calories)per day during the last trimester of pregnancy.This should be provided by increasing total foodintake. Together with the adaptations to absorp-tion efficiency and the metabolic changes alreadymentioned, this will ensure that the additionalneeds for many other nutrients will be covered.

Particular attention should be paid to certainnutrients for which the increase recommended is greater than can be achieved from a dietdesigned to just meet the energy requirement.These nutrients are vitamins A and C, riboflavin,folate and vitamin D. Increasing fruit and vege-table intake should provide extra amounts offolate, vitamins A and C. Taking extra milk ordairy products, which can contribute to the extra energy intake and also supplies protein

Figure 11.3 Some general diet tipsfor pregnancy.


238

and calcium, will also contribute to meeting the riboflavin needs. Vitamin D requirementsmay be a problem, especially in women who arepregnant through the winter and are, therefore,unable to synthesize skin vitamin D. If storeshave not been accumulated during the previoussummer, a supplement of vitamin D is advisableto ensure adequate calcium metabolism. A par-ticular problem may arise in strictly vegetarianwomen of Asian origin, whose vitamin D statusmay be precarious, and in whom supplementa-tion with vitamin D has been shown to be ofpositive benefit for the birthweight and subse-quent growth of the baby.

The NSP content of the diet is important inpregnancy because of the tendency for consti-pation. Including fruit and vegetables andcereal fibre in bread or breakfast cereals canprovide sufficient NSP to relieve problems ofconstipation.

A summary of the dietary reference valuesfor pregnancy is given in Table 11.2.

It should be noted that many of the recom-mendations made by the UK Department ofHealth (DoH, 1991) assume an adequate pre-pregnancy diet, resulting in good nutritionalstatus and stores at the outset of pregnancy.

Where these are not present, extra intakes willbe necessary during pregnancy.

This is a particular problem with ironbecause it is recognized that a substantial pro-portion of women have a chronically low intakeresulting in poor stores. An early check onhaemoglobin and circulating ferritin will con-firm if iron status is adequate or whether sup-plementation is required.

Moreover, where there is a short intervalbetween pregnancies, levels of some nutrients,such as calcium, iron and folate, may be insuffi-ciently restored. It may take 2 years to returnlevels to their original values. Attention to anutrient-rich diet is, therefore, important in thissituation.

Teenage girls who become pregnant are alsoparticularly at risk, as their own growth needsare high and stores may be insufficient.

Other advice on dietary intake includes foodsafety issues. The presence of Listeria monocy-togenes can cause a series of symptoms frommild to severe, but can also result in prematurebirth or miscarriage and meningitis in a new-born baby. This is a relatively rare condition(estimates are 1 in 30 000 in the UK), but preg-nant women are advised to avoid potentially

Summary of dietary reference values for pregnancyTABLE 11.2Nutrient RecommendationEnergy Increase by 200 kcal (0.8 MJ)/day in last trimester onlyProtein Extra 6 g/day; total recommended 51 g/dayThiamin Increase in line with energy: extra 0.1 mg/day; total recommended 0.9 mg/dayRiboflavin Needed for tissue growth: extra 0.3 mg/day; total recommended 1.4 mg/dayNicotinic acid Metabolism becomes more efficient: no increase neededPyridoxine No evidence that increase neededVitamin B12 Little information available about needs: no increaseFolate Increased usage in pregnancy, maintain plasma levels with extra 100 �g/day; total

recommended 300 �g/dayVitamin C Drain on maternal stores in late pregnancy: extra 10 mg/day; total recommended

50 mg/dayVitamin D Seasonal variation in plasma levels of vitamin; 10 �g/day as supplementCalcium Maternal store drawn upon in early pregnancy and enhanced absorption: no increaseIron Iron stores, cessation of menstruation and increased absorption should cover needs:

no increaseMagnesium, zinc Increased needs, but assumed to be met from increased absorptionand copper


SHOULD SUPPLEMENTS BE GIVEN? ❚

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contaminated foods. These include certaincheeses, such as Brie, Camembert and blue-veined cheeses, and meat-based pate. Cookedchilled meats and ready to eat poultry may alsobe a source of contamination. Other microbio-logical contaminants include Salmonella andtoxoplasmosis (mainly from cat litter).

However, there is little evidence to showthat education of pregnant women to improvetheir diet has significant effects. Targeted inter-ventions may make some impact in specificgroups and these are considered below. In gen-eral, encouragement of healthy eating andincrease in nutritional knowledge for the futurebenefit of the family are useful targets.

Should supplements be given?

There have been many studies of the effects ofvarious supplements on pregnancy outcome. Ingeneral, the effects of supplementation duringpregnancy are small.

The provision of a balanced energy and pro-tein supplement to undernourished womenresults in birthweight increases of less than 100g.High-protein supplements may actually result inreductions in birthweight, possibly associatedwith development of a larger placenta rather thanincreasing the size of the fetus. A better under-standing of the metabolic adaptations that occurin pregnant women suggests that the result ofsupplementation is a decrease in the efficiency ofenergy saving by the mother, with a resultinghigher cost of the pregnancy. It is also unclearhow much of the supplement the women con-sume; it may be used to replace intakes ratherthan add to existing nutrient levels.

Evidence suggests that the greatest effects ofsupplementation occur when this is given eitherin the first 3 months of pregnancy or, preferably,before conception. In the latter case, identifyingmothers who have already given birth to a low-weight baby and providing supplements in theinter-pregnancy period has proved to be effect-ive in avoiding a subsequent low weight birth.The Women, Infants and Children Program in theUSA, which provides food or voucher support towomen in low-income groups has demonstrated

a consistent benefit in terms of better health ofthe baby, and reduced need for health and wel-fare support in the future. This is a cost-effectivescheme with greater savings than costs.

In London, supplementation with multivita-mins and minerals, of women who had borne alow birthweight infant and who were found tohave a poor diet (not meeting the majority ofdietary reference values), resulted in a favourableimprovement in folate and iron levels up to 9 months after delivery. However, control subjectswho did not receive the supplements continuedto have low blood levels of these nutrients. Thiswould be an unfavourable start for a subsequentpregnancy and indicates how poor nutrientintakes can be insufficient to restore blood levelsof nutrients in the inter-pregnancy period.

Similarly, supplementation with specificnutrients, such as folate or iron, may be mosteffective if given pre-conceptionally, or in thevery early weeks of pregnancy. Although itoccurs routinely in much obstetric care, there is controversy about the desirability of supple-mentation with iron during pregnancy. Someevidence suggests that pregnancy outcome isoptimal at haemoglobin concentrations between96 and 105 g/L, indicating that this level may bethe most desirable. Haemoglobin levels abovethis value can be achieved by supplementation,but this may be counterproductive.

It could be argued that a low iron status ismerely a marker of a generally inadequate diet,which may be low in other, less frequently meas-ured nutrients. It would, therefore, appear to bepreferable to improve the whole diet, rather thanto focus on specific nutrients, which might resultin an unbalanced intake.

The need to supplement with long-chain fattyacids has also been debated, particularly forwomen whose diet is low in dietary sources. Infantgrowth and development, especially of the brainand retina, is dependent on an adequate supplyof docosahexaenoic acid. Poor status in themother will mean low levels in the infant. Sup-plementation of the mother in late pregnancywith fish oil has been shown to increase levels ofn-3 fatty acids in cord blood of the newborninfant. Supplementation can also increase con-centrations of n-3 acids in breast milk.


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Supplementation with calcium has been usedeffectively to reduce blood pressure in women atrisk of hypertension in pregnancy. The greatestbenefits have been seen in women with lowdietary calcium levels. The amount used is atleast 1 g of calcium per day. Longer term studiesof the offspring from these pregnancies haveshown lower blood pressures in the children.

Who is most at risk inpregnancy?

A number of groups in the population are particu-larly vulnerable to poor pregnancy outcome.

Teenage girls

The nutritional status at conception may bepoor for a number of reasons. Adolescents areless likely to be eating a well-balanced diet. Thisapplies particularly to girls, who may be chronicdieters as a result of the current fashion forslimness. Low intakes of vitamins A and C, folicacid, calcium, iron and zinc have been reported.

Furthermore, if the girl is still growing, herown nutritional needs may be high and, if she continues to grow during the pregnancy, the baby’s development will be compromised. A teenage mother may have social problems,including eating very little to conceal the preg-nancy, having little money, perhaps smokingand living in poor-quality housing. All of thesefactors will contribute to a poorer pregnancyoutcome with a higher incidence of low birth-weight, perinatal mortality, premature deliveryand maternal problems of difficult labour,anaemia and hypertension being reported.

Low income

Women comprise the majority of those existingon low income. The cost of a diet appropriate tomeet the needs of a pregnant woman has beencalculated to be between 40 and 65 per cent ofthe state benefits payable in the UK. For mostwomen in this situation, it is unrealistic tospend this amount on food for themselves, anda nutritionally inferior diet is eaten, containinginsufficient amounts of nutrients to meet the

needs. This leads to a high incidence of lowbirthweight. Of particular concern is the fattyacid profile of the diet, which may include fewlong-chain polyunsaturated fatty acids (such asarachidonic and docosahexaenoic acids) thatare crucial for development of the neural andvascular systems, and are particularly importantin the last 3 months of pregnancy when braingrowth is at its most rapid. These essential fattyacids are found in vegetable oils, green vegetablesand oily fish, which occur less frequently in thediets of the poor. This deficit may have long-term consequences for the growth and develop-ment of their children.

Underweight and overweight women

The importance of adequate but not excessiveweight gain has already been discussed. Infantsborn to underweight women may exhibit inad-equate patterns of growth at 12 months, suggest-ing delays in development. Overweight womenalso have increased pregnancy risks, both forthemselves and the outcome for the baby. Inoverweight women, dieting during pregnancy isnever recommended; a low energy intake duringpregnancy may result in ketosis and pose a threatfor the developing fetus. However, maintaining a reasonable level of activity during pregnancy is desirable to avoid excessive weight gain andbenefit the mother’s physiological fitness. Aerobicexercise may be particularly beneficial for womenwith a predisposition to gestational diabetes, as itenhances insulin sensitivity.

Other situations

Other at-risk situations that may occur are sum-marized in Table 11.3.

Long-term consequences ofintrauterine events

Studies on animals have over many years shownthat the tissues and organs of the fetus gothrough critical periods in their development, atspecific times in uterine life. It has also been clearthat a positive or negative stimulus occurringduring a critical period can have permanent,

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lifelong consequences, even after that stimulushas been removed or cancelled. This phenom-enon is known as ‘programming’, and in evolu-tionary terms is probably an adaptation toimprove the chances of short-term survival,while having longer term consequences that maybe detrimental. These are less important from theevolutionary perspective, if the consequence isdelayed until post-reproductive life. The rele-vance of programming to humans has only beenrecognized from the mid-1980s, and since thenan enormous amount of research has been pub-lished that shows the fundamental impact ofevents in fetal life on subsequent health of indi-viduals.

Early clues to the need for this research camefrom observations that the distribution of coron-ary heart disease in the 1970s in the UK mirroredpatterns of infant mortality at the start of thetwentieth century. This suggested that events inearly life that caused a high rate of infant deathsmight in some way contribute to a higher risk ofcoronary heart disease in survivors. Followingimprovements in living standards in the middleof the twentieth century, coronary heart diseaserates began to show a decrease in the laterdecades of the century. This fall could not be

attributed to any major changes in adult lifestylefactors. Furthermore, as developing countriesare becoming more Westernized, so prevalenceof coronary heart disease and other Western dis-eases is rising there, in much the same way asthey did in the UK in the middle of the twentiethcentury.

Evidence in support of a link came initiallyfrom data contained in birth and developmentrecords of babies born in the early decades of thetwentieth century, together with mortality recordsof those who have since died and measurementsmade on the survivors. A strong negative correl-ation between weight at birth and the incidenceof coronary heart disease later in life was found(Barker, 1998). This did not apply only to babiesthat could be classified as ‘low birthweight’, butwas true across the whole range of normal birth-weights at full term. This negative associationbetween weight at birth and coronary heart disease has since been demonstrated in severaldifferent study cohorts, in the USA, India andNorway.

Furthermore, relationships have been demon-strated between weight at birth and the presenceof some of the accepted risk factors for coronaryheart disease. The evidence suggests that restricted

Possible indicators of nutritional vulnerability inpregnancyTABLE 11.3

Indicator Possible causesLow nutrient stores Adolescent growth spurtat conception Closely spaced pregnancies

Low BMIIntake affected by povertyHistory of dieting/disordered eating

Poor intake during Poor-quality diet due to: pregnancy (evidenced poverty; lack of interest by poor weight gain) in food; smoking; use of drugs or alcohol

Previous low-weight birthIllness/sickness of pregnancyNegative attitude to pregnancyCultural taboos on diet in pregnancy

Pre-existing or gestational Requires special diet/monitoring of food disease/condition and drug balance during pregnancy

Weight gain/weight loss


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growth during uterine life programmes the fetusin a way that increases subsequent risk of cor-onary heart disease and other degenerative dis-eases. As the mechanisms underlying thesefindings are explored, it has become clear thatbirthweight alone is a crude indicator of changesthat have occurred during uterine life. Changesin body proportions, including thinness, length,head and abdominal circumference are able togive more information about possible organs thatmay have been advantaged or disadvantaged inutero. The ratio of the placental to birthweighthas also shown to be a useful indicator. At eitherextreme, an imbalance between these suggeststhat either the placenta was too small to provideadequate nutrients for the fetus, or it was exces-sively large and, therefore, took a greater share ofnutrients for its own development.

At the cellular level, it is understood thatprogramming may:■ alter gene expression, for example, resulting

in different levels of enzyme activity;■ affect cell division, resulting in fewer cell

numbers within a particular organ;■ influence levels of hormone secretion, or

sensitivity of receptor sites to hormones.Examples of these changes have been demon-strated in animal studies, but application of mod-ern experimental techniques will allow more tobe studied in humans to further the understand-ing of processes that happened in the womb.

Lower birthweight has been associated withthe following conditions.

Higher blood pressureA systematic review of 34 studies by Law andShiell (1996) has shown a consistent decrease in blood pressure for each 1 kg increment inbirthweight. The relationship is less clear duringadolescence but is consistent at other ages. Therelationship with blood pressure is also foundwhen the ratio of placental to birthweight is con-sidered. A disproportion between these weights,in either direction from the normal ratio of 1:6, is associated with a higher blood pressure.A number of mechanisms have been postu-lated to explain these findings. Poor nutrientsupply may compromise renal development, withreduced numbers of nephrons that become more

susceptible to raised glomerular pressure, leadingto hypertension. The involvement of the hypo-thalamus, pituitary and adrenals is considered asa probable mechanism. The model proposes thatthe fetus is exposed to higher levels of cortisol.These may originate from the mother, as a resultof physiological stress, and are insufficientlyblocked by low activity of 11-beta-hydroxysteroiddehydrogenase in the placenta and thus reachthe fetus. Downregulation of this enzyme hasbeen demonstrated in the placenta in the animalmodel. Alternatively, the fetus itself experiencesstress and generates high levels of cortisol. Theraised cortisol levels have multiple effects onthe development and sensitivity of blood vesselsas well as the response of the hypothalamus tosignals from blood pressure receptors.

Insulin resistance and diabetes mellitusMany studies have confirmed the relationshipbetween low weight or thinness at birth with agreater risk of impaired glucose tolerance, insulinresistance or Type 2 diabetes in the adult. Raisedplasma insulin concentrations and slower glu-cose clearance after challenge with glucose haveboth been demonstrated in children who werethin at birth. In adults who were thin at birth,lower rates of energy production from glucose inskeletal muscle during exercise have been shown.These findings have led to the hypothesis that thefetal metabolism responds to a reduced nutrientsupply by reducing its utilization of glucose. Thisis achieved by a reduction in levels of insulin and insulin-like growth factor I and increasedcortisol levels. Skeletal muscle growth and glu-cose uptake are both reduced, and amino acidsand lactate are used for energy. Thus, there isreduced muscle bulk, resulting in a thinner baby,and a relatively lower glucose utilization accom-panied by less responsiveness to insulin. If thismetabolic pattern persists into adulthood, it pre-disposes to the insulin resistance syndrome andType 2 diabetes.

A further consequence of programming thatmay determine glucose metabolism affects thesize and function of the pancreatic cells thatsecrete insulin. Animal studies have shown thatrats fed protein deficient diets produced offspringwith fewer pancreatic islet cells and a reduced

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ability to regulate glucose. Such a situation willresult in insulin deficiency in adult life.

Cholesterol metabolism and blood clottingAnimal studies have demonstrated that impairednutrient supply to the fetus in the latter stages of gestation results in diversion of more oxy-genated blood flow to the cranial region to protect development there. As a result, the trunkand particularly the liver becomes relativelydeprived of nutrients, with the potential for per-manent changes to be programmed at this stage.Studies on rats fed low-protein diets have identi-fied changes in levels of enzymes associatedwith lipid metabolism and blood clotting in theliver. Studies in humans have indicated thatinfants born with a relatively larger head andeither a shorter trunk or smaller abdominal cir-cumference, have raised levels of factors pro-duced by the liver. These include blood-clottingfactors, such as fibrinogen, and cholesterol frac-tions. Both of these may contribute to a higherrisk of coronary heart disease in later life.

Other conditionsOther possible conditions that may have fetal ori-gins have been investigated. For many, there isstill only emerging evidence and more research is needed. These include associations of fetaldevelopment with: various cancers, intelligence,obesity, atopy and food allergies, immune status,polycystic ovary syndrome and osteoporosis. Inaddition, ageing processes appear to be associ-ated with growth and nutrition in early life;lower weight at 1 year has been found to be asso-ciated with increased lens opacity, thinner skin,poorer hearing and reduced muscle strength inold age. Figure 11.4 summarizes the fetal influ-ences on later health.

It should be stressed here that not every smallbaby is destined to have a lifetime of ill-health.The effects of programming are inevitably modi-fied by lifestyle factors. However, it is clear fromthe research to date that the greatest risk ofdeveloping degenerative diseases occurs in thosewho had been small at birth, or small at 1 year ofage and who are then exposed to adverse condi-tions in adult life (such as weight gain, smoking,a high saturated fat diet, lack of exercise).

The largest babies, or the ones who had grownwell in the first year of life, were found to havethe lowest risk of developing these degenerativediseases.

These correlations are strong and show up tothree-fold differences in risk between those withthe highest and lowest birthweights, for example,in the development of impaired glucose toleranceand diabetes. If adult BMI is taken into account,the risk increases to almost seven-fold in thosewho also become overweight.

The most tantalizing aspect of this research isto discover what aspects of maternal diet are thekeys that determine fetal nutrition and develop-ment. There is strong evidence that the uterineenvironment is a major determinant of the size of the fetus. Research from embryo implantationstudies shows that the recipient mother has amuch stronger influence on the size of the babythan the donor mother, even though the baby hasthe donor’s genes.

A fetus whose rate of growth is rapid is muchmore susceptible than one growing more slowlyto a change in the nutrient supply. The latterappears to be better adapted to withstand a fal-tering nutrient supply. A key question, therefore,is what determines the setting of the growth tra-jectory. It is suggested, although human evidenceis lacking, that the nutrient availability aroundthe time of conception is critical in determiningthe partitioning of embryonic cells between fetusand placenta, and sets the rates of growth forboth. The availability of nutrients within themother’s womb may itself be determined by herown development as a fetus, when her ovary anduterus were developing. Thus, there is a strongpossibility of cross-generational effects thatdetermine the growth of a fetus. There is someevidence to support this proposal, both fromstudies on rats, where effects of deficiency maytake up to three generations to be normalized, aswell as from human studies following periods offamine in wartime, where effects have beenobserved in the following generation.

Many populations have lived for generationsin an environment where food supply was poorand the workload heavy; these have been associ-ated with slow fetal growth and small babies.Degenerative disease was relatively rare in these


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populations. As Western lifestyles and food habitsspread across the world, there is likely to be a transition phase, where maternal capacity tonourish a fetus may still be hampered by a pooruterine environment. Babies will continue to beborn small, until the effects of better nutritionimprove the overall health of mothers. Thus,

there is likely to be an increase in degenerativedisease, as small babies become overweightadults, poorly adapted to the plentiful food supplies and lower workloads. This transitionphase occurred in the West in the middle of thetwentieth century, with a high prevalence ofdegenerative diseases, but may now be nearing

Figure 11.4 Summary of fetal influences on later health.

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its end, with a decline in some of these diseases.However, developing countries may still be facing the upsurge of diseases, such as coronaryheart disease, as they enter the transition phase,especially in urban areas.

Translating this research into practicaladvice for pregnant women, or those intendingto become pregnant is still very difficult. There is insufficient evidence to pinpoint dietarychanges that should be made, but overall adviceto prepare nutritionally for pregnancy and tomaintain healthy eating throughout mustremain as the guiding principle. The practice ofsupplementing the diet during pregnancy maynot be beneficial, as the determinants of growthare set very early, before the pregnancy is con-firmed. Small babies need to be monitored andthe importance of healthy weight and lifestylestressed in this group, as they have greater vul-nerability to disease than those whose weight atbirth was higher. The next decade may bringmore detailed information about this fascinatingarea of study.

The nursing or lactatingmother

Breastfeeding a newborn infant is the naturalsequel to pregnancy. The process of lactation (ormilk production) does not occur in isolation sincethe mother’s breasts become prepared for lacta-tion throughout pregnancy. By no means allmothers choose to breastfeed their babies. In theUK, prevalence of breastfeeding at birth isaround 64 per cent, although there are great dif-ferences between middle-class mothers, of whomover 80 per cent may start breastfeeding, andlower social class mothers, where the prevalenceis in the order of 25 per cent. For mothers whochoose to breastfeed, it is usually a special andenjoyable experience. Those mothers who decidenot to breastfeed can provide adequate nutritionfor their babies using the many formula feedsavailable. However, certain aspects of humanmilk will not be present in the formula. These arediscussed further in Chapter 12.

If a woman decides not to breastfeed her child,the breasts return to their normal pre-pregnantsize within a fairly short period of time.

The process of lactation

There are two stages involved in lactation: milkproduction and milk ejection (see Figure 11.5).

Milk production or lactogenesis

Milk is made in the mammary glands of thebreast, which contain cells arranged in lobules.The synthesis of milk is stimulated by the hor-mone prolactin released from the anterior pitu-itary gland, which in turn is stimulated by theprocess of suckling by the infant at the breast.Thus, the more the infant suckles, the more milkis synthesized and milk production parallelsdemand.

Some proteins found in milk, such as theimmune factors, enter from the maternal circu-lation, but the majority of the protein content issynthesized by the mammary glands. The fatsthat contain short-chain fatty acids are synthe-sized in the breast, but the long-chain fats arederived from the maternal diet. A mother whoconsumes a high level of long-chain fats will,therefore, have higher levels of them in hermilk. The galactose part of the lactose moleculeis synthesized in the breast, the glucose part isderived from the maternal circulation.

Milk ejection or let-down

The milk that is formed is not released from thebreast until the baby suckles. This initiates areflex in the mother, involving signals to thehypothalamus, which in turn cause the releaseof the hormone oxytocin from the posteriorpituitary gland. It is this hormone that causesthe specialized cells in the mammary gland tocontract and eject the milk into the mouth ofthe infant. The reflex can be inhibited by themother’s mental state: if she is apprehensive,tense or tired, the reflex can fail and milk is notreleased. An understanding of the nature of thereflex, which allows sufficient relaxation andpreparation for feeding, can prevent a great dealof frustration. After about 2 weeks of breast-feeding, the reflex becomes automatic and canbe triggered simply by hearing the baby crying.


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Diet in lactation

As with pregnancy, no special diet is needed inlactation. It must be remembered, however, thatthe food eaten by the mother in the first 4–6 months of breastfeeding (before weaningtakes place) has to meet all of her own needs aswell as those of the baby, which are consider-ably greater than its needs while in the womb.These increased requirements are reflected inthe higher dietary reference values published by

the UK Department of Health (DoH, 1991) andsummarized in Table 11.4.

Energy

The average daily volume of milk producedvaries from mother to mother. Data from the UKand Sweden indicate that the average volume ofmilk produced in the first 3 months of lactationranges from 680 to 820 mL/day. The energy cost

Figure 11.5 The process of lactation.

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of producing this milk, assuming an 80 per centefficiency of energy conversion, has been calculated as 2.38–2.87 MJ (570–690 Calories)per day in the first 3 months. After 3 months,and assuming that weaning begins at around 4 months, the output of milk falls to 700 mL/day,with an energy cost to the mother of 2.45 MJ(590 Calories) per day.

Some of this extra energy can be met fromfat stores laid down in pregnancy, although the extent to which this is mobilized appears to vary between women. It is assumed that, onaverage, 0.5 kg of stored fat is used per month,although women have been recorded as losingbetween 0.6 and 0.8 kg/month during the first4–6 months after delivery. In overweight women,a loss of 2 kg/month may be possible, but feed-ing on demand should continue to ensure thatadequate milk production is maintained. Under-taking intense exercise to speed up weight losscan raise lactic acid levels in the blood, whichwill pass into the milk and affect the taste.

However, moderate exercise is beneficial andshould be encouraged, as long as energy needscontinue to be met.

Dietary energy restriction may affect milkoutput, particularly in the first weeks before lactation is fully established. However, it is alsopossible that milk output is only compromisedwhen body fat stores are below a particularthreshold level. It is also important to recognizethat restricting energy intake to a low level willhave consequences for the quality of the diet,and may result in other nutrient requirementsnot being met. There is a concern that toxicchemical residues, which may be present inmaternal body fat, will be mobilized and secretedin the milk, if fat stores are used as a source ofenergy. There is little evidence, however, onwhich a judgement can be based.

In women who are chronically undernour-ished and, therefore, have very low body fatreserves, lactation can still occur satisfactorilyeven in these apparently adverse circumstances.

Dietary reference values for lactationTABLE 11.4Nutrient Recommended levelEnergy Additional 450–570 kcal (1.9–2.4 MJ)/day at 1–3 months

Additional 480 kcal (2.0 MJ)/day between 3 and 6 monthsProtein To cover protein content of milk, increase by 11 g/day; total recommended 56 g/dayVitamin A To cover content in milk, increase by 350 �g/day; total recommended 950 �g/dayThiamin Increase only in line with increased energy requirementRiboflavin To cover extra content in milk, and its secretion, increase by 0.5 mg/day; total

recommended 1.6 mg/dayNiacin To cover extra content in milk, increase by 2.3 mg/day; total recommended 8.9 mg/dayPyridoxine No evidence exists of a need to increase intakeVitamin B12 To cover the content in milk, increase by 0.5 mg/day; total recommended 2.0 mg/dayFolate To cover the content in milk, and absorption and utilization by the mother, increase by

60 �g/day; total recommended 260 �g/dayVitamin C To cover content in milk and maintain maternal stores, increase by 30 mg/day; total

recommended 70 mg/dayVitamin D To maintain plasma vitamin D levels: recommend a supplement of 10 �g/dayCalcium To cover content in milk and allow for efficiency of absorption by mother, increase by

550 mg/day; total recommended 1250 mg/dayMagnesium To cover content in milk, and allow for absorption, increase by 50 mg/day; total

recommended 320 mg/dayIron Extra content in milk can be met by lactational amenorrhoea; thus, no extra incrementZinc To cover zinc content of milk; no information about enhanced absorption is available;

thus increase by 6 mg/day; total recommended 13 mg/day



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Studies suggest that the greater efficiency ofmetabolism seen in pregnancy carries throughinto lactation, so that costs of maintaining themother’s body remain low, thus providing extraenergy for milk production. However, the nutri-tional content of the milk probably starts to fallfrom the third or fourth month of lactation.

Protein

The protein content of milk supplies the aminoacids necessary for the growth of the baby, andthe additional amount should be provided in themother’s diet. If the diet contains sufficientextra energy to satisfy those needs, then theprotein content will also be adequate. On a poordiet, where the total food supply is inadequate,it is not possible to provide additional protein,but protein levels in the milk are maintained forseveral months even under these circumstances.

General considerations

It can be seen from Table 11.4 that nutritionalneeds in lactation are greater than those in

pregnancy. However, if a mother satisfies herneed for additional energy, then the increasedneeds for all the other nutrients should be met,assuming the extra food eaten is well-balanced.

Nutrients that warrant special attention arecalcium, and vitamins A and D. If it is not pos-sible to increase food intake, then the nutritionalquality of the milk may suffer. The water-solublevitamins, B complex and C, will be present insmaller amounts. The other constituents, namelyfats, lactose, protein and fat-soluble vitamins,may remain at an adequate level for 3–4 months,but will then decline. The weight gain of the babymay slow down or stop at this point, and alterna-tive sources of food will be needed for the baby.

The decision to breastfeed

Human milk is ideally suited to the needs of the human infant. Nevertheless, a significantnumber of mothers do not take advantage of theprocess of lactation for a number of reasons. Thearguments for and against breastfeeding fromthe mother’s perspective are briefly reviewed and summarized in Figure 11.6. An additional

Figure 11.6 Arguments for and against breastfeeding.

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advantage of breastfeeding is that it has beenshown to protect women against breast cancer;this may explain the higher rates of breast cancerin developed than in the less developed countries.

The benefits of breastfeeding are discussedfurther with respect to the infant in Chapter 12.

Because the decision to breastfeed or not isbased on so many deeply held beliefs, it shouldbe respected, and mothers who choose not tobreastfeed should not be made to feel that theyare failing their baby in any way. What mattersfor the mother and infant is that the mother isconfident with what she is doing and can pro-vide all of the nutritional needs that her childrequires. She can achieve this with formula milkor by ensuring that her own nutrition is ade-quate to provide good-quality milk for as longas she wishes to feed her infant.

1 Carry out a small survey among your col-leagues. Ask whether they have opinionsabout breastfeeding and try to relate these totheir own experience of breastfeeding. Thismay include seeing siblings breastfed, havingbreastfed an infant themselves or having seenfriends breastfeeding.■ Is there a gender difference in opinion?■ Is there an age difference?■ Do the opinions you collect match those

given in Figure 11.6?■ Can you add others to the list?

2 In what ways do you think health promotioncould persuade people to breastfeed theirchildren?

Activity 11.2

1 The outcome of pregnancy for both the mother and infant depends on nutritional status of the mother.2 Nutritional status prior to pregnancy may determine fertility and the early development of the embryo.3 During pregnancy, the first 3 months are the most critical from the nutritional perspective, as the

placenta is not fully developed and the fetus depends entirely on the concentrations of nutrients in themother’s circulation.

4 The needs for some nutrients increase more than others. All nutritional needs can be met from abalanced diet, eaten in sufficient amounts. Many adaptations occur in the mother’s body to ensureadequate nutrient supplies.

5 The nutrient supply to the fetus may not only determine the birthweight but also set up the programmefor potential health in future years.

6 Lactation is a sequel to pregnancy and also requires adequate nutrition.7 The quality of the milk is largely protected from shortcomings in the mother’s diet for the first 3 months

of lactation by increased efficiency in maternal metabolism.

SUMMARY

1 Why is it important for a woman to benutritionally fit at the time of conception?

2 Metabolic adjustments occur in a woman duringpregnancy. In the following cases, state whatthe adjustments are and their consequences fornutritional intake or needs:a appetiteb digestive tract functionc metabolic rate.

3 Design a poster or leaflet giving practical dietary advice for pregnancy.

4 Why might the following be particularlynutritionally vulnerable while pregnant:a vegetariansb women on a low incomec young adolescent girls (aged 13–15)?

5 Identify five reasons commonly cited by womenagainst breastfeeding and consider how you mightoffer a positive view to counter each reason.

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Allen, L.H. (ed.) 1994: Recent developments in maternal nutrition and their implications for practi-tioners. American Journal of Clinical Nutrition 59(2) (suppl.), 439–541.

Anderson, A.S. 2001: Pregnancy as a time for dietary change? Proceedings of the Nutrition Society60, 497–504.

Barker, D.J.P. 1998: Mothers, babies and health in later life. Edinburgh: Churchill Livingstone.Czeizel, A.E. 1993: Prevention of congenital abnormalities by periconceptional multivitamin

supplementation. British Medical Journal 306, 1645–8.DoH (UK Department of Health) 1991: Dietary reference values for food energy and nutrients for the


Doyle, W., Crawford, M.A., Wynn, A.H.A. et al. 1990: The association between maternal diet andbirth dimensions. Journal of Nutritional Medicine 1, 9–17.


edn. Cambridge: The Royal Society of Chemistry.Frisch, R.E. 1994: The right weight: body fat, menarche and fertility. Proceedings of the Nutrition

Society 53, 113–29.Godfrey, K.M., Barker, D.J.P. 2001: Fetal programming and adult health. Public Health Nutrition

4 (2B), 611–24.Goldberg, G. 1994: Human pregnancy and lactation: physiological metabolic and behavioural strategies

to maintain energy balance. British Nutrition Foundation Nutrition Bulletin 19(Suppl.), 37–52.Goldberg, G., Prentice, A.M. 1994: Maternal and fetal determinants of adult diseases. Nutrition

Reviews 52(6), 191–200.HEA (Health Education Authority) 1996: Folic acid – what all women should know (leaflet).

London: HEA.Jackson, A.A., Robinson, S.M. 2000: Dietary guidelines for pregnancy: a review of current evidence.

Public Health Nutrition 4(2B), 625–30.Langley-Evans, S.C. 2001: Fetal programming of cardiovascular function through exposure to

maternal undernutrition. Proceedings of the Nutrition Society 60, 505–13.Law, C.M., Shiell, A.W. 1996: Is blood pressure inversely related to birth weight? The strength of evi-

dence from a systematic review of the literature. Journal of Hypertension 14, 935–41.Livingstone, V. 1995: Breastfeeding kinetics: a problem-solving approach to breastfeeding difficul-

ties. World Review of Nutrition and Dietetics 78, 28–54.Marabou Symposium 1996: Early nutrition and lifelong health. Nutrition Reviews 54(2), 1–73.Rasmussen, K.M. 1992: The influence of maternal nutrition on lactation. Annual Review of

Nutrition 12, 103–17.Sayer, A.A., Cooper, C. 2002: Early diet and growth: impact on ageing. Proceedings of the Nutrition

Society 61, 79–85.Yajnik, C. 2000: Interactions of perturbations in intrauterine growth and growth during childhood

on the risk of adult-onset disease. Proceedings of the Nutrition Society 59, 257–65.

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Infants, children andadolescents


❏ describe the nutritional needs of the normal infant and how these are met by human and formula milks;❏ discuss the process and objectives of weaning and consider the problems that might arise;❏ consider the diets of pre-school children and the key nutritional principles to be addressed in this group;❏ discuss the diets of school-age children, including adolescents;❏ consider the special nutritional dilemmas encountered by teenagers.


❏ explain the relative merits of human and formula milks in feeding normal infants and how these may need to bemodified for infants with particular needs;

❏ relate nutritional needs and intakes to the development of the child;❏ explain some of the reasons why intakes may not be nutritionally sound in school age children;❏ suggest ways in which nutritional intakes in adolescents could be improved.

Adequate dietary intake and nutritional statusamong children are important for their owngrowth and development and function. However,there is now also evidence that childhood nutri-tion influences adult health. Research has shownthat intrauterine nutrition influences adult mor-bidity and mortality, but childhood diet andnutritional status can modify the consequencesof being born small. Diet in all the stages ofchildhood needs to be taken seriously because ofits potential for producing normally developedchildren as well as determining their lifelonghealth and thus having an impact on a nation’shealth. With many diets in transition owing tochanging social, economic and environmentalconditions, consideration of the impact of thesechanges on the diets of children is important.Particular issues of concern include the estab-lishment of good dietary habits, together withadequate physical activity to prevent the devel-opment of overweight, adequate intakes of cal-cium to promote bone health, and sufficientintakes of minerals and vitamins in the face of a

culture often centred on fast food. There aremany gaps in our current understanding of children’s food habits and influences on these. It is difficult to obtain good-quality informationabout these and, therefore, health promotioninputs may be missing their target.

Infants

Infants are totally dependent on other people fortheir food supply. During the first year of life,there is very rapid growth, so for its age and size the infant has very high nutritional needs.Neither of these situations normally occur againin a healthy individual. The main aim of infantfeeding is to satisfy nutritional needs in the bestpossible way, and to achieve a healthy infantwho is growing at the appropriate rate anddeveloping normally. Although the main empha-sis here is on the principles of feeding normalinfants, it must be remembered that infants who are premature, ill, disabled or with anyother special needs can also be fed successfully,

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often by only minor adjustment of the normalpractice.

Growth

Babies grow faster in their early months andmore slowly in the latter part of the first year.An infant’s birthweight is doubled within 4–6months and trebles within the first year.

Growth is slower thereafter, and the weightat 5 years is on average twice that of the weightat 1 year. Standard growth curves (see Figure12.1) are used to monitor a child’s developmentin terms of height and weight. They are based onpercentiles, which represent the range of expectednormal results in a group of children. The pos-ition of any one child represents their rank if 100children had been measured. Monitoring weightand height at intervals allows a child’s progressto be followed. Deviations over time from thechild’s usual curve may indicate faulty nutrition,perhaps as a result of concurrent illness. Thismay be seen frequently in children in developingcountries, who may experience periods of infec-tion, possibly often in addition to chronic poornutrition, resulting in slowed growth.

As in uterine life, post-natal growth may beslowed owing to insufficient cell multiplicationor cell growth. The timing of poor nutrition willdetermine which aspect of growth is affectedmore. If fewer cells are made, then it is impos-sible for this to be remedied later by better nutri-tion. However, failure of cells to grow may becompensated by ‘catch up’ growth, if nutritionimproves. Key periods of cell multiplicationoccur at different times for different organs.Brain development, for example, occurs veryrapidly in the first months after birth and cellmultiplication stops by the age of 12–15 months.Although growth continues, the brain is almostat adult size by the age of 5 years. Thus, infancyand childhood are critical periods for nutrientsupply to the brain. There has been considerabledebate about critical periods for fat cell forma-tion and some evidence suggests that overfeed-ing in infancy may encourage multiplication offat cells. These may be associated with higherleptin levels and possible leptin resistance in laterlife. However, this requires further study.

Growth may also be affected by emotionalfactors and stress. Where possible, the causeshould be investigated and rectified as quicklyas possible to prevent long-term consequences.

Nutrition and development

An infant born at full term is able to suck, but isnot able to bite or chew pieces of food, so thatits diet of necessity is a liquid one. The liquiddesigned by nature as food for the newborn ismilk produced by its mother. This provides notonly nourishment, but also immune protectionand developmental stimuli.

Alternative milks have been developed; theseare highly modified to make them suitable forinfants. In Britain, two types of milks derivedfrom cows’ milk are available: whey-dominanttypes based on the dialysed whey protein, andcasein-dominant types based on the entire proteinfraction. Modern milks are as similar in compos-ition to human milk as is possible, however, theylack the immunological and hormonal factors.Modified soya milks and other hydrolysed proteinformulas have also been developed to meet theneeds of children with diagnoses of allergy.

From about the end of the third month of life,the baby can cope with a rusk or cereal mixedwith milk, by sucking it or swallowing it withsaliva. The ability to bite and chew lumps of foodbegins at 5–6 months, and it is at this stage thatan increasing variety of tastes and textures canbegin to be introduced into the baby’s diet. Anability to chew lumpy food by 6–7 months is animportant developmental step and chewing isbest learned at this age. If it is delayed, the childmay have difficulty in learning to chew later. Theability to chew is also related to early speechdevelopment. Early feeding is thus an importantpreparation for verbal communication.

By the age of 1 year, the infant has pro-gressed from a newborn only able to suck liquidsfrom a nipple or teat, to increasing independ-ence of eating, and attempting to feed itself. By this age, a child may have up to eight teeth,which help in the biting and tearing of food.Molar teeth for proper grinding of food developlate in the second year, when chewing abilitybecomes more fully developed.

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Figure 12.1 Example of a standard growth curve used to monitor child development. (©Child Growth Foundation.Copies of the chart may be purchased from Harlow Printing, Maxwell Street, South Shields NE33 4PU, UK.)


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Development of the digestive tractIn the young infant, digestive enzymes are notfully developed and certain dietary componentsmay not be readily digested. Only small amountsof lipase are produced by the pancreas duringthe first 3 months, and pancreatic amylaseincreases only after 6 months. Breastfeeding isbelieved to promote the release of gastrin andcholecystokinin in the infant, and may promoteboth the digestive process and the developmentof the gut. A young infant has the ability toabsorb some undigested protein. This is particu-larly important for the absorption of antibodiespresent in maternal milk or colostrum during thefirst days of breastfeeding. However, it may alsoresult in the absorption of proteins, such as eggalbumen or lactoglobulin from cows’ milk, ifthese are consumed in the early part of infancy.These proteins will generate antibodies withinthe infant and may lay the foundations of futureallergic reactions. There is concern about earlyexposure of infants and children to peanuts insome weaning foods. A rapid increase in theincidence of peanut allergy, which can be lifethreatening, is believed to be linked to this earlysensitization.

Nutritional needs

It must be assumed that the nutritional needs ofthe infant are ideally met by breast milk, when

this is produced in sufficient quantity by a fullybreastfeeding mother. For this reason, the UKDepartment of Health (DoH, 1991) took the viewthat no dietary reference values were requiredfor breastfed infants. Values were, therefore, setfor formula-fed infants, which are based on thenutritional composition of breast milk and theaverage amounts consumed. In addition, someallowance is made in certain cases for poorerefficiency of digestion and absorption of thenutrients in formula milks.

Dietary reference values for infants areshown in Table 12.1.

EnergyEnergy needs are determined primarily by body size and composition, physical activityand rate of growth. Infants have a high basalmetabolic rate owing to the large proportion of metabolically active tissue and the large loss of body heat over a relatively great surfacearea. In the second half of the first year, thegrowth rate slows, but the level of activityincreases as the child starts to crawl and thenlearns to walk around the age of 1 year. Totalenergy expenditure in infants has recently been measured using the doubly labelled watertechnique, which has produced lower resultsthan had been previously reported. Results from studies of energy intakes confirm these results.

Reference nutrient intakes for selected nutrients for infantsTABLE 12.1Nutrient 0–3 months 4–6 months 7–9 months 10–12 monthsProtein (g/day) 12.5 12.7 13.7 14.9Thiamin (mg/day) 0.2 0.2 0.2 0.3Riboflavin (mg/day) 0.4 0.4 0.4 0.4Niacin (nicotinic acid equivalents) 3 3 4 5

(mg/day)Folate (�g/day) 50 50 50 50Vitamin C (mg/day) 25 25 25 25Vitamin A (�g/day) 350 350 350 350Vitamin D (�g/day) 8.5 8.5 7 7Calcium (mg/day) 525 525 525 525Iron (mg/day) 1.7 4.3 7.8 7.8Zinc (mg/day) 4.0 4.0 5.0 5.0

From DoH, 1991. Crown copyright is reproduced with the permission of the Controller of Her Majesty’s Stationery Office.

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Table 12.2 shows the gradual reduction inthe energy requirement per kilogram of bodyweight as growth rates slow down; however, asbody size increases, the total energy needsbecome greater. The energy requirement for chil-dren is up to four times greater than that of theadult, when expressed per unit of body weight.This emphasizes the special need for adequateenergy and explains why a shortfall of energymay have such serious consequences for growth.ACTIVITY 12.1

ProteinIn infants, the role of protein is almost entirely tosupport growth. The infant requires more proteinper unit weight than the adult, and has a par-ticular requirement for the essential amino acidshistidine and taurine. Human milk provides a relative excess of some of the amino acids (gluta-mine, leucine and isoleucine) needed for tissue

synthesis, and relatively lower levels of others(arginine, alanine and glycine). This means thatthe neonate has to be very efficient in transform-ing some amino acids into others to fulfil needsfor tissue synthesis. Adequate amounts of feedshould be provided to allow the protein to beused for growth, rather than to meet the energyneeds. Excessive amounts of protein are undesir-able and may be harmful to the infant, as theyincrease the amounts of waste material to beexcreted in the urine, and might result in dehy-dration. In addition, immature kidneys cannotadequately filter high molecular weight proteins.

FatsFat should comprise 30–50 per cent of an infant’senergy intake and, above this level, it may bedigested poorly. In breast milk, fats supply 50 percent of the energy. Fats are an important part ofan infant’s diet because of their energy density,that is, they provide a substantial amount ofenergy in a relatively small volume. The essentialfatty acids found in milk, and particularly thelong-chain n-3 acids, are important for develop-ment of the brain, vascular systems and retina inearly months of life. In particular, docosa-hexaenoic acid may not be synthesized in suffi-cient amounts by the infant from precursors inthe diet to meet the needs of tissue development.

CarbohydratesCarbohydrate, predominantly in the form of lac-tose, supplies 40 per cent of the energy in aninfant’s diet. Lactose yields glucose and galact-ose on digestion; the latter is essential in the

The estimated average requirement (EAR) for energy for children up to theage of 12 monthsTABLE 12.2

Age Average weight (kg) Requirement/kg EAR (kJ (Cal))(months)

Boys Girlsbody weight

Boys Girls(kJ (Cal))

1 4.15 4.00 480 (115) 1990 (480) 1920 (460)3 6.12 5.70 420 (100) 2570 (610) 2390 (570)6 8.00 7.44 400 (95) 3200 (760) 2980 (710)9 9.20 8.55 400 (95) 3680 (880) 3420 (820)

12 10.04 9.50 400 (95) 4020 (960) 3800 (910)


Using the information in Table 7.6, calculate theequivalent energy needs per kilogram body weightfor adults. Assume that the average adult maleweighs 75 kg and the adult female 60 kg.■ Compare your figures for adults with those for

infants, shown in Table 12.2.■ What is your own energy need per kilogram of

body weight?■ Calculate the protein need per kilogram for

both infants and adults (use the informationin Table 4.5).

Activity 12.1


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development of the brain and nervous system.Undigested lactose is fermented in the digestivetract to lactic acid and lowers the pH. This isbeneficial as many of the pathogenic organismsthat can cause gastroenteritis do not thrive in anacidic environment. Infants can also digest andutilize sucrose, although this sugar is sweetertasting than lactose and can induce a preferencefor sweet foods in the infant. The ability todigest starch is limited.

FluidBecause of their relatively small total body watercontent, babies have a vital need for fluids. Theirsmall body weight/surface area ratio makesthem susceptible to dehydration, for example, inhot weather and illness. As an absolute min-imum, the normal infant requires daily between75 and 100 mL of fluid per kilogram bodyweight, and should be provided with 150 mL/kg,to ensure that all needs are met. Under normalcircumstances, this amount of fluid is providedby the milk feed and no additional water isrequired.

The infant loses water through the skin andrespiratory tract, through sweating in warmenvironments and through the urine and faeces.The volume of urine produced is dependent onthe fluid intake and on the amount of solutes tobe excreted. An adult kidney is able to concen-trate solutes and reduce water loss, if fluid intakeis low, but a baby’s kidneys initially lack thisability. Thus, feeding a diet with a high ‘soluteload’, in particular with high protein and sodiumcontents, results in increased water loss via the kidney. Under normal circumstances, fluidintake should be sufficient to cope with this.However, difficulties may arise if:■ a baby is given an overconcentrated feed

(unmodified cows’ milk is inappropriate forthis reason);

■ amounts of feed are very small (due to illness);

■ there is fluid loss via other routes (vomiting,diarrhoea, sweating);

■ solids are given at a very young age (below2 months).

In each of these cases, additional water shouldbe given to avoid dehydration.

MineralsBabies require a wide range of minerals in theirdiet. These include calcium, phosphorus andmagnesium for bone development, iron and cop-per for red blood cell formation, zinc for celldivision and growth, together with other traceelements. The iron content present at birth hasusually been used in red blood cell formation by4–6 months, and an additional source of iron isneeded at this stage. Calcium and phosphorus arepresent in equimolar quantities in human milk,which matches the ratio in the body. An exces-sive intake of phosphorus can dangerously lowercalcium levels. This is a particular problem inpremature infants and those fed on unmodifiedformula. The minerals in human milk are associ-ated with the protein or fat fractions of the milk,which probably facilitates their availability.

VitaminsThe vitamin content of milk is generally adequate, with the exception of vitamins D and K.Human milk is low in vitamin D and the UKDepartment of Health (DoH, 1991) recommendsthat breastfeeding mothers should take a vita-min D supplement of 10 �g/day to ensure adequate levels in their milk, especially in thewinter months. Formula-fed infants receiveadequate levels of the vitamin.

Breastfed infants are also at risk of low vita-min K intakes. It has been routine practice togive newborn infants a dose of the vitamin inthe first days of life by intramuscular injection.Although the evidence is not clear-cut, there hasbeen concern that this may increase the risk ofchildhood cancer and oral administration of thevitamin is now recommended until the issue hasbeen clarified.

Meeting nutritional needs

A baby’s nutritional needs are generally meteither by the use of human milk from the breastor formula derived from cows’ milk, modified toa composition resembling that of human milk.The continued development of formula milksensures that they come closer to the content of human milk than ever before. In Westernsocieties, mothers are free to make the choice

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between breastfeeding and bottle-feeding, with-out fear that their baby will be disadvantaged inany way as a result of their decision. The pro-fessional consensus is that breastfeeding is bet-ter for the baby, and possibly confers benefits tothe mother. In many poor areas of the world, theuse of infant formula may increase health prob-lems rather than solving them. Where standardsof hygiene are poor, with inadequate water sup-plies and non-existent or poor sanitary facil-ities, it is almost impossible to prepare artificialfeeds with the degree of cleanliness necessary toprevent infection. In addition, poverty maytempt the mother to prepare excessively dilutefeeds in an attempt to extend the supply of themilk powder. This can and does lead to seriousmalnutrition in the infant. In such a situation,the only safe choice for infant feeding is withhuman milk from the breast. The spread of for-mula milk throughout poor regions of the worldhas resulted not only in greatly increased deathsfrom infection in infants, but has also removedthe birth-spacing benefits of breastfeeding.

Breastfeeding or bottle-feeding?

Across the world there are programmes andactivities to promote breastfeeding, since it isrecognized as nutritionally the best way of feeding the newborn infant. The World HealthOrganisation (WHO) and the United NationsChildrens Fund (UNICEF) jointly promote theBabyfriendly Hospital Initiative (BFHI), whichencourages hospitals to put in place a number ofmeasures that will facilitate the initiation andcontinuation of breastfeeding. Some 15 000 hospitals have been certified as Babyfriendlyaround the world, with around 260 in industrial-ized countries.

A series of studies on behalf of the Departmentof Health in the UK has taken place since 1975 to provide national statistics on the incidence,prevalence and duration of breastfeeding andother feeding practices adopted in the earlyweeks and months after birth. The most recentlyreported of these was carried out in 2000(Hamlyn et al., 2002). The survey identified thereasons given by mothers for the choice of

infant feeding method. Most women decidebefore the birth how they will feed the baby. Thedecision is based on the mother’s own attitude tothe idea of breastfeeding, but is also influencedby the views of her mother, friends and partner.Previous experience of feeding is also a stronginfluence.

Breastfeeding is more likely in mothers fromsocial class 1, compared with social class 5.However, there have been marked increases inprevalence among women in social class 5 sincethe earlier surveys. There is also a higher preva-lence among older mothers, ranging from 46 percent in teenage to 78 per cent in mothers over 30 years. Improvements have also been noted inprevalence among mothers educated to age 16(to 54 per cent), where the rates had been lowest,compared with rates in those educated beyondthe age of 19 years (88 per cent prevalencereported).

Reasons cited for choosing breastfeeding aregenerally very positive, including that it is thebest and most natural way of feeding the baby(79 per cent of respondents said this) and that itis convenient (37 per cent said this). Other rea-sons mentioned included that it develops a closerbond with the baby, is cheaper and more natural.Those who choose to bottle-feed have more neg-ative views about breastfeeding, considering thatthey would be tied to the baby and wanted othersto be able to feed it (25 per cent), worrying abouthow much milk the baby receives and generallyfinding the idea distasteful (19 per cent).

The attitude of society in general is import-ant in helping women make the choice, and insupporting and helping breastfeeding mothers.Unfortunately, many people have negative attitudes to breastfeeding, considering it inap-propriate and even shameful behaviour, espe-cially if carried out, however discreetly, in public;this can affect the new mother. The ambivalentview of society about the function of breastscan make it difficult for some women to con-sider feeding their baby themselves.

There has been an increase since 1990 in thenumber of women attempting to breastfeed theirbaby, with 71 per cent starting to breastfeed inEngland and Wales (and 63 per cent in Scotland,54 per cent in Northern Ireland). The overall


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figure for the UK is 69 per cent. However, thenumbers who continue to breastfeed decreasequite rapidly, falling to 52 per cent by 2 weeks,42 per cent by 6 weeks and 28 per cent by 4 months. However, 13 per cent of mothers were still breastfeeding at 9 months. These ratesare lower than in most other north Europeancountries.

The most common reasons for stopping inthe early weeks were given as rejection of thebreast by the baby and painful nipples. However,when feeding continued for more than a week,but had stopped by 4 months, insufficient milkwas the most commonly cited reason for stop-ping. In reality, this should rarely be a reason forfailure to breastfeed, and probably representsinadequate support and information being madeavailable in the first days of breastfeeding whilethe process is becoming established. More helpfor new breastfeeding mothers could increasesuccess rates. An additional reason for stoppingbreastfeeding between 4 and 6 months was thatthe mother was returning to work (mentioned by39 per cent of respondents).

Overall, this survey shows an encouragingimprovement in incidence and prevalence ofbreastfeeding. In particular, improvements haveoccurred in those groups where previous levelsof breastfeeding had been lowest.

Formula milk and breast milk compared

The composition of formula milks available in Britain is governed by a directive from theEuropean Commission (EEC, 1991), and StatutoryInstrument 77 (MAFF, 1995). Derived from cows’milk, they are classified as ‘casein-dominant’,based on the entire protein fraction, or ‘whey-dominant’, containing the dialysed whey protein.Modifications include the addition of lactose,maltodextrins, vegetable oils, various vitaminsand trace elements, and reductions in the level ofprotein, electrolytes and some minerals, such ascalcium.

Bottle-feeding, if carried out correctly, withdue attention to hygiene, appropriate concentra-tions and closeness during the feeding, can pro-vide most of what the infant needs. However, theunique composition of human milk, with over

200 constituents and with a varying content,will probably never be matched by a manufac-tured formula feed. The composition of breastmilk is not constant between women and withinthe same woman for different lactations andeven during the day. The milk secreted towardsthe end of a feed (hind milk) is richer in fat and,therefore, higher in energy value than the foremilk, at the start of the feed. This may play a partin appetite control, with the richer hind milkproviding a feeling of satiety. Obviously, thiscannot happen with a formula feed.

Proteins in milkThe proteins in human milk are predominantlywhey proteins, including alpha-lactalbumin,lactoferrin and various immunoglobulins; caseinforms only 30–40 per cent of the total protein.Although the lactalbumin is a major source ofamino acids, the other whey proteins have anon-nutritional role, in particular, as protectiveagents (see below for their role in immunity).

In cows’ milk, casein comprises 80 per centof total protein, which can form tough, leatherycurds in the stomach and be more difficult todigest. In the formula milks based on whey, thecasein content is reduced (from 27 g/L in cows’milk, to 6.0 g/L). Beta-lactoglobulin, which isnormally found in cows’ milk and is a potentialallergen, is also absent from these formulamilks.

Human milk also contains non-proteinnitrogen compounds, including taurine, urea,and a number of hormones and growth factors.Their functions are still uncertain but may wellhelp with the normal development of the infant.Until their function is clearly defined, it isunlikely that these substances will be includedin formula milks.

Carbohydrates in milkLactose concentrations in human milk aregreater than in cows’ milk, although levels informula are similar. Formula milks may alsocontain maltodextrin as a source of carbohy-drate. Lactose enhances the absorption of cal-cium as a result of the lower pH resulting fromfermentation to lactic acid, which makes thecalcium more soluble.

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Fats in milkAlthough the total fat contents of human andcows’ milks are similar, the fatty acid com-positions are quite different. Modified milkscontain added oils to increase the unsaturatedfatty acid content towards that of human milk.Nevertheless, there remains a much greater diver-sity of lipids in human milk, which contains cho-lesterol, phospholipids and essential fatty acids.Digestion and absorption of fat from human milkis aided by the presence of lipase within the milksecretion, which starts the process of digestionbefore the small intestine is reached. Some milkshave been reformulated to include more essentialand long-chain fatty acids.

VitaminsThe levels of the water-soluble vitamins in milkreflect the maternal levels, and thus rely on asufficient intake by the mother. In the West, it israre for vitamin levels to be deficient in milk dueto maternal undernutrition. Human milk alsocontains binding factors for folate and vitaminB12, which facilitate their absorption. Most for-mula milks contain levels of the vitamins greaterthan those found in human milk. However, apartfrom vitamins D and K, for which intake may betoo low from human milk, there appears to be noadvantage in this.

MineralsLevels of many minerals are modified in themanufacture of formula from cows’ milk. This isbecause their concentrations would generally betoo high for the human infant to cope with. Inparticular, this applies to calcium, phosphorusand the electrolytes. Many of the minerals areassociated either with proteins or fat globules,and this appears to facilitate their absorption.Specific binding factors have been identified foriron and zinc, which make the absorption ofthese minerals from human milk much greaterthan that from formula.

Immunological factorsApart from the nutrients and water, human milkcontains a number of other constituents. Mostimportantly, it contains a range of substancesthat enhance the immune system of the baby.

Among these are:■ white blood cells – T and B lymphocytes,

neutrophils and macrophages;■ immunoglobulins, which are the circulating

antibodies;■ lysozyme, which has specific antibacterial

action;■ lactoferrin, which binds iron to prevent its

uptake by bacteria that need it for growthand replication, and also promotes growthof Lactobacillus sp.;

■ bifidus factor, which promotes growth ofBifidobacteria that prevent the growth ofpotentially pathogenic bacteria;

■ cytokines and growth factors.The overall effect of these constituents is to promote the development of the baby’s ownimmune system and reduce the risk of infection,while it is still immature. Immune factors spe-cific to the environment are produced by themother’s gastrointestinal and respiratory tracts,which then stimulate the mammary glands tosynthesize similar compounds. Thus, the immun-ity provided is ‘tailor made’. Evidence fromaround the world, including both industrializedand developing countries, indicates that thereare lower infection rates in breastfed comparedwith bottle-fed infants.

Other factorsHuman milk may also contain substances passedthrough the mother, such as drugs, alcohol, nico-tine and pollutants. This causes some concern tomothers and, where possible, such agents shouldbe avoided when feeding the baby. However,environmental pollutants may be stored inmaternal body fat and be released during the lac-tation process. At present, there is insufficientevidence to decide the risk from these.

HIV infection may be transmitted throughbreastfeeding. However, whether a woman whois infected chooses to breastfeed is largelydependent on the alternatives available to herand her baby. If these are safe, it is probablybetter to feed with formula; if not, then the rec-ommendation of the WHO is that breastfeedingis the better option. The advantages of breast-feeding in these situations still outweigh therisk of infection from HIV.


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Other milks availableAlternative milks are available for infants whoare allergic to cows’ milk or lactose. The mostwidely available are those based on modifiedsoya protein. These milks contain glucose andcarry a possible risk to teeth. Their use should becarefully monitored. Hydrolysed protein formu-las are available for highly allergic children andthese should be used under supervision.

Special milks for babies born pre-term arealso available, although their use is still contro-versial. It has been recognized that mothers giv-ing birth to pre-term infants, produce milk thathas a higher content of fat, protein and sodium,and less carbohydrate. This would appear to benecessary to sustain the rapid growth of thebaby and to compensate for the lack of reserveswith which it is born. A combination of breastmilk and pre-term formula is considered thebest compromise for these infants.

Future healthIt has been claimed that breastfeeding confersadvantages in terms of the later health of thebaby. Some studies have shown more advanceddevelopment during childhood in those childrenwho received breast milk, even for a short periodin infancy. A meta-analysis by Anderson et al.(1999) showed that breastfeeding conferred anadvantage of 3.2 point increments in cognitivefunction by adolescence. A study of adults aged53 (from the British 1946 birth cohort) con-firmed that breastfeeding was significantly andpositively associated with educational attain-ment, but this was largely accounted for by thecognitive effect at 15 years.

Other possible advantages that have beenproposed include less allergic disease, lowercholesterol levels, less obesity, heart disease andmultiple sclerosis. Breastfed infants have higherlevels of low-density lipoprotein (LDL) and verylow density lipoprotein (VLDL) as infants; thismay be linked to lower cholesterol levels in laterlife, through adaptation of enzyme levels.

Some of these advantages are difficult toshow and require long-term studies. However,using records from the early years of the twenti-eth century, Barker (1994) has shown that menwho were breastfed beyond the age of 1 year

actually experienced higher mortality rates. It issuggested that this is a reflection of inadequatenutrition and possibly restricted growth, sincebreast milk is not a complete food beyond about5–6 months. On the other hand, other work byBarker shows that infants who gained weightwell and had highest weights at the age of 1 year had the lowest incidence of impaired glucose tolerance and cardiovascular disease.Clearly, nutrition in the first year of life has tobe good enough to promote growth and devel-opment for long-term health. However, moreinformation is needed.

Weaning

The process of weaning an infant literally means‘to accustom’ the baby to new foods, and in sodoing to diversify the diet from milk to one con-taining solid foods. The age at which this occursand the foods used vary between different cul-tures and communities, and may be as early as 2 months or as late as 12 months. Neither ofthese extremes is nutritionally ideal. The optimalage of weaning is between 4 and 6 months.

In the UK, the Infant Feeding Survey 2000(Hamlyn et al., 2002) has shown that there hadbeen a move to slightly later introduction ofsolids. Although 24 per cent of mothers hadintroduced solids by the age of 3 months, thiswas less than half the number recorded in 1995.By the age of 4 months, 85 per cent had intro-duced solids and almost all the babies in thesurvey were receiving some solids by the age of6 months.

Early weaning is more common in socialclasses 4 and 5, in the north of England andScotland, among bottle-fed babies and bymothers who smoke.

Why should a baby be weaned?

Developmental advantages ensuing from wean-ing have already been mentioned. Further, fromthe age of 4 months onwards the physiologicaldevelopment of the baby allows more variedfoods to be ingested and digested, and theirwaste products to be excreted. Early weaningtends to result in faster weight gain but, by the

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age of 1 year, differences between infants weanedbefore 8 weeks and those weaned after 12 weekshave disappeared. In addition, there is a smalltendency for infants weaned early to experiencemore respiratory illnesses and cough in the firstyear of life. Early weaning may precipitate anallergic response, and in infants who are at highrisk of developing allergies, weaning as late aspossible is advised.

Weaning has important developmentaladvantages. The ability to manipulate a bolus offood in the mouth and swallow it, to coordinatea utensil and bring food to the mouth and todrink from a cup all help in the development ofmuscles in the face. These are important in theacquisition of speech.

From the nutritional point of view, weaningis required to provide certain nutrients that canno longer be supplied in sufficient amounts bybreast or formula milk. In particular, this appliesto energy, protein, iron, zinc, vitamins A and D.

There is particular concern about iron statusin infants, with low stores and the possibility ofanaemia in 12 per cent of young children. Thelow iron status may result in delayed psycho-motor development and defects in cellularimmunity.

An infant’s stomach capacity is consider-ably smaller than an adult’s, which makes it very important to ensure that the foods offeredcontain enough energy in a compact form.Commonly, the first food introduced to the infantis the local staple cereal. In the West, this may bespecially formulated, designed for weaning andenriched with a number of nutrients. Rice (orother non-wheat cereals) is preferred to wheat,

which may cause gluten allergy to develop. In developing countries, the local staple is used,prepared as a gruel or porridge.

Other purées may then be introduced, forexample, potato, vegetable, pulse or fruit purées,dairy products such as custard or yoghurt. Theseare all smooth with a relatively bland taste, withwhich the infant can gradually become familiar.As the child becomes accustomed to the noveltyof solid foods, minced meat, fish and othersources of protein, such as sieved soft cheese canbe included, together with vegetables and fruitthat have been minced or mashed to retain moretexture.

As chewing ability develops, the pieces offood offered become more distinct, allowingchewing to be practised. ‘Finger foods’ held inthe hand allow the child some independence andhelp to develop coordination, as well as provid-ing some nutritional value. These can includerusks, fingers of toast or pieces of hard cheese.

The diet should aim to provide a variety ofdifferent food groups, to ensure that a range ofnutrients is consumed (Table 12.3). Particularattention may need to be paid to iron and vita-min D sources; vitamin C will help the absorp-tion of iron and should also be provided. Someexamples of suitable foods to provide thesenutrients are shown in Table 12.4.

Milk should remain the cornerstone of theinfant’s diet, as it contains important amounts ofprotein, calcium and vitamins, as well as provid-ing energy. Amounts of milk offered should be600mL at 4 months when weaning starts, but still350mL in the 1-year-old. The type of milk offeredto the infant is also important. The UK Department

Suggested food groups to be included in the diet at 6–9months and 12 monthsTABLE 12.3

Number of servings/day

Food group 6–9 months 12 monthsBread, cereals, potatoes 2–3 At least 4Fruit and vegetables 2 At least 4Milk and dairy products 500–600 mL milk 2–3 servings � 350 mL milkMeat, fish and alternatives 1 1–2Fatty and sugary foods Avoid Limit


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of Health (DoH, 1994) recommends that infantsshould continue to receive breast milk, formula or a ‘follow-on’ milk up to the age of 1 year.‘Follow-on’ milks have been introduced in recentyears, as suitable for infants from 6 months ofage. They are less modified than infant formula,but still contain added nutrients to provide avaluable source of nutrition. Drinks should beoffered in a cup, and the practice of leaving achild with a bottle or ‘trainer’ cup (one with afeeding spout) for periods of time is discouragedas it can lead to pooling of drink in the mouth.This can cause decay of newly erupted milk teeth.

Pasteurized cows’ milk should not becomethe major milk drink until after the age of 1 year.This is because it contains low levels of iron andvitamin D, and may contribute to deficientintakes if taken as the main milk in the diet.However, cows’ milk may be used to make dishescontaining milk, such as custards and sauces.Infants should not be given low-fat milks, suchas skimmed milk or semi-skimmed milk, as thesecontain insufficient fat and, therefore, have alow energy density.

Throughout the weaning process, it is rec-ommended that:■ the child is always supervised during meal-

times;■ sugar and salt are not added to the infant’s

food;■ foods should not be heavily spiced;■ nuts should not be included in the diet;

■ soft-boiled eggs should be avoided becauseof possible contamination with Salmonella;hard-boiled eggs are safe;

■ pâté and mould-ripened soft cheeses (suchas Brie) should be avoided because of therisk of Listeria contamination;

■ drinks other than milk should be offeredfrom a cup from the age of 6 months; theyshould be dilute and unsweetened.

Special ‘infant drinks’ may contain largeamounts of sugar and should be avoided or onlyused rarely and with care. Infants should neverbe left with a sugary drink in a feeding bottle, asnewly erupting teeth may be damaged.

Commercial weaning products are of value.They are often fortified with additional nutri-ents, which is especially useful when the childhas a very small intake, when home-preparedfoods may provide very few nutrients.

Infants cannot cope with large amounts offoods rich in non-starch polysaccharides (NSPs),such as whole grain cereals and pulses, and theseshould not be an important part of the weaningdiet. However, small amounts can be included,and quantities increased when appetite is bigger.

By the age of 1 year, the infant should beeating solids several times per day, and beincluded in family meals. The complete processof weaning may take longer than this, however,and full chewing ability will not be attaineduntil the molar teeth have erupted towards theend of the second year.

Sources of iron, vitamin C and vitamin D suitable for weaningTABLE 12.4Sources of iron Sources of vitamin C Sources of vitamin DRed meat (beef, lamb), Unsweetened fruit juice: diluted Oily fish, e.g. sardines

pork poultry Citrus fruits, e.g. oranges, Eggs and egg dishesLiver, liver sausage satsumas Fortified margarineOily fish, e.g. sardines Summer fruits: strawberries, Breakfast cereals fortifiedEggs and egg dishes peaches, nectarines with vitamin DBeans and lentils Green leafy vegetables Baby cereals fortified withBaby foods fortified with iron Tomatoes, green pepper, peas vitamin DBreakfast cereals with added iron Potatoes Evaporated milkGreen leafy vegetables Some yogurtsDried fruits, e.g. apricots, prunesFish fingers

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Supplements of vitamins A, C and D areavailable; these are recommended for all infantsfrom the age of 1 to 5 years, and for breastfedinfants from the age of 6 months. The daily doseof supplement provides 200 �g of vitamin A,20 mg of vitamin C and 7 �g vitamin D.

It should be remembered throughout that the infant is undergoing a process of learningabout food and, to develop a child with a broadappetite for foods, many different tastes shouldbe offered. Variety in the diet helps to ensure an adequate nutritional intake. Nutrients thatneed attention remain iron, zinc and vitamin D.Refusal of a specific food need not eliminate itcompletely from the diet. It can be reintroducedlater. Important foundations are being laid downat this time and it is essential that the caregivermakes this a pleasurable learning experience forthe infant. Sometimes the weaning process fal-ters and a child that has been gaining weightmay stop doing so. This has been called ‘failure

to thrive’ and is of multifactorial origin. There isno evidence that it is associated with deprivationand neglect. There appears to be an underlyinglack of interest in food in the child, slower eatingand diminished appetite. Delayed progression onto solids and a limited variety of foods eatenhave also been described. Intervention withdietary advice and practical management ofmealtimes can result in rapid improvement, ifthere is no underlying organic cause. The processof weaning is summarized in Figure 12.2.

The child from 1 to 5 years of age

These years provide a time to move from themilk-centred diet of the first year of life to thetypical diet of the family. In nutritional terms,this represents a change from a diet which con-tains approximately 50 per cent fat, no NSP andsimple sugars rather than starches (as seen in the

Figure 12.2 Summary of how towean a baby.


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milk-fed infant), to one meeting or approachingthe dietary guidelines, with 35 per cent fat, 11 per cent non-milk extrinsic sugars and plentyof starch and NSPs. Clearly, there needs to be agradual transition from one to the other.

The food habits developed at this time will bethe foundation for the approach to diet andnutrition for the rest of the individual’s life.During this period, the child will also developsome independence in relation to food, and thismay lead to conflict with the parents. Infantsmore readily accept new foods and tastes. Duringearly childhood there may be an increasingreluctance to try new foods. This served a protect-ive function in the past, as a young child beganto wander off and might have been tempted totry a hazardous food. Exposing children to newfoods is, however, important. Perseverance, whichmay necessitate up to five or ten exposures to thefood can pay off. Modelling on others who areeating the food is a helpful way of persuading a young child to accept it. Finally, presenting anovel food together with a familiar taste can beuseful, for example, as part of a liked dish. Parentshave an important role in determining what foodis available for the child in the home. The attitudeof parents to food is central, and conscious orsubconscious preferences for foods, or attributesattached to a food will be passed on to the child.Foods used as a positive reward (‘have somechocolate for being a good boy’), or a hurdle to beovercome to achieve something pleasurable (‘eatyour vegetables and then you can go out to play’)can foster attitudes to these foods that were notnecessarily intended. Children need guidance andfamily food rules are beneficial to provide aframework in which their own food habits candevelop. Ideally, these should focus on healthyfoods and eating patterns.

Growth is slower than in the first year of lifebut tends to occur in spurts, often accompaniedby surges of appetite. Activity also increasesmarkedly during the second year, as the childbecomes increasingly mobile. Full dentition byabout the age of 2 also increases the dietaryrepertoire. Because capacity remains relativelysmall, between-meal snacks are likely to beneeded in addition to the three main meals of theday. It is important to maintain healthy eating

guidelines in mind when selecting snack foods,since these should be contributing to total nutri-tional intake, rather than being additional to it.Unfortunately, poorly selected snacks, oftencomprising little more than sugar, in drink orsolid form, can seriously compromise nutritionalintake, as they dull the appetite at mealtimes.Snacks can include:■ fresh or dried fruit (although the latter may

stick to the teeth and be cariogenic);■ wholemeal sandwiches with nutritious

fillings;■ raw vegetables as ‘finger food’ to chew;■ dry breakfast cereal;■ low-sugar or savoury biscuits;■ yoghurt or milk;■ popcorn (plain, rather than sugar coated);■ scones or similar plain cakes.

Meals should consist of nutrient-dense foods,with at least 250mL of milk daily, and cereal and bread used to fill up to appetite. Appetiteremains the best guide to overall food needs atthis age.

Food refusal can be a major problem, andcan cause a great deal of stress to parents. Thechild needs a consistent and firm response fromthe parent, so that the association of eating withmealtimes is learned. If the child does not eat at table and is then allowed to snack betweenmeals, disorganized eating habits may developfor the rest of their life. Experimentation withfood within limits is important. Given a widerange of foods to experience, we all develop as individuals in our choice of foods with spe-cific likes and dislikes. Ideally, our childrenshould develop with few dislikes, if we givethem the appropriate guidance and personalexample.

A national study (Gregory et al., 1995) ofchildren aged 1.5–4.5 years, as part of theNational Diet and Nutrition Survey in Britain,found that, on the whole, children were eatinglarge amounts of salt and sugar, and insufficientfruit and vegetables. Although the mean intakeof energy was found to be lower than the esti-mated average requirements, the childrenappeared to be growing well. As a result, it hasbeen suggested that energy requirements mayneed to be decreased by 10–12 per cent from

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their current levels. Other findings included thefollowing.■ Those who had the highest energy intakes

also consumed the most NSP.■ Total sugar intakes represented 29 per cent

of total energy and starches 22 per cent; theintake of non-milk extrinsic sugars com-prised 19 per cent of total energy.

■ There was a reciprocal relationship betweenfat and sugar intakes.

■ Fat intakes were generally between 34 and 36per cent of total energy and, therefore, in linewith Department of Health recommendations(DoH, 1991). It should be remembered thatyoung children should not be rigorously puton low-fat diets, as this can compromise theirtotal energy intake. Other studies show thatlow-fat/high-fibre diets are being given tothis age group, reflecting confusion abouthealthy eating guidelines.

■ Iron intakes were low in a proportion ofchildren: 24 per cent of those aged 1.5–2.5years, and 16 per cent of those under 4 yearshad intakes below the lower reference nutri-ent intake (LRNI), with low ferritin levelsindicative of low stores of iron, and lowhaemoglobin levels resulting in anaemia in1 in 12 of the sample. Apart from help withiron-rich foods, parents may need adviceabout promoters and inhibitors of ironabsorption.

■ Dental caries was found in 17 per cent ofthis age group.In a secondary analysis of these data, it was

found that only 1 per cent of children met thereference nutrient intake (RNI) recommendationsfor iron, zinc, vitamins A and C, and guidelineson non-milk extrinsic sugars (NMES). Two orfewer of the targets were met by 76 per cent ofthe children. Compliance with the recommendedlevels of intake was related to socio-economicstatus, with more children from lower socialgroups, with a head of household in a manualcategory and mothers with fewer educationalqualifications meeting the least number of RNIs/recommendations.

Overall, it can be concluded that the quantityof the diet of this age group in the UK is cur-rently adequate, although certain aspects of its

quality probably need attention. In particular,there needs to be:■ more attention given to iron-containing

foods;■ a reduction in both the amount and fre-

quency of consumption of sugars, especiallyin the form of soft drinks; these could bereplaced by milk or water;

■ a reduction in the consumption of savourysnacks that are high in salt;

■ an increase in the consumption of fruit andvegetables;

■ more attention to the impact of socio-economic factors on food choice in families.

School-age children

Influences on nutritional intakes

When children start school, their eating patternsbegin to be increasingly influenced by factorsother than the home environment. However, itshould be remembered that parents remain the‘gatekeepers’ of what is consumed at home andcan still have a considerable influence by deter-mining what is provided at mealtimes, and whatsnack foods are available for children to helpthemselves. They also continue to serve asimportant role models.

AutonomyA study of 9-year-old children in the UKreported that this group felt that parents had agreat deal of control over their food choices.However, the greatest number (90 per cent)reported control over the content of breakfast,with 2/3 reporting control over snacks and only1/3 reporting control over the amount of foodeaten (Robinson, 2000). This appears to leavechildren with a reasonable amount of autonomyin various aspects of their diet.

Adolescence itself is a time of transition,associated with progress towards autonomy.This is reflected in all aspects of the teenager’slife, but inevitably impacts on food choice andnutritional intake.

Rejection of food selected or prepared byparents is a normal aspect of this developingautonomy. Foods chosen as alternatives may be


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less healthy, as a gesture of independence andperhaps peer solidarity. There is also likely to beexperimentation with foods and adoption ofnovel dietary practices. At other times, the ado-lescent may still want to be part of the familyand eat what is provided in the home.

GrowthGrowth rates are relatively slow during the pre-adolescent years, but growth still occurs non-linearly with surges accompanied by increasesof appetite. Periods of slow growth may beaccompanied by a relatively small appetite and,at such times, particular attention must be paidto the nutrient density of the diet. In adoles-cence, periods of rapid growth take place thathave profound effects on appetite.

School may also be emotionally taxing forchildren, which may affect their food intake. Inaddition, beginning school is often accompan-ied by exposure to many childhood infectionsand periods of (often minor) illness. These canhave an impact on food intake and, if numer-ous, may affect growth.

ActivityApart from growth, activity is the other maininfluence on appetite in this age group. Startingschool may significantly alter a child’s activitypattern, the direction of the change dependingon how active the child was during pre-schoolyears. Children of primary school age tend to be relatively more active in their play and levelsof activity have been shown to decline in a large proportion of adolescents, especially girls.Following the Health of the nation report (DoH,1992), physical activity in children has become afocus of policy in the UK, with recommendationsmade for an increase in activity in this agegroup. There is concern that many hours arebeing spent watching television, playing com-puter games and staying in the house, ratherthan being involved in physical activity or evenjust walking. Estimates from studies in Scotlandsuggest that teenagers may now expend between2 and 3 MJ (500–700 Calories) per day less thantheir peers did 60 years ago. Average time spentwatching television has been shown to be posi-tively associated with increased body weight,

skinfold, fat mass and prevalence of overweightin pre-pubertal children. The reasons for thisassociation are complex.

Societal pressuresPressures from friends will increasingly influencefood intakes as a child goes through school, andthis becomes most notable in adolescence. Inaddition, societal pressures linked to body imagehave a major impact on the food intake of some individuals, especially girls at this age.Adolescence is the peak age for dissatisfactionwith body image and attempts at dieting areprevalent, more so in girls than boys at this age.Changing food trends are particular influences.In recent years, there has been a major shift from traditional meals, and many children andteenagers consume a series of snacks during theday rather than eating ‘normal’ meals. The choiceof foods available in fast-food outlets can be alimiting factor for making healthy selections.

There is also widespread concern about theimpact of advertising on food choices in thisgroup. Food advertising is the single largest cat-egory of advertisement shown during children’stelevision programmes. The majority of these arefor products that are high in sugar and fat andlow in fibre, and include confectionery, snackfoods and breakfast cereals. This trend is alsoseen in other countries, such as the US andAustralia. The advertisements for these foods areoften humorous, animated and easy to follow, sothat they are memorable to children. In contrast,there are no advertisements for foods that shouldform a substantial part of a healthy diet, such asfruit and vegetables. Although advertisements bythemselves do not change food habits, there isconcern that the balance of those shown is inconflict with health promotion messages.

Nutritional needs

Steady growth during childhood up to adoles-cence, increasing per year by 10 cm in heightand 2.5 kg in weight, is reflected by a gradualincrease in the need for nutrients. There is a cer-tain amount of accumulation of stores duringthis time, most notably of body fat, which thenbecomes available to contribute to the fuel

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required for the pubertal growth spurt. Calciumis also laid down and provides some of theneeds for bone growth.

At adolescence, growth rates are greater thanat any other time of life, except early infancy. In most girls, the growth spurt begins betweenthe age of 10 and 13, in boys between 12 and 15 years. In both cases, rapid growth takes placeover a period of 3 years. Girls gain lean tissueand fat, and increase by 20 cm in height and20 kg in weight. In boys, there is a loss of fat anda gain in lean tissue, with increases of 30 cm inheight and 30 kg in weight. These increasesaccount for approximately 40 per cent of adultweight. It is to be expected, therefore, that thenutritional requirements at this time will reflectthis growth.

The timing of the need for additional nutri-ents varies with the individual, and depends onthe onset of growth. In the West, peak appetiteoccurs around the age of 12 in girls and 14 inboys, apparently corresponding to the mostrapid growth period. The demand for new tissuesynthesis results in increased nutrient require-ments for:■ calcium, phosphorus, magnesium and vita-

min D for bone;

■ protein, zinc and iron for muscle;■ iron, folate, vitamin B12 and copper for the

synthesis of extra blood cells to supply itwith oxygen;

■ adequate energy to sustain this synthesis,and the B vitamins to release it.

If energy needs are not met, the growth spurtmay be delayed or reduced. However, energyneeds for growth probably do not exceed 10 percent of total energy requirements at this time.

Once the growth spurt is over, nutrientrequirements settle down to adult levels.

Selected dietary reference values are shownin Table 12.5 for the age groups from 4 to 18years. In addition to these specific guidelines,children’s diets should approach the generalrecommendations on fat and carbohydrates(shown in Table 12.6).

No distinction is made between genders forthe majority of nutrient requirements for chil-dren up to the age of 10 years. After this age,with the onset of the pubertal growth spurt, dif-ferent figures are set for male and female ado-lescents. In part, these reflect the different bodyweights at these ages. However, special needsfor menstrual losses are incorporated in the ironrequirement calculations.

Dietary reference values for children from 4 to 18 yearsTABLE 12.5Nutrient Age 4–6 Age 7–10 Age 11–14 Age 15–18

M F M F M F M FEnergy

(MJ/day) 7.16 6.46 8.24 7.28 9.27 7.92 11.51 8.83(Cals/day) 1715 1545 1970 1740 2220 1845 2755 2110

Protein (g/day) 19.7 19.7 28.3 28.3 42.1 41.2 55.2 45.0Thiamin (mg/day) 0.7 0.7 0.7 0.7 0.9 0.7 1.1 0.8Riboflavin (mg/day) 0.8 0.8 1.0 1.0 1.2 1.1 1.3 1.1Niacin (nicotinic acid 11 11 12 12 15 12 18 14

equiv.) (mg/day)Folate (�g/day) 100 100 150 150 200 200 200 200Vitamin C (mg/day) 30 30 30 30 35 35 40 40Vitamin A (�g/day) 500 500 500 500 600 600 700 600Calcium (mg/day) 450 450 550 550 1000 800 1000 800Iron (mg/day) 6.1 6.1 8.7 8.7 11.3 14.8 11.3 14.8Zinc (mg/day) 6.5 6.5 7.0 7.0 9.0 9.0 9.5 7.0



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There are no dietary reference values (DRVs) given for vitamin D, as it is assumed that sufficient will be synthesized in the skinduring everyday activity. However, some chil-dren of Asian origin may require a dietary supplement.

These dietary guidelines should be met in thesame way as for adults, by eating a diet in linewith the Balance of Good Health, which providesan appropriate balance between the five maingroups shown. Thus, the diet should providemainly starchy carbohydrate sources, fruit andvegetables (five servings per day of each of thetwo groups). In addition, there should be threeservings of milk and dairy produce, and twoservings of meat and alternatives. Intakes offatty and sugary foods should be limited; theymay be included in the diet when the needs forthe other four groups have been met.

It is helpful if meals are planned to includeitems from each of the food groups whereverpossible.

What do children andadolescents eat?

Studies of children’s attitudes to healthy eatingin recent years have shown that in general chil-dren understand the concept of a balanced diet asdescribed in the ‘Balance of Good Health’ model.They are also aware of the relationship betweendiet and health, both present and for the future.Children also demonstrate an awareness of thepotential risk for heart health of excessive fatintakes, and the desirability of a normal bodyweight. The health implications of being too thinand the dangers of eating disorders are also rec-ognized. For this age group, however, social pres-sures are important, and knowledge does notnecessarily translate into behaviour.

A number of studies took place during the1980s and early 1990s on groups of childrenfrom 5 to 17 years of age. In general, these studiesshowed that the health of schoolchildren inBritain is good. There was no widespread evidenceof dietary deficiency, and no biochemical or func-tional improvements were seen with the use ofsupplementation. However, a European study hasreported that the diet of UK children is amongstthe worst in Europe, being high in fat and sugar,low in fibre, iron and calcium and possibly folate.

A new survey of young people aged 4 to 18,which is part of the ongoing National Diet andNutrition Survey programme in the UK was published in 2000 (Gregory et al., 2000). Thiswas a comprehensive study, including 7-day diet-ary records, anthropometric measurements, bio-chemical and clinical assessments, and lifestyleand socio-economic characteristics. Over 1700children responded to the survey and the dataprovide a valuable picture of this group.

Some of the main findings are summarizedhere.

Health-related aspects■ The young people in the survey confirmed

the secular trend, being both taller and heav-ier than the cohort studied in 1982–83.

General recommendationson fat and carbohydratesTABLE 12.6

Total fat 35% of foodenergy

Saturated fatty acids 11%Polyunsaturated fatty acids 6.5%Total carbohydrate 50% of food

energyNon-milk extrinsic sugars 11%Intrinsic and milk sugars + 39%

starchNon-starch polysaccharides 18 g/day

Return to Activity 12.1 and perform a similarexercise for children and adolescents for the fol-lowing body weights:

Age (years) Male weight Female weight(kg) (kg)

5 18 17.7510 31 31.514 49 4818 65 55.5

Activity 12.2

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■ Blood pressure increased with age; it was sig-nificantly higher in those children who usedsalt at table, for boys who smoked and boysin the oldest group who drank alcohol.

■ Physical activity levels were recorded as fairlyactive in the 4–6-year-old children. After thisage, activity decreased with increasing ageand girls were less active than boys.

Dietary patterns■ Foods eaten by over 80 per cent of the

respondents included: white bread, biscuits,chips, potatoes, savoury snacks and choc-olate confectionery.

■ Meat consumed most commonly was chickenand turkey (65–79 per cent of respondents);beef and veal were consumed by 43–63 percent of males and 43–52 per cent of females.Ten per cent of the oldest girls reported thatthey were vegetarian or vegan.

■ Raw and salad vegetables were eaten moreby girls than boys (37–53 per cent of boys,49–66 per cent of girls), but consumption ofgreen leafy vegetables was similar, ataround 40 per cent of the groups.

■ Apples and pears were the fruit consumedmost often, but consumption declinedsharply with age (from 70 to 39 per cent inyoungest and oldest boys and from 66 to 44 per cent in girls). Bananas were the nextmost popular fruit (average consumption

40 per cent), and citrus fruits the least popular(average 25 per cent).

■ Whole milk was consumed most by theyoungest group (75 per cent) and declinedsharply with age. Conversely, the consump-tion of semi-skimmed milk increased withage to approximately 60 per cent in the old-est group.

■ The most popular beverages were carbon-ated soft drinks, consumed by up to 85 percent of boys and 73 per cent of oldest girls.Low-calorie versions were consumed bymore girls than boys. Tea was a more com-mon choice of beverage than coffee.

Nutritional intakesThe survey results were affected by under-reporting, as is commonly found.■ Total energy intakes were below the esti-

mated average requirements (EAR) for all agegroups. In particular the oldest age group of girls and boys reported intakes of only 77 and 83 per cent of their EAR. As bodyweight and height show no evidence of inade-quate energy intakes, it is assumed that theseresults are underreported. Cereals and cerealfoods provided the main source of energy, asfound also in the National Food Surveys.

■ The contributions to the total food energyintake of the main macronutrient groups areshown in Table 12.7.

Contributions of the main macronutrient groups to totalenergy intake for young people aged 4 to 18TABLE 12.7

Macronutrient Contribution to Main contributingfood energy food groups

Protein 13.1% Meat and meat productsCereals and cereal products

Carbohydrate 51.6% (boys) Cereals and cereal products51.1% (girls) Sugar and preserves

Fat 35.4% (boys) Cereals and cereal products 35.9% (girls) (biscuits, buns, cakes and

pastries)Meat and meat products

Non-starch polysaccharides 11.2 g (boys) Vegetables, potatoes and 9.7 g (girls) savoury snacks

Cereals and cereal products


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■ Intakes of non-milk extrinsic sugars pro-vided an average of 16.5 per cent of energy,mainly from carbonated soft drinks andchocolate confectionery.

Micronutrient intakes were generally above theRNI for most nutrients, for most age groups.However, some intakes were below the LRNI, andthe prevalence of this increased with increasingage and was more likely in girls than boys.■ Among the vitamin intakes, vitamin A and

riboflavin were most likely to fall below theLRNI. Further, in the oldest age group ofgirls, there were some intakes below theLRNI for all vitamins studied.

■ For mineral intakes, levels below the LRNIwere found in the youngest age groupsmostly for zinc. With increasing age, agreater range of mineral intakes fell belowthe LRNI. These included iron, calcium, mag-nesium, potassium, zinc and iodine. In thecase of iron, 50 per cent of the oldest groupof girls (aged 15–18 years) had intakes thatfell below the LRNI. Among the oldest boys,magnesium intakes (18 per cent) and potas-sium (15 per cent) were the most commonminerals to fall below the LRNI.

■ Those respondents who took dietary supple-ments generally had higher intakes fromfood sources than non-users of supplements.Supplements affected mean intakes for vita-min A and C, iron and zinc, but did notaffect the intakes below the LRNI.

■ Poor nutritional status identified in bloodanalyses was shown in some individuals forvitamin D, vitamin C, folate, riboflavin andthiamin. In addition, serum ferritin levelswere below the normal range for adults in13 per cent of boys and 14 per cent of girls.This finding was more common in youngerboys (18 per cent affected), but older girls(27 per cent affected).

Other smaller studies confirm these findings.In general, the transition from primary to sec-ondary school is associated with the beginningof greater independence in food choice and isaccompanied by an increased consumption of

less desirable foods and a reduction in desirablefoods, most notably fruit and vegetables.

In addition, socio-economic status results indifferences in the nutritional quality of chil-dren’s diets, with lower intakes of total energyand lower intakes of nutrients when energyintakes had been taken into account. This trendcorresponds to that reported in adults.

School meals

A meal in the middle of the school day is import-ant nutritionally, socially and educationally. Interms of academic performance, it is importantthat children eat in the middle of the day tomaximize their learning opportunities.

Nutritional guidelines for school meals thathad existed since the 1944 Education Act wereabolished in the UK in 1980. Prior to this date,the meal offered at school had to provide one-third of a child’s daily requirements of protein,energy and some minerals and vitamins. From1980, the only obligation that remained was toprovide a meal for those who were entitled to freeschool meals, by reason of low income. Since thisdate, considerable concern has been expressedabout the nutritional adequacy of the diets ofschoolchildren.

Following a period of consultation, MinimumNutritional Standards have been established, tak-ing effect from April 2001. There is once more aduty to provide a paid meals service in schools,and guidance documents have been produced bythe Department for Education and Skills. Schoolshave more autonomy than in the past and at sec-ondary level hold budgets for the provision of meals. This means that many schools are ableto adopt whole-school policies on food andnutrition. The School Nutrition Action Group(SNAG) initiative has provided a framework forthe formation of school-based alliances betweenteachers, pupils and caterers together with helpfrom appropriate health professionals. Many ofthese are in place and they allow the consumersto be involved in the decision-making processand thereby increase their sense of ownership ofthe school meal provision. School managementalso needs to be involved to ensure there is an adequate provision for a lunch break in

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the timetable and that a suitable environmentexists to enable meals to be taken in comfortable surroundings.

When aspects of healthy eating are part ofthe school curriculum, the food service can pro-vide the practical illustration in a positive wayas well as contributing to the pastoral welfare ofthe children.

Some issues about the provision of meals inschool remain to be resolved. These include thefollowing.■ Ensuring that cultural diversity is recog-

nized in the meals provided.■ Improving the uptake of free school meals –

reports suggest that to achieve this a numberof factors, for example, insensitive adminis-tration that results in an associated stigma,the quality of the food, eating environmentand service, all need to be addressed. SomeLocal Education Authorities have introducedswipe cards for all children, so that there isno distinction made at the point of purchasebetween the children receiving free lunchesand those who are paying.

■ Provision of drinking water to accompanythe meals.

■ Monitoring of the provision of the mealsand maintenance of standards. This is a rolefor the appropriate government agency.

Minimum nutritional standardsThe national nutrition standards are based onthe food groups in the Balance of Good Health(see Table 12.8). In terms of defining a healthydiet, they incorporate the following principles:■ a balanced diet with plenty of variety, and

enough energy for growth and development;■ plenty of fibre-rich starchy foods, such as

bread, rice, pasta, potatoes and yams;■ plenty of fruit and vegetables;■ not eating too many foods containing a lot

of fat, especially saturated fat;■ moderate amounts of dairy products;■ moderate amounts of meat, fish or alter-

natives;■ not having sugary foods and drinks too often.

In addition to these general principles, spe-cific nutrients have been identified as importantfor children of school age. These are:■ calcium – important for bone health;■ iron – important for preventing anaemia;■ folate – important for adolescent girls and

young women, but establishing a goodintake in early years forms a sound base;

■ zinc – for normal growth and development.Slightly different nutritional standards have

been established for children in primary and sec-ondary schools. In addition, there are separatestandards for children of nursery school age.

Minimum nutritional standards for school meals (DfES, 2001)TABLE 12.8Food groups Primary school Secondary schoolStarchy foods such as bread, Provide at least one from this Provide at least two from this

potatoes, rice and pasta group daily. Items cooked in group daily. At least one ofoil or fat should not be served these should not be cooked inmore than three times a week oil or fat

Fruit and a vegetable One item of both must be available Two items of both should beevery day. Fruit-based desserts available dailymust be available twice a week

Milk and dairy foods Provide at least one from this Provide at least two from this group daily group daily

Meat, fish and alternative Provide at least one from this group Provide at least two from this sources of protein (cheese daily. Red meat to be served twice group daily. Red meat must bemay be provided as an a week; fish to be served once served at least three times a alternative for primary a week a week; fish to be served at school children only) least twice a week


272

These standards apply to all lunches (hot orcold) provided during term time. There are add-itional recommendations for the provision ofwater, free of charge. Milk to drink should alsobe available every day. It is recommended thatsome hot food be offered daily, especially in thewinter months.

Caterers are also given guidance on goodpractice, which includes the following key points:■ reflect the likes and dislikes of children;■ work with the school to check that healthy

eating principles are being reinforced byboth the curriculum and the lunch service;

■ actively encourage children to have a bal-anced diet;

■ aim to offer a selection of foods, which, overthe week, reflects the proportions in theBalance of Good Health, and make changesgradually;

■ offer a variety of foods;■ use a variety of cooking methods that lead

to minimum destruction of nutrients.In addition to the above, guidance is provided

on various foods within each food group, portionsizes, special dietary requirements and monitor-ing of the nutritional standards. Even though thenew minimum standards have been expressed in terms of food groups, and servings from these,caterers are encouraged to use the CarolineWalker Trust Guidelines on School Meals to

check the nutritional value of the meal provided.These are shown in Table 12.9. This is particu-larly important where children have a free choicein a cash-cafeteria selection. Throughout, cater-ers are encouraged to promote healthy eatingand encourage children in a variety of ways toeat the food provided.

Where children can leave school at lunchtime,caterers have to compete effectively with localfood outlets. Attractive packaging, advertisingand promotions can all help keep children inschool for lunch.

Alternatives to school lunchPacked lunches brought in to school may be ofvariable nutritional content (see Figure 12.3).Confectionery and soft drinks may also beavailable in school, often as a fund-raisingactivity, and may tempt the children to eat theseitems rather than more nutritious foods. In someschools, children can go out of school at lunchtime, and foods purchased away from schoolmay include pizzas, chips, burgers or cakes andsoft drinks. The UK Department of Health sur-vey (DoH, 1989) found that foods eaten out of school were generally of lower nutrient density, especially among the older school-children. In particular, these meals containedless protein, iron, calcium, retinol, thiamin,riboflavin and vitamin D. A small section of the

Summary of Caroline Walker Trust Nutritional Guidelinesfor School MealsTABLE 12.9

Nutrient GuidelineEnergy 30% of the estimated average requirementFat Not more than 35% of food energySaturated fatty acids Not more than 11% of food energyCarbohydrate Not less than 50% of food energyNon-milk extrinsic sugars Not more than 11% of food energyNSP (fibre) Not less than 30% of the calculated reference valueProtein Not less than 30% of the RNIIron Not less than 40% of the RNICalcium Not less than 35% of the RNIVitamin A Not less than 30% of the RNIFolate Not less than 40% of the RNIVitamin C Not less than 35% of the RNISodium Should be reduced in catering practice

NSP, non-starch polysaccharide; RNI, reference nutrient intake. From Sharp, 1993 with permission.

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teenage population have no lunch, with 11 percent of girls and 5 per cent of boys aged 14–16reporting this.

Overall, a well-balanced lunch can providebetween 30 and 40 per cent of the nutrientsrequired in the day. If no food is taken or a verypoor-quality snack is eaten, then the likelihood ofdaily nutritional needs not being met increasesbecause it becomes more difficult to achieve ade-quate intakes from the remaining meals. Eating isa social activity and having lunch with one’speers can provide an important socializationactivity, teaching the individual about food habitsand learning from others. A proportion of chil-dren come to school without having eaten break-fast, or a snack on the way to school. In someschools, Breakfast Clubs have been establishedthat provide food before the school day begins.The School Fruit Initiative aims to provide all primary school children with a piece of fruit inschool each day. This is still being developed, butpilot schemes report a fair measure of success.School milk is also being reintroduced into someprimary schools, to try to address some of thepotential nutritional problems in this age group.

However, it must be recognized that provid-ing healthier choices for children in school doesnot necessarily lead to changes in behaviour.One study reports the outcomes of a 2-year pro-gramme in secondary schools (Parker and Fox,2001). This had a number of dietary targets,

including increasing intakes of high-fibre bread,fruit and vegetables, non-fried potatoes andnon-cream cakes. After 2 years, there was somechange in consumption of high-fibre bread, butother changes were not sustained. This studydemonstrates the challenge of improving dietaryintakes of children in school.

Some potential nutritionalproblems

As part of the development of increasing inde-pendence, children, and particularly teenagers,may encounter difficulties with their diet, whichmight result in nutritional problems. These aresummarized in Figure 12.4.

Vegetarianism

An increasingly common finding among chil-dren and teenagers in the UK is the rejection ofthe omnivorous diet in favour of a vegetarian(non-meat) diet. In addition to the reasons forchoosing to be vegetarian that are discussed inChapter 16, this age group may be subject topeer pressure or initially make the decision as abid for independence from parental control.

Unfortunately, many young vegetarians mayhave an inadequate understanding of the prin-ciples of nutrition, so that the traditional ‘meatand vegetables’ becomes just ‘vegetables’, orcheese omelette, or baked beans on toast. Theremay be little attempt to introduce other dietaryitems, such as pulses, cereals or grains, into thediet to replace the animal foods being avoided. Inthis way iron, zinc and niacin may become inad-equate, as well as calcium, if dairy products areomitted. It has already been mentioned that ironintakes are low in teenagers, particularly girls. Asmall study in London found that anaemia wasthree times more common among vegetarian12–14-years olds, with an incidence of 25 percent, compared to 9 per cent in omnivores.

There is also concern about low calciumintakes and future health. The majority of bonemass is accrued during the teenage years, with high assimilation rates of dietary calcium.Dietary reference values are high to allow for this. If calcium intakes are low, it is likelythat less bone will be made. This may have

Figure 12.3 Example of a healthy packed lunch.


274

repercussions in later life, with an increased riskof osteoporosis.

Many vegetarian meal replacements are nowavailable, based on soya or quorn, which areacceptable and which can help to maintain anadequate nutritional intake, although they can beexpensive as an everyday item. It should beremembered that a well-planned vegetarian dietcan be nutritionally adequate and may be advan-tageous in terms of long-term health benefits.

Teenage athletes

Teenage athletes are particularly vulnerable, ifthey spend a lot of time training and participatingin their chosen sport. This is because the energyneeds for their physical activity must be met inaddition to their needs for growth. Most school-children participate in some sport, which involvesno more than 2–3 hours per week; playing inschool teams may occupy a further 3–4 hours aweek. This amount of extra physical activityincreases nutritional needs slightly, but probablynot beyond the limits of the usual recommendedlevels for nutrients with the exception of energy.

As with adult athletes, there is a particular needfor carbohydrate, preferably in its starchy form, to sustain muscle glycogen levels. School sportsteachers should be aware of this.

Where a teenager aspires to be of nationalclass standard, training may take up much moretime, often from a very young age. This imposesconsiderable nutritional needs both for energyand associated nutrients in line with theincrease in energy. Energy needs may be 50 percent greater than those for an average teenager.Meeting these necessitates eating an enormousamount of extra food, which can be quite daunt-ing for a teenager. There may be reluctance to do this for fear of becoming overweight, orappearing greedy. However, full athletic poten-tial and normal growth cannot be achievedwithout the appropriate nutritional input.

Pregnant teenagers

Pregnancy is associated with changing nutri-tional requirements. When these are additionalto the high needs of adolescence, there is a riskthat the intake may not be adequate to meet

Figure 12.4 A summary of potentialnutritional problems encountered bychildren and teenagers.

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both. Approximately 1 per cent of all concep-tions in England and Wales are in girls under16; this represents 9400 pregnancies.

In addition to the nutritional needs, theremay be social and emotional factors that com-pound the nutritional difficulties. Dietary habitsof pregnant teenagers have been shown to bemore erratic than those of pregnant adults andlow levels of vitamins A and C, folate, calcium,iron and zinc have been recorded. If the preg-nancy is unwanted, as is often the case, the girlmay try to limit weight gain or even diet to loseweight. There may be parental rejection and shemay leave home, which can reduce her opportu-nities to obtain a healthy diet.

Attendance at antenatal clinics may be erraticor non-existent, so monitoring of the pregnancyto anticipate problems and obtain advice aboutdiet may be missed. Unsurprisingly, there is anincreased risk to both mother and fetus in teenagepregnancies. Maternal mortality may be 2.5 timesgreater at the age of 15 than between 20 and 24;the infant is likely to be of low birthweight, and isat higher risk of morbidity and mortality from anumber of causes.

A teenager who becomes pregnant needs toincrease her nutrient intakes and gain sufficientweight to allow the normal development of herbaby. She requires foods with high nutrientdensity and cannot afford to include low nutri-ent density foods in her diet. She may alsorequire supplements.

Dieting

Dissatisfaction with body image is a prevalentphenomenon in Western societies, affecting morefemales than males. This is transmitted to chil-dren from their parents and inevitably influencesattitudes and behaviours in children. The prefer-ence for slimness is strongly related to the child’scurrent body weight, but a desire to be thinner isfound among those with a normal body weightand also those that are underweight. The desirefor a thinner body has increasingly been reportedin pre-adolescent children. Over half of teenagegirls questioned reported feeling fat and wantingto be thinner; the figure for boys in this studywas approximately 20 per cent.

Dieting is a natural corollary to this dissatis-faction, with over 40 per cent of teenage girlsreporting past attempts at dieting, and 23 percent reporting being on a diet at the time ofstudy. A further 6 per cent claim to be dieting allthe time. The intensity and duration of dieting isalso variable, with some diets lasting only a fewdays, but other girls reporting continuing theirdiets for more than 4 weeks.

Dieting practices may be variable. Some mayreduce fat, snack or total energy intake, andincrease fruit and vegetable intake. However, upto 15 per cent are reported to use extreme weightloss measures, such as fasting, skipping meals(usually breakfast), vomiting and using diet pills.Filling up on diet drinks to prevent hunger is alsoreported. Dieting can become a habit, establish-ing a pattern of chaotic eating. The food intake iscontinually restrained; if the restraint slips, abinge may occur, with large amounts of ‘forbid-den’ foods being eaten. However, restraint is verysoon re-established. Changing to a vegetariandiet may be part of a dieting strategy and be perceived as a means of weight management.

This type of dietary intake pattern can lead toinadequate energy and nutrient consumption,with subclinical deficiencies developing andimplications for future health. In particular, poornutritional status at the beginning of pregnancymay harm the fetus. Low iron status may lead topoorer cognitive abilities, and low zinc statusmay depress immune function and lead to higherrates of infection. Finally, poor status of antioxi-dant nutrients may facilitate damage at cellularlevel, which may in years to come result indegenerative diseases. In its most severe form,disordered eating can develop into bulimia ner-vosa or anorexia nervosa, both of which carryserious health risks. In the extreme, anorexiamay result in death. Adolescent girls tendingtowards thinness should be counselled about thedangers for their future health. A body massindex of 18 or less is a useful criterion for theneed to intervene.

Dieting is less of a problem among boys,although anorexia has been reported in up to 5per cent. In some, an obsessional preoccupationwith sport as a means of weight control mayreplace the vomiting and purging used by girls.


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Usually adolescent boys are more concernedabout becoming taller and stronger, and con-centrate more on body building than restrictingtheir body size.

Nutrition and IQ

In the late 1980s, research was published whichsuggested that supplementing the diets ofschoolchildren with vitamins and minerals couldimprove results in non-verbal intelligence tests.However, the results of these studies have notbeen supported by other work. In addition, thereis no information about the original nutritionalstatus of the children who were supplemented. It is possible that children who are malnourishedcould benefit from supplementation and showimproved mental functioning. However, there isno persuasive evidence currently available that,in children who have a normal diet, supplemen-tation with minerals and vitamins can improvemental abilities.

Smoking and alcohol use

Both smoking and the use of alcohol are becom-ing more common among older children and

teenagers in the UK. A quarter of 15-year olds arereported to be regular smokers and the rate ishigher among girls. Alcohol interferes with theabsorption and metabolism of a number of nutri-ents including amino acids, calcium, folate, thi-amin and vitamin C. If the intake is modest, theseeffects are probably of little concern. However,binge drinking may have a more serious impacton nutrient levels. Among 15–16-year olds, 15 per cent of girls and 26 per cent of boys claimto be drinking more than 10 units per week, oftenin binges. This sort of drinking may also beaccompanied by vomiting, which removes nutri-ents from the body. Ultimately, nutritional statusmay be affected. In addition, alcohol itself willhave damaging effects on the organs of the body,just as in an adult.

Smoking increases the free-radical load inthe body and, therefore, the requirement forvitamin C. This should be provided in greateramounts to those teenagers who smoke. A par-ticularly vulnerable situation exists in thoseteenagers who are dieting and smoking, to helpcontrol their hunger and their weight. In thiscase, nutrient intakes may be inadequate tooffer protection against the harmful free rad-icals in cigarette smoke.

1 The transition from infant to teenager and young adult involves enormous changes in body size andcomposition. The constituents of the new tissues must be obtained from the diet. Thus, at all stages ofthis process, nutritional requirements are high.

2 Human and formula milk can provide the nutritional needs of the infant, although human milk conferssome immunological and developmental advantages.

3 The process of weaning should start at 4 months. It parallels stages of development but is nutritionallyimportant.

4 Between the years of 1 and 5, the child consolidates the early experience with food, and becomes moreindependent. Growth rates are slower but, because appetite can be small, the nutrient density of the dietis of great importance.

5 The diet of the school-age child is increasingly affected by external influences. It is important that well-balanced diets are provided at home. It must be recognized that children need to exercise choice in theirfood intake, as part of development. However, a sound foundation of education about food can makethese choices healthier.

6 Teenagers are more vulnerable than the other age groups to peer pressure and may pass throughphases of experimentation with food. Again, a core of well-balanced food provided at home can ensurethat good nutrient intakes are maintained.

SUMMARY

REFERENCES AND FURTHER READING❚

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Anderson, J.A., Johnstone, B.M., Remley, D.T. 1999: Breast feeding and cognitive development: ameta-analysis. American Journal of Clinical Nutrition 70, 525–35.

Barker, D.J.P. 1994: Mothers, babies and diseases in later life. London: British Medical Journal.Child Growth Foundation 1995: Boys/girls growth charts. London: Child Growth Foundation.Decsi, T., Koletzko, B. 1994: Polyunsaturated fatty acids in infant nutrition. Acta Paediatrica

83(Suppl. 395), 35–7.DfES (UK Department for Education and Skills) 2001: Healthy school lunches for students in second-

ary schools. London: DfSE.DoH (UK Department of Health) 1989: The diets of British schoolchildren. Report on Health and

Social Subjects 36. London: HMSO.DoH (UK Department of Health) 1991: Dietary reference values for food energy and nutrients for the


DoH (UK Department of Health) 1992: The health of the nation: a strategy for health in England.London: HMSO.

DoH (UK Department of Health) 1994: Weaning and the weaning diet. Report on Health and SocialSubjects 45. Report of the Working Group on the Weaning Diet of the Committee on MedicalAspects of Food Policy. London: HMSO.

EEC 1991: Commission Directive on infant formulae and follow-on formulae. Official Journal of theEuropean Communities L175, 35–49.

Food Standards Agency 2001: The balance of good health. Information for educators and communi-cators. London: Food Standards Agency.

Gregory, J.R., Collins, D.L., Davies, P.S.W., Hughes, J.M., Clarke P.C. 1995: National diet and nutri-tion survey: children aged 1.5 to 4.5 years. Volume 1: Report of the diet and nutrition survey.London: HMSO.

Gregory, J., Lowe, S., Bates, C.J. et al. 2000: National Diet and Nutrition Survey: Young people aged4–18 years. Volume 1. Report of the Diet and Nutrition Survey. London: The Stationery Office.

Hamlyn, B., Brooker, S., Oleinikova, K., et al. 2002: Infant feeding 2000. London: The Stationery Office.Hill, A.J. 2002: Developmental issues in attitudes to food and diet. Proceedings of the Nutrition

Society 61, 259–66.

1 a Prepare a table summarizing the nutritionaland non-nutritional differences betweenhuman milk and formula milk.

b Do you have more points under thenutritional or the non-nutritional heading?Try to account for this.

2 Write a short article for a ‘Parenting’ magazinein answer to the question ‘Why does my 18-month-old child have an erratic appetite?’Include some practical advice.

3 a What are the main nutritional principlesunderlying the balance of the diet suitable forchildren aged between 5 and 10 years?

b What problems might be encountered?c Which nutrients might be most at risk?

4 At what ages are teenage boys and girls most nutritionally vulnerable and for whatreasons?

5 Suggest some ways in which teenagers couldbe targeted for nutritional advice.

6 For the 11–16 year age group, how importantnutritionally do you consider the followingmeals to be? Explain your viewpoint:a midday mealb breakfastc snacks.

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MAFF (Ministry of Agriculture, Fisheries and Food) 1995: The infant formula and follow-on formularegulations. Statutory Instrument 77. London: HMSO.

Parker, L., Fox, A. 2001: The Peterborough Schools Nutrition Project: a multiple intervention pro-gramme to improve school-based eating in secondary schools. Public Health Nutrition 4(6),1221–8.

Robinson, S. 2000: Children’s perceptions of who controls their food. Journal of Human Nutritionand Dietetics 13, 163–71.

Ruxton, C.H.S., Kirk, T.R., Belton, N.R. 1996: The contribution of specific dietary patterns to energyand nutrient intakes of 7–8 year old Scottish schoolchildren. Journal of Human Nutrition andDietetics 9, 5–31.

Sharp, I. 1993: Nutritional guidelines for school meals. Report of an Expert Working Group. London:The Caroline Walker Trust.

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Adults and the elderlypopulation


❏ review the dietary guidelines that have been made for adults in the UK;❏ identify the particular needs of men and of women;❏ review the nutritional aspects of a vegetarian diet;❏ consider the effects of alcohol consumption on the achievement of dietary goals;❏ discuss some human situations that may influence diet and so affect the attainment of the guidelines, including

belonging to an ethnic minority group, having a low income, retirement and ageing.


❏ discuss the dietary recommendations and guidelines that are in existence in the UK for adults, and explain thereasoning behind them;

❏ explain the background to the special dietary needs of men, and particular diet-linked diseases, which theguidelines are aiming to prevent;

❏ discuss why women may be considered a nutritionally vulnerable group at certain stages of their life, andwhether the dietary guidelines address their problems;

❏ discuss the advantages and disadvantages of following a vegetarian diet;❏ explain why members of some ethnic minority groups consume different diets and the implications of this for

dietary guidelines;❏ discuss the implications of living on a low income in meeting dietary recommendations and goals;❏ show how social, psychological and emotional circumstances may affect an older person’s diet and the

implications of these for meeting nutritional guidelines.

Dietary reference values and nutritional guide-lines have, of necessity, been devised for the popu-lation as a whole. It would be both impracticaland confusing to set a great number of differentrecommendations for various subgroups in thepopulation. The guidelines current in the UK arevery much in line with those in other Westerncountries and are the result of a wide consensus.

As discussed in Chapter 3, the progresstowards achieving these guidelines is slow and insome cases trends in consumption appear to bemoving contrary to the desired direction. It hasbeen suggested that the guidelines are too ambi-tious as they set goals that only a very small

amount of the population currently meet. Anintermediate set of guidelines, closer to the actualpatterns of consumption in the population, maybe a more realistic target.

It is also important that a ‘whole-diet’approach is adopted. Many people at presentmistakenly believe that, if they change just oneaspect of their diet, they are already eating morehealthily. For example, there has been an increasein use of low-fat spread and semi-skimmedmilk. These changes are desirable, but they donot go far enough towards a healthier diet. Suchchanges may result in a lower energy intakefrom dairy fat, which is then replaced by fats

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contained in biscuits or processed conveniencefoods. More extensive changes to the diet, forexample, becoming vegetarian may have anumber of positive health effects but, at thesame time, increase risks from unforeseen con-sequences in the diet.

In addition, it should be recognized that thereare many groups within the population who, fora diverse number of reasons, cannot achieve thetargets. All of these groups will be considered inthis chapter, exploring the reasons why they mayhave different needs, and considering some ofthe barriers that prevent them achieving dietaryguidelines.

Adult men

Many dietary guidelines around the world origin-ated from a concern about morbidity and mor-tality from coronary heart disease. Consequently,they were based largely on findings from studiesof men, since almost all the early studies targetedgroups of men. In addition, their primary focuswas related to intakes of fat, which for manyyears has been the major dietary factor linked to coronary heart disease development. Only in more recent years have dietary guidelineswidened to include other dietary components,

such as starchy carbohydrates, alcohol, salt andother micronutrients, including the antioxidantvitamins.

Do men have problems achieving theseguidelines and are they appropriate?

Most men understand that they are at risk of heartdisease, although many adopt the attitude that ‘itwon’t happen to me’. Consequently, motivation tochange dietary habits may not be very great. Thismay be sustained by social norms, which, in somecultural subgroups, expect men to have a trad-itional diet that contains plenty of meat and not to eat the more ‘feminine’ salad, fruit and vege-tables. Some acceptance of a need to changespreading fat was achieved by the initial advertis-ing of a polyunsaturated margarine in the UK asthe ‘margarine for men’.

Among some men there is also a generalreluctance to be concerned about their health,reflected in lower attendance rates to health ser-vices by men than by women and a lower uptakeof screening services. Exposure to informationabout healthy eating is generally less amongmen, as women gain this information from mag-azines (often in association with articles on cook-ery or weight loss), from information at healthcentres and supermarkets. In all cases, men haveless access to these sources.

Further, traditional education philosophyexcluded boys from learning about food andnutrition at school; the National Curriculum inthe UK has introduced some teaching abouthealth and diet to all children.

Concern about body weight is much lessamongst men, although current trends in the UKshow that more men than women are over-weight. In addition, the distribution of body fatin men, with a greater tendency to depositabdominal fat (apple-shape) means that over-weight is a greater health risk.

Traditionally, more men have been smokersand heavy drinkers, although in both cases ratesin women have increased in the last twodecades. These are lifestyle factors, which maycompound risk in several chronic diseases thatalso have nutritional risk factors. Men, there-fore, are at nutritional risk and it is important

Refer back to Chapter 3 to remind yourself of thebasics of a healthy diet.What are the dietary reference values – what arethey based on?■ Are they to be used for assessing the diets of

individuals?■ Why are healthy eating guidelines produced?■ What is the difference between dietary refer-

ence values and healthy eating guidelines?■ What were the nutritional targets set in the

‘Health of the nation’ report?■ How are these converted into a practical way

of planning diets?■ How does the Balance of Good Health help

consumers to achieve a healthy diet?

Activity 13.1

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that attempts to change to a healthier diet aremade, encompassing whole diet changes.

Studies show that, when changes are made,results are better in the younger age group thanin older men. In addition, men in the highersocial classes are more likely to make changes.Therefore, greatest benefits are seen here. There isa need to target men to increase their awarenessof the importance of dietary change as well as exercise, and other lifestyle factors, such asdrinking and smoking, in a more active approachto disease prevention. This will be easier toachieve in some groups than others; regrettablythose with the greatest need for change are often the ones who are most difficult to reach.Imaginative approaches on the part of primaryhealth care teams and health promoters areneeded. These can include health promotion inthe workplace or through social clubs, perhapsrelated to support of sporting activities.

Adult women

There is a dilemma in trying to devise an optimaldiet for women, as different stages in a woman’slife may require different nutritional priorities.

A very important point to remember is thatwomen generally have a smaller food intakethan men, related to their lower energy needs.Within this smaller intake, however, they stillneed to obtain all of the nutrients essential for

good health. Consequently, they have less mar-gin for error in their diet – most of what they eathas to be nutrient rich. Eating too much ‘emptyenergy’ will result in an insufficient intake ofmicronutrients and possible health risks.

Most of the specific health issues for womenhave been discussed in other parts of this book;they are highlighted here to remind the readerof the vulnerability of the female to poor nutri-tion at various ages.

A female adolescent requires a certainamount of body fat to be present for normalreproductive activity to begin. Yet, during thistime of life, many adolescent girls feel an enor-mous pressure from society to restrict theirweight gain and achieve a slim body shape.These two goals are difficult to reconcile, withthe result that some girls do not start to men-struate or, having started, stop again, as theirbody weight falls. This has implications for bonehealth in later life, in particular, because adoles-cence is also the time when the bone assimilatesits minerals and achieves most of its final mass.Once into her early twenties, a woman is nolonger able to add significant amounts of cal-cium to her bones, with the result that, if thebone mass is not optimal, she may developosteoporosis in her early old age.

In early adult years, a woman may want tohave children. Research dating back to the Dutchhunger winter in 1944–45 (when the populationof Holland suffered severe food shortages for aperiod of 8 months), but replicated in manystudies since then, has shown that an adequateamount of body fat is needed for normal fertility.The normal development of the fetus is threat-ened if the woman is underweight. More recentwork shows that various vitamins and mineralsmust be present in sufficient amounts from thebeginning of the pregnancy to avoid low birth-weight and associated risks to the child, both inits early and later life.

Certain diseases are also a particular threatfor women. Women experience anaemia muchmore commonly than men, principally becausethe iron lost in blood during menstruation is notreplaced adequately from the diet. Both cancerof the breast and heart disease cause a largenumber of deaths, and are believed to have a

Work with a partner on this activity. Imagine you are given the brief of tackling one aspect ofhealth promotion for a group of men (it could be reducing alcohol intake, losing weight, takingmore exercise or altering the diet). Make somesuggestions about:■ which group of men you would like to use as

your client group;■ which aspect of health promotion you would

like to tackle;■ how you might go about identifying the prob-

lem, and trying to suggest solutions.What do you think are going to be the main barriersto success?

Activity 13.2


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dietary component. In addition, osteoporosis isa condition that causes disability in many moreelderly women than men.

Physical activity, which is beneficial in pro-moting health, has for many years been moresocially acceptable for men than for women.There is now an increase in women taking part insport, but problems of time and access to sportsfacilities still bar many women from being moreactive. There may be a reluctance also to exposea less than perfect body in the gym.

Social research shows that a woman’s foodchoices tend to be dictated more by the likes and dislikes of her partner and children than byher own preferences, even when she is the onewith the major responsibility for food provisionwithin the household. Thus, even if a womanmight want to eat a healthier diet, she may experi-ence pressure from her family to minimizechange.

Finally, it must be recognized that womenrepresent the majority (in the UK, 65 per cent) of those living in poverty, with its associatedeffects on nutrition. As a result of these conflictsand dilemmas, women generally have morenutritional problems than men.

Vegetarians

There has been a steady increase in the UK in thenumber of people who reject meat from theirdiet and follow some variant of the vegetariandiet. Surveys suggest that between 5 and 10 percent of the population may be following someform of vegetarian diet. Numbers tend to begreatest in females and among teenagers andyoung adults, although people of all ages arerepresented. The move to vegetarianism mayinitially include the rejection only of red meat,but might further also exclude white meats, fishand, occasionally, other animal products such aseggs and cheese. Thus, the diet is based on cer-eals, pulses, nuts, vegetables and fruit. Many vegetarians, but not vegans, also include dairyproducts and eggs. Various categories of vege-tarianism have been defined according to thefoods of animal origin that are included in thediet (e.g. a lacto-ovo-vegetarian will eat cheeseand eggs, a pescarian will eat fish).

The reasons for adopting a vegetarian dietvary, but may include:■ compassion for animals and concerns about

animal welfare;■ rejection on ethical grounds of the intensive

production methods used in animal hus-bandry and food production;

■ concern over Western overindulgence infood, and exploitation of poorer countriesand world resources;

■ dislike of the taste, texture or smell of meat;■ concern over the safety of meat and animal

products in the light of ‘food scares’, such asSalmonella, bovine spongiform encephalop-athy (BSE) and the use of antibiotics;

■ religious or cultural reasons.From a nutritional perspective, an ideal diet is

one that contains a wide variety of foods, provid-ing maxiumum opportunities to meet nutritionalrequirements. However, it cannot be said thatfoods of animal origin are an essential part of sucha diet, and there are many populations around the world who exist on diets that are exclusivelyplant based. Problems of deficiency may arisewhen there is overreliance on a limited number offoods, or foods of limited nutritional value, forexample, cassava, yam and maize. Where thequantity of food supplied by such a diet is suffi-cient, and the diet contains a variety of plantfoods, then nutritional adequacy is not a problem.This is generally the case in Western societies anda well-planned vegetarian diet may provide agreater diversity of foods than one based aroundmeat, including more vegetables, pulses and nuts.As a result, many nutrients may be present ingreater amounts than in an omnivorous diet.However, meat and animal products are rich in a number of minerals and vitamins that may not be sufficiently replaced in a vegetarian diet.

In general, a well-balanced vegetarian dietcontaining grains, vegetables and nuts is likelyto provide more of the following nutrients:folate, vitamin C, carotene, thiamin, vitamin Eand potassium.

Nutrients about which there may be someconcern, especially if the diet lacks dairy prod-ucts, include the following: protein, iron, cal-cium, iodine and zinc, vitamin B12, vitamins A and D, and n-3 fatty acids.

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It is particularly important that attention ispaid to these nutrients in the diets of vegetarianinfants, children and adolescents (see Chapter 12).For adults, there is little evidence for a defi-ciency of most of these nutrients; however, anumber are discussed below.

Vegetarians are probably more prone to iron deficiency anaemia because of the poorerbioavailability of iron from plant-based diets.Attention should be paid to maximizing absorp-tion by including enhancing factors, such asfoods containing vitamin C in the diet. VitaminB12 occurs only in foods of animal origin and,therefore, their strict exclusion will be a riskfactor for deficiency. Many foods designed forvegetarian diets, such as meat substitutes, arefortified with the vitamin, but vigilance isneeded to ensure an adequate intake.

Vitamin D status may be compromised whenthe vegetarian diet is also very high in phytateand low in calcium, as has been reported insome macrobiotic diets and among people ofAsian origin in the UK.

Lower intakes of the long-chain n-3 fattyacids are also a feature of vegetarian diets thatexclude fish. Levels of these fatty acids are lowerin plasma of adult vegetarians and also in themilk during lactation. These fatty acids have arole in the development of the retina and centralnervous system in the infant, and the signi-ficance of these lower levels for infant develop-ment is being studied.

More interest has been focused on the posi-tive aspects of a vegetarian diet, in relation tosome of the chronic diseases prevailing inWestern societies. Studies of adult vegetariansshow that they have similar energy intakescompared with omnivores. However, the bodymass index of vegetarians is on average 1 kg/m2

lower than in matched omnivores. The reasonsfor this are unclear, but may be attributable tolower fat or alcohol intakes. One of the reportedconsequences of the lower body weight is alower blood pressure, which may confer advan-tages in terms of stroke and coronary heart disease.

Data from five cohort studies (Key et al.,1998), including 76 000 subjects, has shown thatvegetarians had a 24 per cent reduction in

mortality from coronary heart disease. Mortalityin semi-vegetarians, who ate fish only or meatless than once per week, was intermediate betweenmeat eaters and vegetarians. It is proposed thatthese differences can be attributed to lowerintakes of saturated fat in vegetarians, andrelated lower plasma total cholesterol concentra-tions. In addition, vegetarians tend to havehigher intakes of polyunsaturated fatty acids,especially linoleic acid and dietary fibre. Both ofthese will also affect cholesterol levels, and therisk of coronary heart disease.

Higher intakes of dietary fibre are also pos-sibly responsible for lower rates of constipation,diverticular disease, appendicitis and gallstonesthat have been reported among vegetarians. Atpresent, there is no firm evidence that vegetar-ian diets protect against cancers.

Overall, a planned vegetarian diet can meetmany of the dietary guidelines and contribute tobetter health. There are a number of possibleshortcomings from the exclusion of meat anddairy products, and these nutrients should bereplaced from other foods. A badly constructedvegetarian diet will, however, carry no healthadvantages and may be hazardous to long-termhealth. The possible advantages and disadvan-tages of a vegetarian diet are summarized inFigure 13.1.

Minority ethnic groups

Many people around the world for a variety ofpolitical or economic reasons move to and settlein a country that is not their own. In doing so,they become immigrants to that country. If theculture of the host country is similar to that ofthe immigrant’s own mother country, settlementis relatively easy. If there are many cultural,religious and language difficulties, the immi-grant may experience alienation in the hostcountry. If the immigrant is a refugee forced toleave the home country, the psychological chal-lenges of adjustment may also create difficultieswith the diet.

Food habits are one of the aspects of animmigrant family’s culture that may undergolittle adjustment, resulting potentially in somenutrition-related problems. These may be the


284

result of a number of factors that impinge onthe diet.

When traditional foods are eaten, the dietarymix may seem quite different from that of thetypical host country diet. Consequently, some ofthe guidelines that have largely been createdaround a ‘British’ diet may not be applicable. It isnecessary, therefore, to explore two main issues:■ what do some of the larger minority ethnic

groups in Britain eat, and what conse-quences does it have for their health?

■ should the dietary guidelines be applied tothe traditional diets eaten, and how can thisbe achieved?The main groups of immigrants in the UK are

Europeans (including people from SouthernIreland and those of Eastern European andMediterranean origin), Asians from the Indiansubcontinent (including Indians, Pakistanis andBangladeshis), people of Afro-Caribbean originfrom Africa or the West Indies, and Chinese peo-ple, from Singapore, Hong Kong and Vietnam aswell as some from China. There are many othergroups that have settled in the UK from every

country in the world, but numerically these aremuch smaller, and have not been studied as an identified group, although it is possible thatnutritional issues do exist. People belonging tominority ethnic groups including those of mixedrace in the UK represent about 8.8 per cent of theUK population (2001 figures).

The Europeans, together with the smallgroups of immigrants from various parts of theglobe not mentioned above, have not as a groupbeen reported to experience nutritional difficul-ties or possible deficiencies in Britain. It is pos-sible that, like any other individual, they mayexperience personal dietary problems, whichmay be exacerbated by factors related to theirethnic origin.

Features common to many members ofethnic minority immigrant groups

Newly arrived immigrants may share the common feature of belonging to a socially dis-advantaged sector of society, even if they wererelatively well off in the home country. This may

Figure 13.1 The possible advantages and disadvantages of a vegetarian diet.


285

be reflected in various aspects of life, includinglow income or unemployment, poor housing,poor educational opportunity and less access tohealth care. All of these may have a bearing onnutrition. In those who maintain the traditionaldiet, the higher cost of some imported foods andthe need to travel to specialist shops may limitthe amount of food eaten.

The traditional diet may be modified by thesubstitution of some ‘British’ foods to replaceunavailable traditional items. Unfortunately, the British foods chosen are often those of poor-est nutritional quality, such as highly refinedprocessed items like cakes, biscuits, crisps andsoft drinks. These are not nutritionally compar-able to the traditional items they may be dis-placing. In this way, a well-balanced traditionaldiet, by attempting to become integrated into the British diet, becomes nutritionally poorer. Itis important that, where some adaptation to theBritish diet occurs, the foods chosen should benutritionally adequate.

For the children of some of these families,especially those new to the UK, school mealsmay pose a major dilemma. If the child has beenbrought up from infancy eating only a trad-itional diet, foods presented in school may becompletely unfamiliar both in content, style ofpresentation and expected way of being eaten.In time, peer pressure may encourage these chil-dren to sample British foods and, if they enjoythem, they may eventually request them athome. It should be pointed out, however, thatmany of the children in British schools who are of minority ethnic group origin are second-or even third-generation children of formermigrants, who no longer consider themselves asanything other than British, and have perhapsbeen eating the typical British diet for the wholeof their life. Traditional foods may be somethingthat they eat only in the presence of members ofthe older generation or occasionally at home.

A different problem exists at the oppositeend of the age spectrum, as some of the earlymigrants into Britain in the late 1950s and1960s reach retirement and old age. For many ofthese, life has remained very traditional. This isparticularly true for the women who may havenever worked, or integrated much with the local

population. Services such as meals on wheels or luncheon clubs may not provide appropriatemeals. Because of this, the person may beexcluded from receiving this provision. In someparts of Britain, special ‘ethnic’ meals on wheelsare provided for the local population, but thisservice is not widespread. In most cases, theolder generation of immigrants rely on theirchildren and grandchildren to provide them withfood, if they cannot cope themselves. Welfareservices are gradually recognizing the need toencompass the needs of ethnic elders in theirprovision.

Asian immigrants

Much attention has been focused by nutritionistson the South Asian immigrants from Bangladesh,India and Pakistan. In addition, smaller numberscame to Britain from Africa, in particular Ugandaand Kenya.

Religion is an important part of the culturefor most of these groups, and many are follow-ers of one of the three major religions found inAsia: Hindu, Islam and Sikh. All three have spe-cific dietary laws, which have an impact on thefoods consumed and may result in nutritionalconsequences. The main features of the reli-gions and their dietary prescriptions are out-lined below.

Hindu religionThis is an ancient religion, one of whose mainprecepts is the sanctity of life and the transmi-gration of the soul. As a consequence, there is aprohibition on the taking of life, including thatof an animal for food. Thus, traditionally Hindusare vegetarian, eating only plant foods, or foodsfrom animals that do not include killing – forexample, dairy products. Eggs may be avoidedby some Hindus, particularly women, as they areseen as a potential source of life. The cow isdeemed sacred, and its products are prized in thediet. Orthodox Hindus will adhere strictly to thedietary laws, but some who are less strict mayeat meat, but usually not beef or pork (the pig isconsidered unclean).

Fasting, which means either total abstinencefrom food, or alternatively the eating of ‘pure’


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foods – fruit, yoghurt, nuts and potatoes – maybe a regular occurrence.

IslamFollowers of Islam are Muslims. The religiousteachings in the Koran encompass most aspectsof life, including dietary laws, as well as rules onfasting. Muslims are permitted to eat the flesh ofruminant animals (which excludes pork), poultryand fish (some but not all exclude shellfish). Theanimal must be ritually slaughtered by a regis-tered butcher; the meat is bled and sacrificed toAllah. It is thus made ‘halal’. Meat prepared inthis way is available in Britain, either fresh orfrozen. Milk and dairy products are not a majorpart of the Muslim diet in the UK, although theyare eaten increasingly, as the diet becomes moreBritish. Even though meat is allowed in theMuslim diet, the amount actually eaten may notbe very large. This is especially true for womenwho normally eat last, giving the larger share tothe men in the household.

All Muslims over the age of responsibility(early adolescence) are required to fast from sun-rise to sunset for a 4-week period each yearknown as Ramadan. The actual number of hoursof fasting depends on the time of year in whichRamadan falls. When it occurs in the summermonths, there may be up to 16 hours of fasting aday, but perhaps less than 8 hours in the winter.In the early years of the twenty-first century, thefast falls in October/November/December, and ismoving back through the year into the Autumnmonths. Ramadan is associated with eating duringthe hours of darkness, with special foods beingprepared, many high in fat and sugar. Familiesrise before dawn to eat; this alleviates the prob-lems of hunger during the day. Ramadan finisheswith special celebrations, again involving particu-lar foods prepared only at this time of the year.

SikhismThis religion developed comparatively recently(in the sixteenth century) and incorporates somefeatures of both the Hindu religion and Islam.Dietary restrictions are less than in either ofthese religions: eggs or meat are not prohibited,but some Sikhs may believe in the transmigra-tion of the soul and are vegetarian.

Very few eat beef, and pork may be con-sidered unclean, as with the other religionsdescribed above. Animals for meat must bekilled in a prescribed manner by a single blow tothe head; meat produced in this way is known as‘khatka’.

General featuresTraditional Asian meals may consist principallyof the staple (a rice or wheat dish), together withone or several side dishes, which provide the gar-nish or flavour part of the meal. Fruit is morelikely to be eaten for dessert rather than a sweetcooked dish. Sweets may be prepared for specialoccasions, rather than everyday. The mostWesternized meal may be breakfast, which mightinclude cereals and toast, rather than the trad-itional leftovers from the previous day. In theHealth Survey for England 1999 (DoH, 2001),which considered the health of minority ethnicgroups, consumption of red meat and fried foodswas reported to be high among Bangladeshigroups, and the diet was also low in fibre. TheIndian diet contained least amounts of red meat(for religious reasons), lowest fat levels and had ahigher fibre content.

Asian women tend to have a more markeddomestic role in the traditional household.Particularly for these women, integration withthe British community may be slow. Changeoccurs most quickly in those communities wherethe women have roles outside the house: goingout to work, or meeting others.

Afro-Caribbean immigrants

Immigrants to Britain from the Caribbean arepredominantly of African descent, althoughsome may be of Indian origin. The cultural out-look of these groups has been influenced by lifeboth in the Caribbean and Britain. Several eth-nic subcultures exist, linked to the island of ori-gin. Traditional Caribbean food habits may bekept by significant numbers of this populationand are likely to be diverse. Generally, they posefew nutritional problems, apart from obesity.

The diet is largely based on cereals, such ascorn, rice and wheat, and starchy vegetablesincluding potatoes. These may be served in the


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form of spicy stews or soups, containing manydifferent vegetables. Many of the traditionalfoods, such as mangoes, breadfruit, cassava,green bananas, plantain and yams, are availablein West Indian specialist shops, indicating thatthey have remained an important part of the diet.The diet is higher in carbohydrate (50 per cent),lower in fat (32 per cent) and alcohol (2 per cent)than the equivalent white British diet. Food pat-terns may be different among this populationand dietary assessment requires specialist know-ledge (see Sharma and Cruickshank, 2001).

One of the subgroups of the West Indiancommunity are the Rastafarians who aspire toreturn to Ethiopia, which is seen as the Africanhomeland. There is a strong adherence to theBible, and many of the dietary laws are basedon a very strict interpretation of Bible writings.In its strictest form, the diet is vegetarian, con-taining no meat or animal products. It is basedpredominantly on fruit, vegetables and cereals.However, because pulses are not a major item in the West Indian diet, the vegetables tend to be starchy roots and leafy vegetables, both of which contain little protein. There can be alack of vitamin B12 in the diet. In other ways,however, the diet may be considered healthy,with a prohibition on alcohol, convenience andprocessed foods, and a low salt intake. As withall dietary laws, the extent to which the diet iskept will vary between individuals. However, asRastafarianism is perceived as conferring anidentity to the individual, there is a considerablemotivation to keep to the dietary laws.

Chinese immigrants

The Chinese have a food culture very differentfrom that of the indigenous British population,which has remained largely unchanged despitelong periods of settlement in Britain. Althoughsome British foods are included in the diet, usu-ally being requested by the children, these formonly a small part of the daily intake. The dietincludes rice as a staple, and meat, fish, fruit andvegetables prepared in many diverse ways.

Food is perceived by older Chinese as notjust providing nutrients but contributing to theoverall balance of the energy in the body. This is

described in terms of hot and cold (or male andfemale, yin and yang) properties. Foods areascribed such properties according to the effectsthey are believed to have on the body (not on theactual temperature of the food). In addition, par-ticular stages of life, such as pregnancy, as wellas illness, alter the body’s balance. An appropri-ate selection of foods can restore the balance.For example, if children eat a school meal that isconsidered ‘hot’, they will be given a ‘cooling’food to restore their balance when they returnhome. Thus, rather than avoiding British foods,the Chinese simply accommodate them, andadjust other foods eaten accordingly. There areno reports in the British literature of nutritionalproblems associated with the Chinese diet.

Potential nutritional consequences

Vitamin D deficiency began to appear amongchildren of Asian immigrants in the early 1970s.Initially, it was believed that the cause waslinked to the skin pigmentation, which reducedthe synthesis of vitamin D on exposure to sun-light. However, this was not supported by resultsof measurements of vitamin D synthesis afterultraviolet exposure in light- and dark-skinnedindividuals. A further possibility was that thetraditional dress of many Asian immigrantsrequired that the body be covered, allowing littleexposure of the skin and minimizing vitamin Dsynthesis. This may contribute to the deficiency,but is unlikely to be the sole explanation.

Investigation of the diet of affected andunaffected individuals has shown that mostvitamin D deficiency occurs in those who followthe most strictly vegetarian diet. Diets that con-tain no meat, eggs or dairy produce appear to be the most rachitogenic (rickets causing) amongthe Asian population. It has been suggested thatthe high content of dietary fibre and phytatereduces the availability of calcium and removesvitamin D from the body in the faeces. In add-ition, the lack of animal products directly reducesvitamin D intake. A strict vegetarian diet hasalso been found to lead to rickets amongRastafarian children. Health promotion cam-paigns among the Asian population have largelyreduced the occurrence of rickets among the


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children, although low plasma vitamin D levelsare still recorded. The problem of osteomalaciain adults (women, in particular), however,remains and appears to be difficult to prevent byeducation.

Anaemia arises in these groups from inad-equate intakes of iron, folic acid or vitamin B12,or a combination of these. Iron deficiency arisesin infants because of prolonged milk feeding,and inadequate use of iron-rich weaning foods.This has been found in both Asian and Afro-Caribbean families. Pregnant women are also atrisk, in particular those who are vegetarian.Language barriers, especially among thosenewly arrived in the country, may prevent themseeking or accepting medical advice to treat theanaemia.

Folic acid deficiency also occurs in pregnantwomen, whose needs are increased to supportfetal cell division. Prolonged cooking of vege-tables and reheating from day to day destroys allpotential folate in these foods. This is particu-larly a problem when the diet is vegetarian.

Vitamin B12 deficiency is particularly foundin vegetarian immigrants, being seen most inthe Hindu population in the UK. It may coexistwith iron and folate deficiency, and has alsobeen linked to a higher than average occurrenceof tuberculosis.

Studies on the incidence of dental cariesshow that pre-school children in immigrantgroups throughout Europe tend to have a higherprevalence of dental caries than the indigenouspopulation. This is particularly true among theAsian communities and is believed to be associ-ated with a higher intake of sugar-containingdrinks, including milk, and a higher frequencyof consumption of sugar products.

Obesity, diabetes and heart disease are thenewer diseases among the Asian population atpresent. Central obesity is particularly commonamong the South Asian groups, especiallyamong women (DoH, 2001). The incidence ofboth diabetes and heart disease is higher amongmembers of Asian minority groups than theindigenous British population. This may seemsurprising, since the traditional diet is rich instarchy carbohydrate and contains large amountsof vegetables, in line with dietary guidelines.

Recent work has shown that Asians have higherplasma levels of lipoprotein(a) than Europeans.This increases coronary heart disease risk. Inaddition, the Westernized diet and lifestyle con-tribute to increasing body mass index with cen-tral fat deposition, insulin resistance and raisedblood lipids. These combine to produce an ele-vated risk for both heart disease and diabetes. Akey factor in prevention is physical activity,which can help to reverse many of these trends.However, uptake of physical activity is low inmany members of these groups.

For all of the immigrant groups, the trad-itional diet more closely resembles the dietaryguidelines than does the current British diet. Itis important that minority ethnic groups areencouraged to retain their traditional dietarypractices, perhaps incorporating some of thestaple foods available in Britain. They should bediscouraged from including the unhealthyBritish dietary practices into their traditionalpatterns.

One of the most disadvantaged groups arerefugees, who may come from many differentcountries. There is a high level of food insecur-ity in these households, particularly within thefirst two years of arrival in the UK. It is difficultto reach people in these groups, but childhunger is likely to be common, and signifi-cantly associated with recent arrival and receiptof fewer benefits.

Low income and nutrition

People on a low income may be living inpoverty. This is a relative term: it can be takento mean an absolute lack of material posses-sions but, in Western society, it is more com-monly used to reflect disadvantage in relationto the rest of society. In practice, the definitionvaries between different organizations. Twodefinitions that are used are:■ people receiving less than half of the aver-

age income (whether from employment orstate benefits); and

■ people having to spend more than 30 percent of income on food.Numbers of people in poverty have been

increasing in Europe throughout the last decades.

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It is documented that people in these situationshave poorer health in almost every measure usedto assess health, with excess morbidity and mor-tality at all ages. Various groups are particularlyvulnerable to poverty. These include the following.■ Families with children, in particular, where

there is a lone parent or where neither par-ent is in employment.

■ Women, owing to the traditional dependenceof women on a male breadwinner, their trad-itional role as carers of children and theirpoorer pension rights as a result of incompleteemployment records. In two-adult householdswhere the woman is the sole wage earner, theincome is usually lower than in those with amale wage earner.

■ People with a disability, owing to pooreremployment prospects and higher than aver-age living costs.

■ Members of minority ethnic groups, owingto a higher unemployment rate and a greaterrepresentation among the low paid. In add-ition, there are now many refugees and asy-lum seekers throughout Europe who areoften in severe financial hardship, whichalso reflects on their nutritional intakes.

■ Young people who have left school but havenot been able to find work. They have verylow entitlements to benefits and may not besupported by their families, leading perhapsto homelessness and a life in poverty.

■ Homeless people have major problems inachieving an adequate food intake. They mayhave additional problems that compromisenutritional status, such as alcohol or drugabuse. Alcohol may provide a substantial pro-portion of the energy intake. Studies on thisgroup find that they are up to four times morelikely to be underweight and have a diet thatis low in a wide range of nutrients. Sheltersfor the homeless and soup kitchens are animportant source of nutritional provision andattention to the quality of the food couldmake a difference to the status of this group.Income is not the only factor contributing to

poorer health experienced by people in thesegroups. One of the main factors is likely to betheir diet, but poorer housing, low self-esteem,poorer educational opportunity and lifestyle

habits detrimental to health, such as smoking,all make a contribution.

Characteristics of the diet

Expenditure on food is described as elastic,which means that when income is limited andother, fixed, expenses have to be met, the foodbudget can be trimmed accordingly. However,those on a limited income may spend up tothree times more, proportionately, on food com-pared with the average UK family.

The expenditure on food is cost efficient; theannual National Food Survey consistently showsthat the lowest income groups obtain morenutrients per unit of money spent. Table 13.1shows some of the foods typically bought by thelow-income and high-income groups, and inTable 13.2 the amount bought per 1 pence ofexpenditure is shown.

Studies such as these of the foods eaten typ-ically show that low-income families rely moreheavily on white bread, whole milk, sugar, eggs,meat products and margarine, and consume lessreduced fat milk, poultry, carcass meat, fish,fresh vegetables (excluding potatoes), fruit,brown and wholemeal bread. Vegetables andpotatoes are more likely to be processed ratherthan fresh. There is also less variety of foodseaten; for example, among pregnant women inEdinburgh and London, the poorest had onlyhalf the number of different foods in their dietcompared with the richer women. The diet is,therefore, more likely to be monotonous, withfew new additions.

Table 13.2 shows that, for every food group,those households with a lower income buy more(by weight) for their money. This applies to evensimple products, such as confectionery or softdrinks. Overall, expenditure is also less, with amean expenditure of £22.03 by group A and£14.07 by group D recorded by DEFRA (2001).

This cost efficiency often necessitates shop-ping around to find the best value for money,which may be time consuming. Some poorer resi-dential areas may have limited shopping facilities,and the term ‘food deserts’ has been coined todescribe this situation. Access to the wider choiceof foods in larger supermarkets may be limited by


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lack of transport or insufficient resources to makethe trip worthwhile. In general, about 30 per centof the British population have no access to a carand are, therefore, dependent on public transportfor their access to more distant shops. In addition,the temptation of a large variety of foods on offermakes a stark contrast with the amount of moneyavailable. Consequently, local and often smaller

shops may be used, where both choice and valuefor money are likely to be less. There may also bea problem of a lack of storage facilities, necessi-tating frequent purchases of perishable items.Shopping becomes a chore, with little scope forenjoyment. It should also be noted that ‘value formoney’ in terms of quantity of food purchaseddoes not necessarily equate to nutritional value.

Types of foods eaten by the highest (A) and lowest (D) incomegroups studied by the National Food Survey 2000 (consumptionin g/person per week) (calculated from DEFRA, 2001)

TABLE 13.1

Food Income group

A DWhite bread 175 375Wholemeal, brown and other bread 258 174Breakfast cereal 155 110Biscuits 108 143Milk 464 833Cheese 111 88Meat and meat products 849 971Fats and oils 149 200Sugars and preserves 90 142Potatoes (fresh) 568 776Fresh green and other vegetables 857 581Processed potatoes and vegetables 462 581Fruit 895 573Fruit juice 483 211

‘Value for money’ of foods bought by high-income (A) and low-income groups (D) (amount purchased in grams per 1 pence spent) (calculated from DEFRA, 2001)

TABLE 13.2

Food Income group

A DMilk, cream and cheese 9.3 13.8Meat and meat products 1.9 2.8Fish 1.3 2.0Fats and oils 3.8 6.0Sugar and preserves 7.0 12.9Vegetables and potatoes 6.3 10.4Fruit 6.8 9.0Bread 7.8 11.5Cereals 4.2 6.3Soft drinks 22.1 31.3Alcoholic drinks 2.3 3.8Confectionery 1.6 2.0

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The cheaper foods bought may have poorer nutritional content; for example, cheaper meatproducts contain more fat and salt, cheaper veg-etables may be less fresh and have lower vitamincontents.

Nevertheless, families try to maintain con-ventional eating patterns to lessen the impact oflow income, often eating cheaper versions of‘mainstream’ meals. Also, parents endeavour toprotect their children against the effects on thediet of poverty, buying foods that the childrenprefer. As a consequence, children in low-income families may actually receive more oftheir favourite foods than children from better-off households. To achieve this, parents in sev-eral studies record missing meals. Protecting the children also means that the family meal isfocused on what the children prefer and will eat,rather than the likes and dislikes of other familymembers. Eating may cease to be a pleasure andbecomes simply a means to ward off hunger.

Food selection is made from a rational per-spective, with a view to the meal it can producein the most economical way. Therefore, foodsthat may require preparation and addition ofseveral other ingredients to constitute a mealare less attractive. A ready-made product, suchas a meat pie, needs few additional items to

make it into a complete meal, in contrast to aleaner meat, which itself contains less energyand requires vegetables, pasta, potatoes, bread,etc. to make a meal. Predictability of portionsize and number also helps in meal planning.

As one of the primary concerns is to feelsatiated after a meal, foods that provide a largeamount of energy for a small financial outlaymay be preferred. Consequently, foods high infat and sugars will be more satisfying than alow-fat, low-sugar food and will provide a cost-efficient source of energy. The cost to supply420 kJ (100 Calories) from a variety of snackfoods is shown in Table 13.3. Not all are nutri-tionally poor; for example, bread and milk canprovide a cheap nutritious snack.

Nutritional implications

Current dietary advice (discussed in Chapter 3) isto eat more fruit, vegetables and starchy carbo-hydrate, and to reduce the intake of fats, particu-larly from whole fat dairy products and meatsrich in saturated fats. In addition, the consump-tion of fish is encouraged. The National FoodSurveys show that the trend towards a healthierpattern in the diet is more marked in the higherincome groups surveyed and, in many cases,

Cost of common snack foods, in pence, to supply 420 kJ(100 Calories). Values calculated from Food Standards Agency(FSA, 2002b) and at 2002 supermarket economy prices

TABLE 13.3

Food Costs to provide 420 kJ (100 Calories) (pence)

Digestive biscuits 2Wholemeal bread 2Kit Kat (chocolate wafer) 6Crisps 7Milk 7Banana 10Chocolate bar 12Peppermints 13Coca cola 13Sponge cake 15Yogurt 21Orange/satsuma 35Apple 42


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is moving in the opposite direction in the poorergroups. Thus, although there is a small down-ward trend in fat intake in poorer families, moreof that fat is still saturated, and fruit and greenvegetable consumption in one study was foundto be equivalent to two apples and ten Brusselssprouts per person per week.

Evidence collected in many centres aroundthe UK has shown that the costs of a ‘healthierbasket’ of foods are greater than for a ‘lesshealthy’ basket. The difference in price variesbetween regions of the country, but may repre-sent an excess cost of 20 per cent for the ‘health-ier’ basket. In addition, the access to many of thehealthier items may be more limited in the areaswhere the poorer families may shop.

The stresses of living on a low income mean that health concerns are not one of thehighest priorities, even though evidence sug-gests that the desire to eat more healthily exists.Knowledge about what constitutes a healthierdiet is also present among poorer families,although it may be fragmentary. Reports haveshown that, if there was more money to spend,then this would be used to buy more fruit, vege-tables and leaner meats. At present, for suchfamilies, the cost of the food takes precedenceover issues of taste, cultural acceptability andhealthy eating.

Members of these families run the risk ofhaving lower intakes of many of the micronu-trients. In particular, these include iron, zinc,calcium, magnesium and potassium, as well as the vitamins, especially vitamin C, folate,riboflavin, niacin, beta-carotene and vitamin E.Many of these are the ‘antioxidant nutrients’,which are believed to be especially important tohealth. At the same time, the diet may be low innon-starch polysaccharides (NSPs) and polyun-saturated fats, but contain excessive amounts of saturated fat and sugars. The consequencesfor health are likely at all ages. Links with nutri-tion have been discussed also in the relevantsections of the book; a summary is providedhere.■ Infants are less likely to be breastfed,

although there has been an increase in preva-lence reported in the Infant Feeding 2000Survey (Hamlyn et al., 2002). Breastfeeding

is protective against infection in early life,enhances gut development, and may protectagainst allergy and eczema. It is also associ-ated with better school performance in childhood and a higher IQ for children bornpre-term.

■ Infants in low-income families have ahigher consumption of infant formulae,potatoes, confectionery, squashes and softdrinks, and a lower consumption of milkproducts and fruit. Nutrient intakes arehigher in saturated fats and cholesterol, andlower in carotene and vitamin C.

■ Toddlers have slower growth and slowerrecovery from infection, but also more havea high body mass index (BMI), more dentalcaries and higher blood lipids. Their diets arehigher in saturated fatty acids, sugars, starchand sodium (present in higher amounts inprocessed foods that form a larger part of thediet). There are lower intakes of NSPs, beta-carotene, vitamin C, iron, zinc, calcium andiodine.

■ Older schoolchildren have lower intakes ofmost vitamins and minerals, lower levels ofactivity and poorer bone accretion. Thereare higher rates of anaemia among teenagegirls and lower iron status, which probablyimpacts on cognitive ability. If the poor ironstatus continues into pregnancy, there arehigher risks of stillbirth, low birthweight,and increased risk of hypertension and heartdisease in the offspring later in their lives.

■ Lone parents have a greater likelihood offalling below the lower reference nutrientintake (LRNI) for many nutrients, the greatertheir ‘poverty index’. (This was assessed on anumber of lifestyle factors associated withlow income.) Pregnant women have gener-ally lower intakes of energy and nutrients,poorer weight gain and higher occurrence oflow birthweight babies. This has implica-tions for their future health and perpetuatesthe intergenerational effects of deprivation.

■ Older adults have lower nutrient intakes,poorer immune status and higher risk fromall diet-related diseases.

■ Special dietary requirements are more diffi-cult to follow.

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Practical help

Attempts have been made to devise sample dietsthat would be nutritionally sound and at thesame time cost no more than a low-incomebudget could afford. One such was the ‘tenpound diet’ produced by Ministry of Agriculture,Fisheries and Food (MAFF; see Leather, 1992),which gave precise amounts of 26 different foodgroups/items, which could be used to plan mealsfor 1 week within this budget. Many people feltthat this diet was socially unacceptable, as itexpected people on a low income to eat differ-ently from the rest of society.

More practical help is reported by theNational Food Alliance, which brings togethermany local projects engaged in empoweringpeople on low income and enabling them to worktogether in low-cost cafes, food cooperatives andother support groups. In this way, access to andeducation about food are improved, the feelingsof isolation are reduced and self-esteem can beenhanced. In association with these more socialimprovements, there can be a better diet and agreater interest in food and eating healthily.

Further work was undertaken on a strategyon food and low income by the Low IncomeProject Team (DoH, 1996). This aimed to bring

about a better understanding of the costs ofhealthy eating and facilitate access to healthierfoods by involving policy makers and providersof the food. As part of this initiative, ways ofmapping price and availability of healthy foodhave been developed. This can then be used toidentify areas that serve their local communitypoorly in terms of healthy food and attempt to address this. Local projects as part of theGovernments initiative on Social Exclusion inthe UK are helping local groups around thecountry to improve their access to better qualityfood; this may be through, for example, localstreet markets, ‘Get Cooking’ clubs or commu-nity cafes.

Older adults

In this discussion, the term ‘elderly’ is used torefer to men and women of pensionable age. Inthe UK, this generally means 65 years or over formen and over 60 years for women. The upperend of this age spectrum is not defined, but thereare increasing numbers of people over 100 yearsold in the UK (the majority are women).

In 2001, 18.3 per cent of the population inthe UK or 10.8 million people, was over retire-ment age (65 in men and 60 in women). Thetotal numbers of the elderly are increasing inmost Western countries: by 2030, it is estimatedthat one in four of the adult population will beaged over 65 years. In the UK, the greatestincrease in the early part of the twenty-first century will be particularly in the over-85 agegroup, with a smaller relative increase in theover-75s. The numbers between 60/65–74 willfall slightly, reflecting the lower birth rates in the1930s and during the Second World War. Theover-85 group are the most vulnerable sector ofthe retired population, and the most likely toexperience nutritional problems. However, it isanticipated that the increased knowledge ofnutrition among younger adults, and the con-sumption by some of a healthier diet, will reducethe occurrence of nutritional problems as theyget older. Current statistics suggest that an aver-age of 13 years of disability for men and 16years for women may be expected at the end oftheir life. The proposals of the ‘Health of the

Keep a record of your expenditure on food for aperiod of 1 week. Use the Balance of Good Health(FSA, 2001) to break down this expenditure intothe main food groups.■ Which of the groups costs you the most and

which the least?■ Is it possible for you to change your expenditure

on food?■ Could you spend less during the following

week?Prepare a plan of which food groups you couldbuy less and which more during the next week.How easy do you find this exercise?Make a list of the constraints that operate for you in trying to be more economical in your foodexpenditure. Which could you overcome, and whichare beyond your control?

Activity 13.3


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nation’ white paper of adding ‘years to life andlife to years’ are particularly relevant in thisgroup.

In making general statements about the vul-nerability of the elderly population, it is import-ant to remember that there is considerablevariation between individuals, as at any age.Preparation for retirement and a healthy old ageshould have begun earlier in life, with theacquisition of good eating habits and a healthylifestyle, involving both physical and mentalstimulation. Several studies confirm that healthand good nutrition coexist in the elderly, andwhen one begins to deteriorate, often so doesthe other.

Why are some elderly persons at risk?

Elderly people are at increasing risk of havingmarginal nutrition resulting from the ageingprocess itself and its impact on social factors, aswell as an increased incidence of disease. Thesefactors are summarized in Figure 13.2. Ageing isbelieved to be the result of an increase in oxida-tive stress and dysregulation of cellular function

over time. Supplementation with several antioxi-dants, most notably vitamins E and C has beenassociated with a reduced risk of age-associatedchronic diseases as well as maintenance of cognitive function.

It is helpful to consider how ageing affectssome of the body’s systems, which may in turncontribute to poor nutritional status.

Sensory systemChanges to the sensory system will have animpact on both the ability to obtain food as wellas its enjoyment. Loss of hearing or visual acuitymay restrict shopping as well as social contacts,leading to isolation. Loss of sensitivity to tasteand smell, which is a normal feature of ageing,can reduce the attractiveness of food. Elderlypeople may actually complain that food does nottaste ‘as it used to’. This is more likely to be areflection of their failing sense of taste, ratherthan a change in the food itself. Enhancingflavours with herbs and spices can overcomesome of these problems. However, it should alsobe recognized that a zinc deficiency can con-tribute to loss of taste acuity.

Figure 13.2 Factors resulting in increased risk in older adults.

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Gastrointestinal systemThe loss of teeth and wearing of dentures shouldnot have a major impact on food intake. It isreported that 57 per cent of the 65–74 age grouphave none of their own teeth, with 75 per cent ofthose over 75 similarly affected. Although moreelderly people are keeping their teeth for longer,there is still a substantial proportion of thisgroup dependent on dentures. If the dentures arebadly fitting, not checked regularly or even notworn at mealtimes because of discomfort, thedietary intake may suffer. Foods that are coarse,tough or require prolonged chewing may beavoided, possibly resulting in unbalancedintakes. Saliva flow is less in an older person,which may result in poorer oral hygiene andassociated infections adding to oral discomfort.

There is a reduced secretion of acid, mucusand enzymes in the stomach in old age, and adecrease in pancreatic function. Gut motility isslowed and this may prolong the digestionperiod to compensate for the poorer enzymesecretions, but a more likely result is constipa-tion. An adequate intake of dietary fibre (NSPs)as well as sufficient fluids is, therefore, desirable.The use of laxatives is to be discouraged, espe-cially those based on mineral oils, which candeplete the body of fat-soluble vitamins. Thereduced gastric secretion may produce a lowerlevel of intrinsic factor for vitamin B12 absorp-tion, as well as reduced solubilization of ironand its consequent absorption.

Kidney functionThe amount of active renal mass declines withage and is on average 30 per cent less at 80 thanat 30 years. Consequently, the kidneys may havea poorer ability to concentrate the urine, as wellas eliminating waste products more slowly.Therefore, fluid balance will be under less pre-cise control. In addition, thirst mechanisms are less sensitive. Thus, an elderly person runsthe risk of dehydration, if fluid intake is not consciously maintained. Sometimes, the addedproblem of incontinence, or even a reluctance tohave to get up in the night to empty the bladder,may discourage an individual from drinkingenough. Consequences of dehydration includeconfusion, dry lips, sunken eyes, increased body

temperature, dizziness and low blood pressure.An intake of eight cups (1.5–2 L) of drink per dayis recommended.

Lean tissueThere is a progressive loss of lean tissuethroughout life, although the actual extentdepends on lifestyle factors. On average, 40 percent of the peak tissue mass may be lost by theage of 70 years. This results in reduced basalmetabolism and, consequently, a reduced energyrequirement. The loss of lean tissue also resultsin a loss of strength and this may discourage anelderly person from engaging in even gentlephysical activity. Thus, it is clearly important tominimize the loss of lean tissue by maintainingphysical activity throughout life. This also main-tains appetite and promotes an adequate nutri-tional intake. There may be little change in totalbody weight associated with losses of lean tissuebecause of an increase in the amount of body fatwith age. The loss of lean tissue also represents areduction in both total body water and potas-sium in the overall composition of the body.

MobilityIt is estimated that over 50 per cent of adultsover the age of 65 years suffer from one form of disability and 33 per cent suffer at least onetype of severe disability. Arthritis, hypertension,heart disease, hearing and visual impairments,orthopaedic impairments and diabetes are themost frequent problems that pose difficulties forthis age group in carrying out daily activities. Inaddition to these, older adults suffer from pro-gressive bone loss, leading to increased bonefragility and susceptibility to fractures, knownas osteoporosis. This is discussed in greaterdetail in Chapter 10. There is an increased risk ofsustaining fractures with age. After the age of 50years, the lifetime risk of an osteoporotic frac-ture is 40 per cent for a woman and 14 per centfor a man. Hip fracture has the highest costs interms of morbidity and mortality. It nearlyalways necessitates hospital admission, with anaverage length of stay of 30 days. Only aboutone-third of these patients regain their formermobility. Deaths within the first 6 months after a hip fracture are approximately 20 per cent.


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There are many factors that interact to increasesusceptibility to osteoporosis that results in afracture. Genetic factors play a role, and theseinteract with environmental and dietary factors.Prevention of fracture depends on attention tolong-term diet, as well as maintenance of musclestrength and balance in old age to reduce therisk of falling. Supplementation of elderly peoplewith calcium and vitamin D has been effective inreducing fracture risk, and is a well toleratedtreatment. The use of drugs that slow boneresorption may also be preventative. It is import-ant for the nutritional well-being of this agegroup to maintain mobility as long as possible.

The immune systemThis becomes less efficient with age, with theresult that there is a higher risk of infection. Inparticular, there are lower levels of T-lympho-cytes, as well as an increased production ofautoantibodies. A poor nutritional status, in par-ticular, with relation to protein, zinc and vitaminlevels, can contribute to poor immune function.This may expose the individual to more minorinfections, but also increase the risk of moreserious problems, such as pneumonia or woundinfections.

The brain and nervous systemCognitive function may decline with age and thisis another factor that hinders independent living.Dementia is the most common cause of cognitiveimpairment, and is defined as a significant mem-ory impairment and loss of intellectual functions.Increased oxidative stress and an imbalance inantioxidant status may both contribute to thedecline in cognitive function. A study in the USAfound that plasma levels of vitamin C, E and A,carotenoids and selenium were correlated withmemory function among people aged over 60years (Perkins et al., 1999). The same surveyfound that 7 per cent of elderly Americans suf-fered from poor memory. Antioxidants protectthe integrity of blood vessels in the brain and,therefore, maintain circulation. This may also beeffective in protection against stroke, which isthe most common cause of vascular dementia.Other studies have shown that oxidative injury ispresent in the brains of patients with Alzheimer’s

disease and may play a role in its development.Various components of brain tissue appear to beaffected, including lipids, proteins and DNA, andit is likely that several different antioxidants maybe needed to protect the whole range of mol-ecules. In addition, a number of B vitamins espe-cially vitamin B6, B12 and folate may play a rolein the development of dementia through theirinvolvement in the metabolism of homocysteine.Elevated levels of homocysteine have been impli-cated in development of cognitive impairment.Therefore, maintenance of an adequate dietbefore old age may be protective against some ofthe degenerative changes in the brain, and inturn facilitate better nutrition in old age.

Other factorsIn addition, an elderly person is more vulner-able to many degenerative diseases, which oftendevelop over a considerable number of years.These may include atherosclerosis, arthritis,lung diseases and cancers. All of these maydirectly affect dietary intake. Drug treatment forthe disease may have an effect on appetite,digestion, absorption, excretion or metabolismof nutrients. Patients suffering from a numberof chronic conditions may be taking severaldrugs, which can interact with one another andproduce side-effects, such as nausea, diarrhoea,constipation or confusion.

Factors affecting nutritional status

In addition to ageing and its consequences,social and environmental factors may affect thenutritional status of an elderly person.

Inadequate intakeThere are many contributory factors influencinga poor food intake. These are summarized inTable 13.4.

Physical/medical factors■ Reduced mobility, from rheumatism, arthritis

or as a consequence of a stroke or lung dis-ease, may be sufficiently severe to make theindividual housebound or even bedfast.

■ Dentition and the state of the mouth play animportant part in the food intake.

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■ Appetite may be reduced by coexisting dis-ease or by its treatment, for example, diseaseof the gastrointestinal tract, associated withnausea and vomiting or discomfort after eating, will severely limit appetite.

■ Various drugs used in the treatment of avariety of illnesses may also have a depress-ing effect on the appetite.

■ Mental illness and depression are also likelyto affect food intake; there may be a com-plete disregard for eating with a loss of timesense so that mealtimes are ignored.

Social factors■ Availability of money: many of the retired

live on a fixed income. They may spend in excess of 30 per cent of their income onfood – considerably more than the UK aver-age of 9.5 per cent.

■ Lack of education about the importance ofnutrition and the existence of out of datebeliefs about food may prevent the elderlyindividual having a healthy diet, and mayrender them vulnerable to cranky notionsthat they see in the media.

■ Social isolation may be the result of retire-ment, re-housing, death of friends and rela-tives, breakdown of the nuclear family orillness. Several studies have shown that foodintake was less and nutritional status pooreramong those living alone and experiencingisolation. In particular, the widowed andmen were more acutely affected than thelong-term single and women. Conversely,where an effort was made to share food andeat in company, the food intake was better.

Psychological factors■ Depression, often the result of bereavement,

is probably one of the major causes of inad-equate food intake in an otherwise healthyperson and may persist for many years,resulting in malnutrition.

■ Altered mental function, with memory lossand unusual behaviour, may also occur andresult in erratic eating. There is an increase in the numbers of people cared for in the community rather than in institutions. It isimportant that the nutritional needs of theseindividuals are addressed. Severely dementedpatients are cared for in nursing homes andhospitals, where food and care are provided.It is still important, however, that nutritionalintakes are monitored and checked for adequacy.

■ Consumption of large amounts of alcoholmay be a coping mechanism for depressionor bereavement. The problems associatedwith excessive drinking may worsen otherconsequences of ageing.

Less efficient digestion and absorptionRelatively little is known about the effects ofageing on the functioning of the digestive tract.Reduced secretion of stomach acid and pancre-atic enzymes may result in poorer digestion andabsorption. There may also be minor malab-sorption syndromes, associated with a decreasein the intestinal mucosal surface and broader,shorter villi. Absorption may also be reduced asa result of chronic use of laxatives. The extentof these changes in a normal elderly person is,however, unknown.

Factors contributing to poor food intake in the elderlyTABLE 13.4Physical/medical factors Social factors Psychological factorsMobility Money available DepressionSelection of foods bought Food storage/preparation Bereavement

facilitiesFood preparation Education/knowledge Mental illness

of nutritionDentition Social isolation AlcoholismAppetite

DiseaseDrugs


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Altered needsMany bodily functions become less efficientwith ageing.■ There is decreased nutrient uptake by cells,

so that an apparently adequate intake for ayounger person may not produce the samelevels in the cells in an elderly person.

■ Energy needs decrease with ageing because ofthe reduction in basal metabolic rate conse-quent on reduction in lean tissue mass as wellas reduced activity. The latter is a culturalphenomenon and attempts are being made to change perceptions about the importanceof physical activity in older people. In manysocieties, people remain active to a very oldage, yet in Britain activity levels are generallyvery low in this age group. A reasonable levelof activity will ensure adequate energy intaketo cover the expenditure and incidentally provide sufficient other nutrients in the diet tomeet requirements. Conversely, a low activ-ity level may result in such low intakes ofenergy that basic nutritional requirementscannot be met. Thus, there is an importantnutritional argument for maintaining activ-ity levels. In addition, activity will help topromote cardiovascular fitness and maintainmuscle mass.

■ Protein needs may be higher as protein syn-thesis, turnover and breakdown all decreasewith advancing age. Homeostatic mechanismsregulating protein levels in the body may beless efficient in elderly people. In addition, illhealth, trauma and disease states may upsetthe equilibrium. Insufficient energy intakemay also compromise protein balance, as pro-tein will be used to meet energy needs.

■ The presence of disease and its treatment bydrugs may affect nutritional needs and theeffects may be exacerbated by drug inter-actions. Further problems may arise in a con-fused patient who fails to take drugs atprescribed times. Up to 60 per cent of drugstaken by the elderly are obtained withoutprescription. One of the commonest isaspirin, which interferes with the absorptionof vitamin C and may cause bleeding alongthe gut. It may thus cause a vitamin C deficiency or anaemia. Laxatives are also

frequently obtained without prescription andcan deplete the body of potassium, causingdepression and affecting cardiac function.

What is the nutritional state of older adults?

A major survey of diet and nutrition in peopleaged over 65 was carried out in Britain between1994–95 as part of the National Diet andNutrition Survey programme. The results werepublished in 1998 (Finch et al., 1998). The studycovered free-living individuals as well as a sam-ple living in institutions. Some of the mainfindings are summarized.■ The foods and drinks consumed by the

largest proportion of the sample were: tea(95 per cent), potatoes (87 per cent), whitebread (74 per cent) and biscuits (71 per cent).Whole grain breakfast cereals were eaten by50 per cent of the sample, and the mostcommonly used type of milk was full fat.Butter was the most popular fat used. Themost commonly consumed meats were hamand bacon, followed by beef, veal and meatdishes. Fish was eaten by 36 per cent of thesample. Cooked vegetables were consumedby up to 66 per cent of the group. Less thanhalf the group ate fruit. Sugar was used by55 per cent of the sample. Alcoholic bever-ages were consumed by fewer than 20 percent of the sample. In general, these findingssuggest a dietary pattern that is quite trad-itional and shows relatively low uptake offoods such as semi-skimmed or skimmedmilk, low-fat or polyunsaturated spreads, orsalads. The eating pattern of the older sub-jects and those living in institutions waseven more traditional.

■ More people are retaining their teeth intoold age than was the case in the past. Thestate of dentition has an impact on the foods chosen, and limits intakes of fruit anduncooked vegetables. The quality of the dietwas strongly related to the oral health of the subjects, with higher nutrient intakes inthose subjects with some natural teeth. Thedifference in nutrient intake with dentalstate was not significant in the group in

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institutions. However, these subjects hadmore dental plaque and caries, and consumedmore sugar than the free-living subjects.

■ Energy intakes were generally below the esti-mated average requirements (EAR) and were15 per cent less than recorded in the previoussurvey, 25 years ago. However, more of the subjects were overweight (65 per cent offree-living sample) than previously and it isassumed that energy intakes were adequatefor needs. More people in institutions (16 percent) than in the community (4.5 per cent)were underweight. In general, energy intakesdecreased with age in men but not in women.

■ Proportions of macronutrients in the diet werein line with intakes across the adult popula-tion and did not comply with dietary guide-lines. Intakes of NSP did not meet the dietaryreference value (DRV), and there was a posi-tive correlation between NSP intake and number of bowel movements.

■ Average intakes for minerals and vitaminsexceeded the reference nutrient intake (RNI).However, in both groups, there were num-bers of individuals in whom the intakes fellbelow the LRNI. In general, subjects in insti-tutions were less likely to have such lowintakes. This could be linked to the use ofmilk and fortified foods in the menus. Thefindings are summarized in Table 13.5.

■ Intakes of sodium and chloride were abovethe RNI in both groups of subjects. In the

free-living group, systolic blood pressurelevels were positively associated with urin-ary sodium/potassium ratio.

■ In those subjects whose intake of non-milkextrinsic sugars (NMES) was within the nor-mal population range of 8-15 per cent oftotal energy, there was no evidence thatmicronutrient intakes were compromised.Micronutrient intakes were however mar-ginally lower at NMES intakes outside thisrange. In general, micronutrient intakesreflected energy intake.

■ Biochemical assessments showed subopti-mal indices for a number of nutrients. Theseare indicated in Table 13.6.

■ Subjects from the community who were inmanual social groups had lower averageintakes of nutrients per unit of energy, buthigher intakes of sodium.

■ Lower intakes of energy were seen in bothmen and women who lived alone, comparedto those who lived with others. In men livingalone, this also resulted in lower intakes perunit energy of some nutrients. This was notthe case in women.Overall, these findings demonstrate that the

diet of older adults in Britain is largely compar-able to that of younger adults. However, dietarychoice may be affected by factors such as socialclass, household composition and dentition, aswell as state of health and age. Changes in dietaryintake will lead to poorer indices of nutrients and

Percentages of elderly subjects with nutrient intakes from foodsources below the LRNI (data adapted from Finch et al., 1998)TABLE 13.5

Nutrient Free-living subjects Subjects in institutions(average for men and women) (average for men and women)

Vitamin A 4.5 1Thiamin, niacin, vitamin B12 1 1Folate, vitamin B6 4 5 (folate), 2 (B6)Riboflavin 7 3Vitamin C 2 1Iron 3.5 5.5Calcium 7 0.75Phosphorus 22 30Potassium 28 65Zinc 6.5 8.5


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may lead to poorer health. Institutional care canhelp to maintain nutrient intakes.

What are the nutritional requirementsfor the elderly?

There is still a lack of reliable data about thespecific nutritional needs of elderly people andresearch is needed. In part, this is related to theheterogeneity of the group, which makes gener-alized recommendations difficult. In practice,most recommendations for nutrients are extrapo-lated from those for younger adults and, assuch, may be inappropriate.

The principal guidelines for a healthy dietapply equally in those past retirement age. Inmany ways, it becomes even more importantthat nutrient-dense foods are eaten, since asmaller food intake increases the risk of nutrientneeds not being met.

It should also be remembered that dietaryreference values (DoH, 1991) and comparablefigures published in other countries apply tohealthy individuals. It may be that the presenceof disease in certain older people may alter theirnutritional needs. Therefore, it can be concludedthat nutritional requirements are probably simi-lar in the elderly to those in younger adults, butindividual differences may occur, owing to par-ticular circumstances. These may include healthproblems, decreased physical capacity, presenceof drug–nutrient interactions, possible depres-sion and economic constraints.

Advice about diet to people who have retiredcould include the following:■ enjoy food;■ follow basic healthy eating guidelines relat-

ing to fat, fibre, salt and sugar by using theBalance of Good Health (FSA, 2001);

■ recognize that snacks can be an importantpart of the diet;

■ make sure that fluid intakes are adequate;■ keep some food stocks in the house for

emergencies;■ try to spend some time outdoors, especially

in the spring and summer;■ if alone, try to arrange to share meals with

friends/neighbours;■ ask for help with shopping when necessary;■ try to keep active;■ remember that food provides warmth.

In planning diets for an elderly person, par-ticular attention should be paid to nutrients thathave been identified as being ‘at risk’ in studiesof this age group. These include: vitamin D, vita-min E, thiamin, pyridoxine, folate, vitamin C andvitamin B12, as well as iron, zinc and calcium.Energy and protein intakes must be adequate toallow protein to be used for wound healing andtissue repair rather than for energy needs. Inpatients receiving diuretic therapy, potassium ormagnesium levels may be at risk. A diet contain-ing a variety of foods fitting in with the Balanceof Good Health, a sufficient intake of fluids and a moderate activity level will ensure good nutri-tional status in an elderly person.

Prevalence of suboptimal indices for nutrients inelderly subjects (adapted from Finch et al., 1998)TABLE 13.6

% in institution % in free-livingFolate 40 15Vitamin C 40 15Riboflavin 40 40Thiamin 10–15 10–15Vitamin D 37 8Zinc 7–15 2Iron (low haemoglobin)Men 52 11Women 39 9

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It should be recognized, however, that prob-ably the most common nutritional disorderamong the elderly in Western society is obesity.As at any other age, this is multifactorial in ori-gin and is detrimental to health. If the over-weight is very longstanding, the likelihood ofsuccessful, significant weight loss in an elderlyperson is small. Nonetheless, in cases of dia-betes, hypertension and arthritis, weight loss isdesirable and should be actively encouraged.

The most vulnerable elderly people are thosewho are ill and frail. It is necessary to identifythose at risk as rapidly and efficiently as pos-sible, before they enter a spiral of deficiency andinadequate intake, leading to further deficiency.Ten major risk factors have been identified:■ depression/loneliness;■ fewer than eight protein-containing meals/

week;■ long periods without food;■ little milk drunk;■ high level of food wastage;■ disease/disability;■ low income;■ inability to shop;■ sudden weight change;■ fruit and vegetables rarely in the diet.The presence of several of these factors points toincreased nutritional vulnerability and the needfor intervention.

Community services available for the elderlyin the UK include the provision of luncheon

clubs and day centres for those who are reason-ably mobile, and ‘meals on wheels’ and homehelps for those elderly who cannot get out, orare incapable of fully looking after themselves.They provide social contact as well as helpingthe nutritional status.

Approximately 5 per cent of the elderly inBritain are in institutions, including hospitalsand residential or nursing homes. These are themost vulnerable subgroup, since it is largelybecause they are ill, infirm and incapable ofcaring for themselves that they live in these set-tings. The diet provided by the institution maybe nutritionally incomplete, particularly withrespect to vitamins C and D, although othernutrients have also been shown to be low. Theremay be problems for the individual withappetite, eating and swallowing. Many diseaseprocesses may make an adequate nutritionalstatus difficult to achieve, or assess. However,every effort should be made to ensure that theelderly in institutions are properly fed. NationalCare Standards, including nutritional standards,were introduced in 2002 in the UK.

Finally, it should be remembered that,although some of the retired population doencounter nutritional problems, the great major-ity live a reasonably healthy life and succeed in caring adequately for themselves. A positiveoutlook and a continued interest in life areimportant prerequisities. When interest in foodwanes, a decline in health will surely follow.

1 The principles of the balanced diet apply to all adults; however, particular emphasis may be needed onsome aspects rather than others in certain situations.

2 Men may have less access to information and be less prepared to make changes for a variety of reasons.3 For women, nutritional needs differ at stages of the life cycle. Pressures from society, demands of

pregnancy and their own health may provide conflicting messages about how to interpret the dietaryguidelines.

4 Ethnic minority group members may have a traditional diet that is healthy but, by becomingWesternized, there is a reduction in nutritional quality of the diet.

5 A vegetarian diet can be a positive contributor to health but may lack some nutrients if not well planned.6 Low income may be a major barrier to consuming a healthy diet.7 A nutrient-dense diet is important with increasing age, as nutritional needs remain high but appetite

decreases. Maintaining physical activity can help to promote appetite.

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Appleby, P.N., Key, T.J., Thorogood, M. et al. 2002: Mortality in British vegetarians. Public HealthNutrition 5(1), 29–36.

British Nutrition Foundation 1995: Vegetarianism, a briefing paper. London: British NutritionFoundation.

Buttriss, J., Hyman, K. 1995: Focus on women: nutrition and health. Proceedings of a conference.London: National Dairy Council.

Davies, L., Knutson, C.K. 1991: Warning signals for malnutrition in the elderly. Journal of theAmerican Dietetic Association 91, 1413–17.


DoH (UK Department of Health) 1991: Dietary reference values for food energy and nutrients for theUnited Kingdom. Report on Health and Social Subjects No. 41. Report of the Panel on DietaryReference Values of the Committee on Medical Aspects of Food Policy. London: HMSO.

DoH (UK Department of Health) 1996: Low income, food, nutrition and health: strategies forimprovement. A Report by the Low Income Project Team for the Nutrition Task Force. Wetherby:Department of Health.

DoH (UK Department of Health) 2001: Health survey for England. The health of minority ethnicgroups. London: The Stationery Office.

Dowler, E., Calvert, C. 1995: Nutrition and diet in lone-parent families in London. London: FamilyPolicies Study Centre.

Dowler, E.S., Turner, S., Dobson, B. 2001: Poverty bites; food health and poor families. London: ChildPoverty Action Group.

Finch, S., Doyle, W., Lowe, C. 1998: National Diet and Nutrition Survey: people aged 65 years andolder. Volume 1. Report of the diet and nutrition survey. London: The Stationery Office.

Food Standards Agency 2001: The balance of good health. London: FSA.Food Standards Agency 2002a: Food portion sizes, 3rd edn. London: The Stationery Office.Food Standards Agency 2002b: McCance & Widdowson’s The composition of foods, 6th summary

edn. Cambridge: Royal Society of Chemistry.Gonzalez-Gross, M., Marcos, A., Pietrzik, K. 2001: Nutrition and cognitive impairment in the elderly.

British Journal of Nutrition 86, 313–21.

1 a The female body can experience severalmajor biological changes during the lifecycle. In what ways might these affect thedietary advice given to women?

b Do you believe that dietary advice given tomen should vary with their life stage?

2 a What are the main threats to health affectingmembers of the Asian community in the UK?

b What changes to diet and/or lifestyle couldbe of benefit?

3 For what reasons does living on a low incomepose a threat to eating healthily and/or having ahealthy lifestyle?

4 Prepare a leaflet designed for those who carefor the elderly, summarizing the main principlesof eating healthily at this age.

5 a Discuss with a group of fellow students, oryour tutor, some of the reasons why peoplegenerally appear to have difficulty achievingthe dietary goals. What sources might youuse to check how well goals are beingachieved to help you in this discussion?

b Identify ways in which meeting goals couldbe made easier.

c Who might need to be involved in b above?

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Grundman, M., Delaney, P. 2002: Antioxidant strategies for Alzheimer’s disease. Proceedings of theNutrition Society 61, 191–202.

Hamlyn, B., Brooker, S. Oleinikova, K. et al. 2002: Infant feeding 2000. London: The StationeryOffice.

Hill, S.E. 1990: More than rice and peas. Guidelines to improve food provision for black and ethnicminorities in Britain. London: Food Commission.

Key, T.J., Fraser, G.E., Thorogood, M. et al. 1998: Mortality in vegetarians and non-vegetarians: a collaborative analysis of 8300 deaths among 76000 men and women in 5 prospective studies.Public Health Nutrition 1, 33–41.

Leather, S. 1992: Less money, less choice: poverty and diet in the UK today. In National ConsumerCouncil, Your food: Whose choice? London: HMSO, 72–94.

National Food Alliance 1994: Food and low income: a practical guide for advisers and supportersworking with families and young people on low incomes. London: National Food Alliance.

Nutrition Society 1995: Nutrition for the elderly (Symposium). Proceedings of the Nutrition Society54(3), 617–99.

Perkins, A., Hendrie, H.C., Callahan, C.M. et al. 1999: Association of antioxidants with memory in amultiethnic elderly sample using the Third National Health and Nutrition Examination Survey.American Journal of Epidemiology 150, 37–44.

Ritz, P. 2001: Factors affecting energy and macronutrient requirements in elderly people. PublicHealth Nutrition 4(2B), 563–8.

Schofield, C., Stewart, J., Wheeler, E. 1989: Dietary variety during and after pregnancy in Scotlandand England. Journal of Human Nutrition and Dietetics 2, 7–18.

Sellen, D.W., Tedstone, A.E., Frize, J. 2002: Food insecurity among refugee families in East London:results of a pilot assessment. Public Health Nutrition 5(5), 637–44.

Sharma, S., Cruickshank, J.K. 2001: Cultural differences in assessing dietary intake and providingrelevant dietary information to British African-Caribbean populations. Journal of HumanNutrition and Dietetics 14, 449–56.

Van Staveren, W.A., de Groot, L.C., Burema, L. et al. 1995: Energy balance and health in SENECAparticipants. Proceedings of the Nutrition Society 54(3), 617–29.

Williams, B. 1995: Westernised Asians and cardiovascular disease: nature or nurture? Lancet 345,401–2.

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Diet and coronary heart disease


❏ define what is meant by coronary heart disease and describe its development;❏ describe the lipid hypothesis for heart disease aetiology;❏ study some of the ways in which evidence about heart disease causation has been collected;❏ identify some of the suggested risk factors;❏ describe the suggested role of dietary factors in the development and prevention of heart disease.


❏ explain the physiological processes involved in the development of heart disease;❏ discuss the origins of the lipid hypothesis of heart disease;❏ describe some of the other dietary factors that play a part in heart disease aetiology;❏ explain the suggested interaction of antioxidant nutrients as protective factors;❏ propose and explain dietary advice for the prevention of coronary heart disease.

Coronary heart disease, together with other diseases of the circulatory system, is one of themajor causes of death in the Western world.Worldwide mortality due to coronary heart dis-ease and stroke accounts for approximately 20per cent of all deaths, and numbers are increas-ing as the world population becomes relativelyolder. Throughout Europe, cardiovascular diseaseaccounts for about 40 per cent of overall mor-tality, the majority of these deaths are attributableto coronary heart disease, most of the remainderto stroke. Across Europe there is an East–Westgradient, with higher mortality rates in centraland Eastern Europe than in Western Europe. Thedifferential between the highest and lowest mor-tality approaches a factor of 5. There are alsohigher rates of coronary heart disease, but notstroke, in Northern Europe than in the South,and the variation between North and South isapproximately 2.5.

Death rates from coronary heart disease varybetween the countries of the UK. The rates are

highest in northern parts of England, Scotlandand Northern Ireland, and lowest in the southeastand London. Heart disease rates among women inthe UK are some of the highest in the world. InScotland, the rate amongst women aged 35–74 isten times greater than that in Japanese women.

People born in the Indian subcontinent liv-ing in the UK have heart disease rates 36 percent higher than those in the population as awhole. Those in people originating from theCaribbean countries are lower than in the popu-lation as a whole, by 55 per cent in males and24 per cent in females.

In the UK, the age-standardized death rateof people under 65 from circulatory diseaseswas 70 per 100 000 of the population in 1995. InFrance, which has the lowest rate in Europe, thedeath rate at the same time was 36 per 100 000.In 2001, there were 120 891 deaths in the UKfrom coronary heart disease alone. All of thecirculatory diseases taken together account for41 per cent of mortality in England. In addition,

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angina and other circulatory disorders, someresulting in stroke, are leading causes of ill healthand disability.

Changes in rates ofcardiovascular disease

Most Western European countries, including theUK, have experienced a downward trend in heartdisease rates since the 1980s and early 1990s. Themost encouraging trends have been among theyounger age groups. Rates have fallen by 40 percent in the under 65s in the last decade. However,in the countries of Eastern Europe, such asHungary, Poland and Romania, rates increased.

In the USA, Australia, New Zealand andJapan, rates have shown a dramatic reduction inthe last 15–20 years, but the causes are unclear.The White Paper, Saving Lives – Our HealthierNation (DoH, 1999) has set the target in the UKto reduce deaths from circulatory diseases by 40 per cent by 2010. This is estimated poten-tially to save 200 000 lives over this period.

Traditionally, coronary heart disease has beenviewed as a disease of men because, in middleage, mortality is higher in men. However, afterthe menopause, women become increasinglysusceptible to the disease and death rates of thetwo sexes are similar. Since women generally livelonger than men, many more suffer from heartdisease in old age. As a result of this perception,much of the early research has been focused onthe disease in men, and both research and treat-ment in women has lagged behind. More recentstudies have included women among the subjects.

There are many changes that occur in diet andenvironmental influences that make it very diffi-cult to pinpoint those having the major effects.Positive factors may include health educationthat affects, for example, the intake of fats, fruitand vegetables and increases physical activity. Onthe other hand, negative factors may include thesocietal shift in dietary intake to more ‘fast food’,as well as political changes (such as in EasternEurope during the 1990s), which cause stress, andincrease alcohol intake and smoking rates.

Projections for the future indicate that preva-lence of cardiovascular disease will continue torise, despite some encouraging trends. This is

attributable to the better treatment and survivalafter heart attack, albeit with increased morbidity.A further reason is the age profile of most popu-lations, with an increase in the proportion ofolder people, who are at increased risk of thesediseases.

This chapter will focus on coronary heartdisease, as this is the major manifestation ofcardiovascular disease in Western Europe. Inaddition, much more of the research in this areahas been on the dietary determinants of coronaryheart disease, rather than stroke.

What is coronary heartdisease?

A heart attack (myocardial infarction) can resultin sudden death. It occurs when the blood andhence oxygen supply to a part of the heart fails,because of a blockage in the vessels supplyingthe muscular walls of the heart. This makes theheart unable to continue working normally tosupply blood to all the parts of the body and,most crucially, to the brain. If a large part of themuscle is deprived of oxygen, the heart attackmay be fatal. Failure of a smaller part of the heartmuscle may allow the rest of the heart to continueworking and maintain the circulation.

These events are, however, the culmination ofa process that may have been developing grad-ually over a long period of time, involving a seriesof changes to the walls of the coronary arteries.The process may be described in terms of athero-genesis and thrombogenesis (see Figure 14.1).

Injury to the coronary arteries

The blood vessel walls are continually exposedto wear and tear by the flow of blood. The wallis not completely smooth, especially where thereare divisions of the vessels into smaller channelsand associated branching. Blood flow becomesturbulent here, rather like the flow of a riverwhere streams are joining or there is someobstruction to the flow.

Prolonged raised blood pressure will alsoincrease stress on the walls. As a result, the wallof the vessel is continually repairing itself inresponse to the damage, using the blood platelets

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and forming minute blood clots. New collagenand smooth muscle cells may be laid down tostrengthen the wall. Over a long period of time,these areas may become thicker and, since theyare no longer perfect, become more permeableto substances and particles in the blood. Manyfactors contribute to the normal functioning of the endothelial surface of the blood vessel,including relaxing factors and growth factors,and these are considered to be important in main-taining functional integrity.

Fibrous plaque formation

The progression from the previous stage is notcompletely clear. It is normal for blood vesselwalls to be permeable to substances required bythe tissues, such as lipid-soluble material neededfor metabolic processes. It is now believed thatpartly oxidized lipids present in low-densitylipoprotein (LDL) entering the blood vessel wallare recognized as ‘foreign’ and are not allowed topass through the endothelium of the blood ves-sel. Their presence attracts monocytes (a type of

white blood cell), which adhere to and then enterthe blood vessel wall. Various factors are nowknown to influence the adhesion of the mono-cytes, including nitric oxide (endothelial relaxingfactor) and antioxidants (particularly vitamin E).

Having penetrated the blood vessel wall, themonocytes are converted to macrophages, whichare scavenger cells whose purpose is to destroythe damaged lipids. However, the macrophageitself then cannot leave the wall and so thesescavenger cells accumulate, laden with fat, andgradually coalesce to produce ‘foam cells’. Whenthese die, the fat they contain remains in the walland becomes the origin of the fatty streaks thatare believed to be a contributing factor in theatherogenesis of the heart disease process.

The fatty streaks also attract blood plateletsand fibrin, which attempt to ‘seal off ’ the dam-aged area. In the process, these clot-formingentities actually contribute to thickening, pro-ducing a fibrous plaque and ultimately harden-ing the blood vessel wall. Smooth muscle cellsare laid down under the influence of growthfactors, derived from platelets and other blood

Figure 14.1 The development of coronary heart disease. LDL, low-density lipoprotein.

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components. The plaque area grows, protrudingprogressively into the lumen of the vessel andfurther interfering with the blood flow.

Thrombosis and heart attack

Eventually the fibrous plaque becomes unstableand ruptures, releasing fatty contents into thecirculation. These attract components of the clot-ting mechanism and a thrombus (or clot) is likelyto form. If the blood vessel is already narrow atthis point, the clot may block the flow of blood.The fibrous plaque components themselves mayalso become lodged in the vessel. Both of theseprocesses will cause a myocardial infarction, ifthe blockage is in a coronary blood vessel. Whenthe narrowing and thrombosis occur in a bloodvessel supplying the brain, a stroke (or cerebro-vascular accident) will be the result.

Various physiological and dietary factors areinvolved in the processes described above. Anunderstanding of these is emerging from themany studies of coronary heart disease and itsassociated risk factors. The developments inmolecular biology have added a new dimensionto these studies, so that mechanisms that wereoriginally only suggested as a possibility are nowbeing described in detail at the molecular level.As more information becomes available, it clari-fies some aspects but it also demonstrates thatthe picture is highly complex.

Studying coronary heartdisease

The study of coronary heart disease is hamperedby the absence of a close animal model formyocardial infarction, although aspects of thedisease process can be mimicked in various ani-mals. However, to obtain the most relevant data,studies are performed on human populationsand, for ethical reasons, are limited in the scopeof experimental work that can be done. Much ofthe research is, therefore, based on epidemi-ological data obtained from populations withhigh and low rates of heart disease, and attemptsto associate these with diet and lifestyle charac-teristics. A number of approaches have beenused. Dietary lipids have been the main focus of

attention because of the lipid nature of the fibrousplaque contributing to the narrowing of the bloodvessels.

Origins of the lipid hypothesis

Cross-community comparisonsThe most widely known of the early studies is Keys’ Seven Country Study, which comparedfat intakes and serum cholesterol levels withsubsequent 10-year coronary heart disease inci-dence in men aged 40–59 from seven countries(Keys, 1970). The strongest correlation was foundbetween the percentage of energy derived fromsaturated fat in the diet and increased risk ofheart disease. These results were compared morerecently in a 25-year follow up of the subjects.In communities with a high incidence of heartdisease, the intake of saturated fatty acids typic-ally ranges between 15 and 25 per cent of the energy intake. At the extremes, saturated fatintakes in East Finland are 22 per cent and inCrete are 8 per cent of the energy. The corres-ponding rates of coronary heart disease are 1074and 26 per 10000 (age standardized rate), respec-tively. There was also a weaker, negative correl-ation between intake of polyunsaturated fatsand heart disease.

Although these relationships could be seenacross different population groups, with varyingdiets and cultures, they are more difficult to findin comparisons of individuals within one country.Nevertheless, it has been possible to produce anequation that predicts the change in serum chol-esterol, given changes in the dietary intake ofsaturated and polyunsaturated fats. Two suchequations have been produced by Keys andHegsted. The Keys formula shows that saturatedfatty acids (excluding stearic acid, C18) raiseplasma cholesterol levels by twice as much aspolyunsaturated fatty acids can lower it. This maynot always be exactly so predictable for any one individual because of other behavioural orgenetic factors. However, the ratio of polyunsat-urated (P) fatty acids to saturated (S) fatty acidsis a useful means of expressing the desirableproportion in the diet. Where the ratio is low(P/S � 0.2), the population generally has a highblood cholesterol level and a high risk of coronary


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heart disease. Increasing the P/S ratio to 0.5–0.8has been considered a desirable goal, as heartdisease rates are lower in populations where thenormal diet approaches these proportions.

This basic premise is the first principle of the lipid hypothesis and is widely accepted. Thecorollary and the second principle, that both riskand mortality from heart disease can be reducedby lowering cholesterol, is still debated. Viewshave become polarized and the lack of consensushas been widely publicized in the media, withresulting confusion for both health professionalsand the general population.

Prospective studiesThese involve studying a cohort of individualsover a number of years and measuring thoseparameters that are believed to be related to heartdisease. Over time, some individuals will developthe disease; it is assumed that they share particu-lar characteristics, not seen in the unaffectedmembers of the population. One of the bestknown of these studies is that in Framingham,Massachusetts, where a cohort of over 5000individuals were first recruited in 1948. Dataregarding their cardiovascular health and manypossible causal factors have been systematicallycollected, using standardized methods of meas-urement. Data from the Framingham study haveshown that raised serum cholesterol, high bloodpressure and cigarette smoking are three majorcontributory risk factors in heart disease. Thestudy also showed the comparative level of riskwith increasing serum cholesterol levels. Asnewer risk factors are discovered, the data fromFramingham can be reviewed to investigate otherrelationships. A newer data set is informationfrom a sample of over 100 000 female nurses inthe USA, from whom medical and dietary infor-mation has been collected, and who are beingfollowed up prospectively. A review of tenwithin-population studies (Caggiula and Mustad,1997), showed a positive significant relationshipbetween intakes of saturated fat and coronaryheart disease.

Intervention studiesThe second principle of the lipid hypothesissuggests that, if a raised serum cholesterol level

is associated with an increased risk of heart dis-ease, then lowering it should reduce the risk.Many trials have attempted to demonstrate thisby using advice, dietary manipulation, lifestylechanges or drug intervention either separatelyor in varying combinations.

In some studies, those with no pre-existingevidence of heart disease have been targeted(primary prevention). The main drawbacks of thisapproach are the size of the subject group neededto demonstrate any benefits and the difficultyof evaluation.

Some community projects have been success-ful, most notably the North Karelia project inFinland, where a programme of health educationwas targeted at the whole community, aimed atreducing the very high incidence of heart disease.Evaluation has found measurable improvementsin the average values for key parameters, mostnotably a 13 per cent decrease in serum choles-terol. This was attributed to changes from butterto vegetable oil margarines, from whole fat tolow-fat milk and from boiled to filtered coffee. Inaddition, blood pressure fell as a result of reducedsalt intakes, and an increase in fruit and vegetableintake. Overall, coronary heart disease mortalitydeclined by 55 per cent in men and 69 per cent inwomen. These results imply that some individ-uals have achieved substantial changes. However,such large projects can also have very disap-pointing results. For example, the World HealthOrganisation (WHO) Collaborative study, target-ing factory workers in several European coun-tries, achieved some reduction in heart diseasemortality in Belgium and Italy, but not in the UK.

More specifically, focused trials recruitingthose at high risk of heart disease have had mixedresults. The Multiple Risk Factor Intervention Trial(MR FIT) found that both the study and controlgroups showed an improvement in mortality rates.This demonstrated the difficulty of human stud-ies, where diet is not a constant variable. Figure14.2 shows the relationship between plasmacholesterol and heart disease from this study.

A review by Truswell (1994) of 14 studiesfrom the 1960s and 1970s, in which saturatedfatty acids were exchanged with polyunsaturatedfatty acids, found that the average cholesterollevel was lowered by 10 per cent. This was

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associated with a 13 per cent reduction in coron-ary events and a 6 per cent reduction in mortal-ity. Where cholesterol reduction was more thanaverage, there was an even greater decrease incoronary events and mortality.

Trials using cholesterol-lowering drugs (e.g.Helsinki Heart Study, Lipid Research Clinic Trial)have also demonstrated that it is possible toreduce heart disease mortality. However, both ofthe trials mentioned also found an increase innon-cardiovascular mortality in the study group.Findings of this nature led to concern about the safety of cholesterol lowering in subjectswho have not experienced heart disease. TheScandinavian Simvastatin Survival Study (1994)achieved a 25 per cent reduction in plasma chol-esterol and 42 per cent fewer coronary deaths,and no excess mortality in the treated group.

Secondary prevention targets those whoalready possess signs or symptoms of heart dis-ease, or who have suffered a heart attack. Inrecent years, interventions have introduced otherdietary manipulations as the lipid hypothesis has become more sophisticated. Some of thesestudies have achieved excellent results. TheDART study (Burr et al., 1989) showed thatadvice to eat fatty fish resulted in a reduction of29 per cent in mortality within 2 years; this wasnot seen in a group advised about fat intakes or about cereal fibre intake. The Lyon Diet HeartStudy (De Lorgeril et al., 1994) increased the

levels of alpha-linolenic acid as part of the dietaryintervention, and achieved a 70 per cent reduc-tion in mortality and 73 per cent fewer non-fatalcoronary events. Addition of long-chain n-3 fattyacids to the diet, resulted in a 20 per cent reduc-tion in coronary heart disease mortality (GISSIPrevenzione Investigators, 1999).

It is clear that the lipid hypothesis does notfully explain all the causes of coronary heartdisease. In particular:■ the saturated/polyunsaturated fat relationship

is an oversimplification of the link betweendiet and heart disease;

■ some of the saturated fatty acids have morepotent effects than others;

■ the role of different polyunsaturated fattyacids in the atherosclerosis process is deter-mined by the position of the first double bondin the chain and hence the fatty acid family;

■ further evidence suggests that monounsatu-rated fatty acids are important in determiningdevelopment of coronary heart disease;

■ the trans fatty acids that are found in the dietmay also have a role.

We shall return to these issues later in the chapter.

Risk factors

Coronary heart disease is a multifactorial condi-tion, determined by the interaction of differentcombinations of factors, known as risk factors.Many of these have now been identified. A riskfactor does not necessarily cause the disease nordoes its presence mean that an individual willdefinitely develop heart disease. They can, how-ever, help to explain cross-cultural and inter-individual differences. Although the factors aremodulated by individual susceptibility, the pres-ence of several factors in any one individual doessuggest that there is a greater chance of develop-ing disease. In addition, there are synergisticeffects between the risk factors. For example, thecalculated risk from smoking is much greater inan individual who also has raised blood choles-terol levels than in one whose levels are in thenormal range. Adding the extra risk factor ofraised blood pressure further elevates the risk byan amount greater than that seen for hyper-tension alone. This is illustrated in Figure 14.3.

Figure 14.2 The increase in risk with increases inserum cholesterol levels. CHD, coronary heart disease.(From Martin et al., © 1986 The Lancet Ltd 1986.Reproduced with kind permission.)


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It should also be remembered that the develop-ment of heart disease is a process and that riskfactors may be involved at different stages.Therefore, some may contribute to the layingdown of fatty deposits in the blood vessels, andothers influence the formation of a thrombosisor determine the response of the heart muscle toa lack of oxygen supply.

The main risk factors associated with heart dis-ease are shown in Figure 14.4. Some of the factorsare believed to increase risk and others to reducerisk. Therefore, any high risk factors can be ame-liorated by enhancing those that reduce the risk.

Genetic predisposition

This may be associated with increased risk. Oftenthose who develop heart disease have a strong

family history of the disease. It has even beensuggested that any advice to reduce heart dis-ease risk should only be targeted at those with afamily history, as this will account for most ofthe new cases. Equally, it should be rememberedthat there may be a genetic predisposition to notdevelop heart disease.

Age

It was stated earlier in this chapter that the riskof heart disease increases with age in both menand women. Morbidity statistics show the peakage in men to be 55–64 and in women 75–84.This implies that the disease develops over aperiod of time, which is in line with the proposedmechanisms described earlier. In women, there isa relative protection against the disease duringthe reproductive years and an increase in inci-dence after the menopause. This also accountsfor the gender differences in risk in middle age,with a higher risk seen in men than womenbefore the ages of 50–55.

Social class

Contrary to the common perception, it is not the ‘stressed businessman’ who is most likely todevelop heart disease. The highest incidence ofthe disease is in the lowest social class andshows an inverse class gradient. Standardizedmortality ratios for England and Wales showthis quite clearly for both genders. Furthermore,

Figure 14.3 Additive effects of risk factors on damageto coronary arteries. (From Grundy, 1988. Copyright 1988, American Medical Association. All rightsreserved.)

Figure 14.4 Main riskfactors in the developmentof coronary heart disease.

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improvements in heart disease rates have beenlargest in the professional classes, so that thegap between these and the unskilled groups iswidening (Figure 14.5). There is also a differencein height between social classes in the UK, thosein the higher social classes being taller. Thisresults in an inverse relationship between heartdisease and height.

Birthweight

Individuals who were born small for gestationalage have been shown in a number of studies tohave a higher risk of coronary heart disease. Inaddition, there is an increased risk of many of therisk factors, such as hypertension, raised choles-terol levels and higher levels of the blood clottingfactors. Those individuals who were thin at birth,with less well-developed skeletal muscle are alsoat risk of glucose intolerance, which may resultin Type 2 diabetes in adult life. This in its turnmay also result in a higher risk of coronary heartdisease, as it is associated with some of the otherfactors mentioned above. The risk seems to begreatest in those people who become overweightas adults having been small infants. Maintenanceof a normal body weight helps to minimize therisk. More information about these associationsis presented in Chapter 11.

Geographical location

Crude heart disease prevalence trends indicatethat the disease occurs more commonly in north-ern latitudes and is less common nearer theequator. It has been suggested that low levels ofultraviolet light during winter months may insome way be responsible perhaps via a mechan-ism involving vitamin D levels. This would alsolink with the increased incidence of heart attacksin winter. Immigrants tend to experience the heartdisease risk of their host country after a relativelyshort period of time. However, as has alreadybeen mentioned, it has been found that some of the immigrant groups in the UK have muchhigher heart disease rates than the indigenouspopulation. Thus, although environmental fac-tors play an important part, other mechanismsare also involved.

Disease

Of the many diseases affecting humans, diabetesis one of the most prevalent and people withType 2 diabetes have an increased risk of heartdisease, often associated with obesity and raisedlipid levels. The insulin resistance syndrome thatoccurs in these cases is associated with centralobesity and a number of metabolic abnormalities,

Figure 14.5 Social class and gender differences in heart disease mortality. SMR, standardized mortality ratio; itcompares the true mortality of population with the experience that would have been expected if it had a standardmortality rate. An SMR in excess of 100 indicates mortality rates higher than expected in a standard population.(From DoH, 1994. Crown Copyright is reproduced with the permission of the Controller of Her Majesty’sStationery Office.)


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affecting carbohydrate and fat metabolism, andresulting in raised lipid levels and poor oxidativecapacity in skeletal muscle and liver (see Chapter5). The current guidelines on dietary manage-ment of diabetes stress reduced fat intakes tominimize the risk. Previously, recommendeddiets controlled carbohydrate intakes strictlyand allowed much higher fat intakes, whichexacerbated the problem of heart disease.

There is some reported evidence that achronic inflammatory state associated with thepresence of infective organisms (e.g. Helicobacterpylori, found in the stomach, Chlamydia pneu-moniae, which can cause respiratory infection, oreven oral bacteria that cause gum disease) mayelevate cytokine levels, which affect the endothe-lial function of the blood vessel, and may facili-tate immune responses and trigger clottingmechanisms. Patients with periodontal diseasehave been shown to have higher levels of plasmaclotting factors. Conversely, bacteria responsiblefor periodontitis have been found in atheroscle-rotic plaques. C-reactive protein (CRP), a markerof inflammation has now been shown to correlatewith incidence of heart disease.

Smoking

Similar proportions of men and women (28 per cent) are smokers in England. Smoking ismuch more prevalent in manual social classesand in lower income groups. Persuading at-risksubjects to stop smoking can result in a signifi-cant reduction of their heart disease risk. It isthought that the free radicals that enter the bodyfrom cigarette smoke contribute to the diseaseprocess by causing peroxidation of lipids. Thealtered lipids are then taken up by macrophagesin the blood vessel walls and contribute to thefatty streaks. A further potential effect of smok-ing is the reduction in oxygen-carrying capac-ity of the red blood cells owing to higher levelsof carbon monoxide, which can exacerbateischaemia in tissues fed by narrowed blood ves-sels. Dietary intake studies also show that smok-ers tend to have poorer diets and consume lower levels of antioxidants from fruit, whichcompounds the risks from free radicals. Thereappears to be a clear linear relationship between

the numbers of cigarettes smoked per day andheart disease risk.

High blood pressure

The Health Survey for England (Erens andPrimatesta, 1999) showed that 40.8 per cent ofmen and 32.9 per cent of women were hyper-tensive, with a higher prevalence of high bloodpressure in more economically deprived groups.A higher proportion of those subjects with highblood pressure were also found to be phys-ically inactive, have high total cholesterol andlower levels of high-density lipoprotein (HDL)cholesterol.

Raised blood pressure is one of the maincontributors to heart disease, possibly because itpotentiates the damage to blood vessel walls andincreases the transfer of substances across theblood vessel wall. Both of these may play a part in the development of the fibrous plaque.Reduction of blood pressure by drug treatment,weight loss or dietary modification is likely to beof benefit. Better control of hypertension mayaccount for some of the reduction in heart dis-ease seen in Western countries in recent years.

Raised blood lipids

Above normal levels of cholesterol, especially inthe low-density lipoprotein fraction, are stronglylinked with increased risk of heart disease, as evi-denced by many studies. Those individuals withfamilial hyperlipidaemias have a well-recognizedhigh risk of developing heart disease, often at avery young age. Recent interest has focused onthe possible role of lipoprotein(a), closely relatedto LDL, but carrying an additional apoproteinmolecule. Raised levels of this molecule appear tobe more strongly linked to myocardial infarctionthan even LDL. These may explain the high inci-dence of heart disease in South Asians in the UK.Chylomicrons and very low density lipoprotein(VLDL), both of which are rich in triglycerides,are elevated in some individuals, resulting inprolonged lipaemia (presence of fats in the blood)after meals. These raised levels seem to be causedby a defective rate of clearance from the circula-tion by the enzyme lipoprotein lipase (LPL). Both chylomicrons and VLDL are likely to be

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atherogenic and constitute risk factors. Moreattention is now being focused on dietary factorsthat contribute to raised levels of the VLDL frac-tion. Measures to reduce blood lipid levels inindividuals as well as population groups couldresult in reduced incidence of heart disease.

Weight

Early studies, such as the Seven Countries Studyby Keys, failed to find a causative effect of over-weight on heart disease risk because many of theother risk factors are also aggravated by a higherbody fat content. Using more sophisticated ana-lyses, it is now clear that excess body fat is adirect contributor to coronary heart disease, aswell as acting indirectly through many of therisk factors, such as diabetes, hypertension andraised blood lipids. In particular, when body fatdistribution is taken into account, and people aredivided into ‘apples’ (those with predominantlyabdominal fat deposits) and ‘pears’ (peripheral fatdeposits, mostly around the buttocks and hips),a strong relationship with heart disease is seenfor ‘apples’. In general, the relative risk of cardio-vascular disease for individuals with a body massindex (BMI) 30 is about 2–3 times that of peoplewith a BMI 25. The use of waist circumferenceas a guide to the need for weight loss is a usefulquick measure to indicate increased risk. Actionlevels for weight loss based on waist measure-ments are discussed in Chapter 8. Weight loss bydietary restriction and with physical activitycan improve all the modifiable risk factors andthus reduce the risk of coronary heart disease.

Physical activity

A proportion of people have been shown to haveminimal levels of physical activity. The HealthSurvey for England (Erens and Primatesta, 1999)found that 20–25 per cent of men and womenreported no physical activity in the 4 weeks priorto the survey. However, 37 per cent of men and25 per cent of women reported activity at therecommended level. This includes activity ofmoderate intensity for at least 30 minutes on atleast 5 days of the week. The remaining subjectshad activity levels between these limits.

Many long-term studies have found lowermortality in those who have a more active life-style, compared with more sedentary controlsand, therefore, exercise has been promoted asdesirable in the reduction of heart disease risk.Changes to activity levels are followed by changesin risk of death, with an improvement of riskseen in previously sedentary subjects who beginan activity programme. Even moderate levels of activity appear to confer benefit, althoughthe evidence is stronger for men than women.The mechanisms involved are unclear but, at abasic level, activity helps in the maintenance of energy balance and prevents development ofoverweight. Exercise has been shown to increasethe beneficial high-density lipoprotein. Abdom-inal fat deposits appear to be particularly sensitiveto mobilization by exercise and, in individualswith central obesity, even moderate exercise can produce improvements in the metabolic profile. Other possible beneficial effects includechanges in clotting factors (linked to endurance-type exercise) or in the density of capillaries inthe tissues, which provides protection againstischaemic damage, if blood vessels become narrowed. Inactivity may be as important a riskfactor as hypertension, smoking or hypercho-lesterolaemia.

Psychosocial factors

These are less well defined than other factors.Data from the Whitehall studies show higher ratesof heart disease in lower employment grades,with the gradients being steeper for women thanmen (see Ashwell, 1996; DoH, 1994). It is sug-gested that stress and lack of social support maybe linked to coronary heart disease.

Dietary factors

There are several constituents of the diet forwhich there is evidence of a link with heart disease. Most notably this applies to the fatsthat have been linked with lipid levels in theblood. In addition, other components, such astotal energy intake, dietary fibre (non-starchpolysaccharides), sugar, salt, alcohol and anti-oxidant nutrients, have all been studied in


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relation to stages in the development of heartdisease. The dietary risk factors are summarizedin Figure 14.6.

FatsDietary cholesterolMeat, egg yolks and dairy products containfairly large amounts of cholesterol and manypeople concerned about their blood lipids havein the past attempted to reduce their intake ofthese foods. However, changing the amount ofcholesterol in the diet has only limited effectson blood cholesterol concentrations in mostpeople. This is because several compensationmechanisms exist. Only about half of the chol-esterol ingested is absorbed from the gut; a typical dietary intake of 400 mg/day will, there-fore, only result in the absorption of 200 mg of

cholesterol. The essential nature of cholesterolin the body means that the body synthesizes theremainder of its needs, about 1 g of cholesterolper day. If dietary intake increases, the amountsynthesized is reduced to compensate; this isachieved by regulating one of the enzymes –hydroxymethyl-glutaryl coenzyme A (HMG-coA) reductase – in the cholesterol synthesispathway in the liver through a negative feed-back mechanism. In addition, HDL activity canalso increase to scavenge excess cholesterolfrom the tissues for removal in bile.

However, control is not exact and an increasein cholesterol intake in the diet can raise bloodcholesterol levels. It has also been shown thatthere are individual, genetically determined dif-ferences in response to dietary cholesterol, withhyporesponders and hyperresponders. This makes

Figure 14.6 A summary of dietary risk factors for coronary heart disease. HDL, high-density lipoprotein; LDL,low-density lipoprotein; MI, myocardial infarction; PUFA, polyunsaturated fatty acid.

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it difficult to generalize about the effect of dietarycholesterol.

Saturated fatty acidsOriginally, it was postulated that all saturatedfatty acids in the diet were equally harmful,causing an elevation of blood cholesterol/LDLlevels. It is now recognized that myristic acid(C14) is the main fatty acid responsible for rais-ing the serum cholesterol level. This contributesto the formation of fibrous plaques and isdescribed as atherogenic. Both lauric acid (C12)and myristic acid also suppress the clearingmechanism at LDL receptors, which removes LDLcholesterol from the circulation, thus contributingto raised circulating levels. Palmitic acid (C16)has probably less effect on cholesterol levels inthe blood than originally suggested by Keys.However, palmitic acid is the main saturated fattyacid in most diets and, therefore, has an import-ant effect because of its prevalence. In addition,the different fatty acids appear to have varyingeffects on the formation of thrombi in the blood.Myristic acid and stearic acid (C18) are considered to be the most thrombogenic, togetherwith trans fatty acids. A reduction in thrombo-genic effects is associated with monounsaturatedfatty acids, seed oils and fish oils.

Monounsaturated fatty acidsMonounsaturated fatty acids (MUFAs), particu-larly oleic acid (18:1), were originally believedto be neutral in their effect on blood cholesterollevels and were not included in the original equa-tions of Keys and Hegsted. Studies of heart dis-ease prevalence among peoples in Mediterraneancountries showed a lower rate than expected. Thediet in these countries (particularly Greece andsouthern Italy) contains more MUFAs, especiallyoleic acid from olive oil, than is found in northernEuropean diets. This led to the suggestion thatthis type of fatty acid may be protective againstheart disease. It should, however, be remem-bered that there are many other features of aMediterranean diet and lifestyle, such as largeintakes of fruit, vegetables and wine, which maybetter explain the lower prevalence of heart disease. However, a number of studies have now confirmed that substitution of some of the

saturated fats in the diet by MUFAs results in areduction of LDL cholesterol, equal to about halfof that achieved by n-6 polyunsaturated fattyacid (PUFA) substitution. In addition, however,there is an elevation of HDL cholesterol, an effectnot obtained with n-6 PUFAs.

The proposed mechanism is an increase inLDL clearance by the liver as a result of increasedreceptor activity. In addition, as MUFAs containonly one double bond, they are more resistantto the harmful effects of free radicals, whichattack PUFAs and can lead to the early stages offibrous plaque formation. Observed effects onthrombogenesis have also been reported, withreduced levels of clotting factor activation. Over-all, MUFAs are considered to be a beneficial com-ponent of the diet, with no harmful effects on theknown risk factors for coronary heart disease.New equations predicting the change in totalserum cholesterol consequent on modificationsto the dietary intake of MUFAs, in addition to sat-urated fatty acids (SFAs) and PUFAs, have nowbeen developed based on metabolic ward studies(e.g. Mensink and Katan, 1992). It should, how-ever, be remembered that, in terms of weight con-trol, the intake of MUFAs, as of other fats in thediet may need to be regulated.

Polyunsaturated fatty acidsPolyunsaturated fatty acids in the diet originatefrom two main sources: n-6 acids from plantfoods and n-3 acids mainly from marine foods,and it is now recognized that the two familieshave different effects on coronary heart diseaserisk factors. Other roles in the body have beendiscussed in Chapter 5.n-6 PUFAs. Fatty acids from this family havea LDL cholesterol-lowering effect, independent ofany change in saturated fat intake. The effect isachieved, it is believed, by increasing the removalof LDL from the circulation by enhancing theactivity of the LDL receptor sites, which thusopposes the effect of the saturated fatty acids on these receptors. Although n-6 PUFAs are alsoreported to reduce HDL levels in the blood, this isto a smaller extent than the effect on LDL and,consequently, the HDL/LDL ratio increases.

The n-6 PUFAs in membrane lipids are, how-ever, vulnerable to free radical attack, resulting


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in peroxidation. Once established, this producesa chain reaction with further peroxide formationand potential for further damage. At present,there is little evidence that high intake of n-6PUFAs in any way contributes to enhanced per-oxidation in the body, but the vulnerability ofthe double bonds in these molecules suggeststhat this could be a possibility. Accordingly, it isadvisable to be cautious about excessively highintakes of PUFAs and intakes should be below10 per cent of total energy. European recommen-dations (EURODIET, 2001) are that intakes of n-6PUFAs should not exceed 5 per cent (range 4–8per cent) of total energy.n-3 PUFAs. The n-3 fatty acids reduce VLDLlevels and hence may eventually cause a reduc-tion in LDL. The effect is linked to a more rapidclearance of VLDL rich in n-3 PUFAs than thosecontaining SFAs, resulting in less post-prandiallipaemia on a n-3 PUFA-rich diet. However, themain interest in these fatty acids is associatedwith their action on blood clotting, which arosefrom studies on Greenland Eskimos who, despitea diet high in fat, have very low rates of heartdisease. In addition, these subjects have pro-longed bleeding times. Their diet contains a largeamount of marine foods providing high levelsof long-chain n-3 PUFAs. Chapter 5 describes therole of the essential fatty acids in the formationof prostaglandins and related eicosanoids. Then-3 series of prostaglandins and eicosanoids hasless aggregating potency than those made fromthe n-6 family. In addition, the vasoconstrictingeffects on blood vessel walls are less. The over-all effect is that the n-3 series is less likely toproduce inflammation, thrombosis or increasesin blood pressure. All of these responses are likelyto reduce the risk of heart attack. Ingestion ofsignificant amounts of n-3 PUFAs is believed todisplace the n-6 series from enzyme sites, so thatn-3 series eicosanoids are produced. Research hasattempted to ascertain the ratio of n-6:n-3 PUFAsin the diet that could ensure optimal outcomes inrespect of coronary heart disease. Current advicefor populations based on EURODIET (2001) is thatn-3 PUFAs should constitute 1 per cent of totalenergy, providing a n-6:n-3 ratio of 5:1.

Data from the DART study (Burr et al., 1989)also suggested that the higher intake of n-3 acids

stabilizes the rhythm of the heart and allows it to continue beating normally during a heartattack, ensuring a higher chance of survival.The Lyon Heart Study (De Lorgeril et al., 1998)demonstrated a significant protective effect ofadditional alpha-linolenic acid together with a Mediterranean diet. Supplementation withlong-chain n-3 PUFAs in the GISSI trial (GISSIPrevenzione Investigators, 1999) caused a reduc-tion in total mortality. It is on the basis of studiessuch as these that an increase in n-3 PUFA intakeis recommended, either by increasing fish consumption, or inclusion of more sources ofalpha-linolenic acid in the diet.

Trans fatty acidsAs discussed in Chapter 5, the naturally occurringunsaturated fatty acids have a cis orientation;trans fatty acids are produced by chemical alter-ation of the molecule. This occurs in the stomachsof ruminants and result in a dietary intake ofnaturally formed trans fatty acids in foods such asmilk, dairy products, beef and lamb. In addition,the diet contains artificial trans fatty acids pro-duced during food processing or manufacture offat spreads by hydrogenation (approximately 65per cent of the total intake). These fats are usedin the manufacture of biscuits, pies, cakes andpotato crisps. Most trans fatty acids have so farbeen monounsaturated, predominantly trans-oleic acid. The manufacture of high PUFA mar-garines, using emulsifier technology and thedeodorizing of vegetable oils has resulted inincreased levels of trans PUFAs, including bothn-6 and n-3, and there could be an increasedintake of trans-alpha-linolenic acid in the future.

Studies suggest that large amounts of transfatty acids (greater than currently consumed inthe UK) raise LDL cholesterol and depress HDL,albeit to a smaller extent than seen with lauricand palmitic acids. Other evidence points to anelevation of lipoprotein(a) by up to 30 per cent.Current intakes in the UK are in the range of4–6 g per person, but the top 2.5 per cent of consumers may take in more than 12 g/day.Intakes are higher in the USA, with an averageof 8.1 g/person per day.

Overall, trans fatty acids have an adverseeffect on both LDL and HDL, and this appears to

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be greater than that following an equal amountof saturated fatty acids. Nevertheless, since sat-urated fat represents a greater proportion of fatintake, reducing these is of greater importance.Consideration should perhaps be given to includ-ing information about trans fatty acids in nutri-tional labelling. It is recommended that transfatty acids should comprise no more than 1 percent of total energy intake.

Conjugated linoleic acid (CLA) is a trans fattyacid formed during the conversion of linoleicacid to oleic acid by rumen bacteria. It is foundin milk and dairy produce, and in beef andlamb. Animal studies have shown an anticancerand antiatherogenic activity by this acid, andcurrent research is investigating potential healthbenefits.

Total fatWhen total fat intake was studied by Keys (1970)in the Seven Countries Study, it was found thatthere was an association with serum cholesterollevels and heart disease mortality. However, thiseffect was dependent on the saturated fat intake.More recent data have suggested that the totalfat intake may be closely linked with the activ-ity of Factor VII, one of the clotting factors, andmay thus have a role to play in the thrombosisphase of the aetiology of heart disease. The cur-rent view is that total fat intake needs to becontrolled in individuals who are not within theideal body weight range. In these cases, a reduc-tion in fat, together with increased physical activ-ity is a useful contribution to reducing the riskof coronary heart disease. In people who are at ornear their ideal body weight, the balance of fatsshould be the main focus, rather than aiming tochange total fat intakes.

Total energyA low energy intake has been associated with a high incidence of heart disease. Low levels offood intake not only contain small amounts ofenergy, but also low nutrient levels, includingmany of the other protective factors that are necessary to sustain normal physiological func-tioning in the body. It is thought possible thatthis level of intake is a consequence of a lowenergy output and a sign of a sedentary lifestyle.

In addition, low levels of physical activity areassociated with increased body weight, which initself is considered to be a risk factor. The incor-poration of physical activity into everyday lifeis probably the best way to escape from thiscycle.

SaltThe possible links between salt intake and hyper-tension have been discussed in Chapter 10. Sincehypertension is a recognized risk factor in coronary heart disease, it can be argued thatreducing salt intake in those who are susceptiblemight reduce their risk of heart disease. However,it is now clear that a broader dietary approach canbe more effective in reducing blood pressure. Datafrom the Dietary Approaches to Stop Hyper-tension (DASH) trial showed a dietary changethat included low-fat dairy products, nuts, fruitand vegetables resulted in greater reductions inblood pressure than salt restriction alone (Appelet al., 1997). The DASH diet included increasedintakes of potassium, calcium and magnesium,as well as lower sodium intakes, and it is nowrecognized that all of these factors are effectivein changing blood pressure. These findings addfurther support to the importance of potassiumintakes in the control of blood pressure.

CalciumFor many years it has been noted that the inci-dence of coronary heart disease is lower in thosegeographical areas that have hard water. Severalmechanisms have been put forward, with sup-porting evidence. Dietary calcium combines withfats, especially saturated fatty acids producingsoaps, which remain unabsorbed and are excretedfrom the body. In a study of British and Frenchfarmers, calcium intake was inversely related toblood levels of triglycerides. In addition, therewas an inverse relationship with platelet clottingactivity. Finally, as discussed above, calciumintakes are inversely related to blood pressure,as has been demonstrated in a number of largecohort studies. In general, calcium intakes, espe-cially from dairy produce, appear to be associatedwith a lower risk of coronary heart disease andlow-fat cheese may be considered a constituentof healthy diets.


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AlcoholHeavy drinking in excess of 55 units for men and35 units for women per week is associated withraised triglyceride and VLDL levels, and thusincreases heart disease risk. In addition, bingedrinking has been associated with sudden deathdue to myocardial infarction or stroke. However,a moderate alcohol intake (within ‘safe’ limits) hasbeen shown to have a protective effect againstheart disease. The mechanisms appear to involveboth the atherogenesis and thrombogenesisaspects of coronary heart disease. A number ofstudies have found an increase in HDL levels onalcohol consumption, which falls within 24 hourswhen alcohol intake stops. The elevation of HDLis approximately similar to that achieved byphysical activity. In addition, moderate alcoholintake has been shown to reduce platelet aggre-gation. In large amounts, alcohol can causeplatelet aggregation. In this case, alcoholic beverages that contain antioxidants, such as redwine, may be protective.

The relationship between alcohol consump-tion and heart disease is usually found to followa J-shaped curve, with increased risk in non-drinkers and heavy drinkers. The lowest riskoccurs in the middle range of alcohol intakes,taking 2–4 drinks per day on 3–4 days per week.Ideally, consumption should be with meals, as isseen in Mediterranean countries. There has beendebate about the type of alcoholic drink that maybe most beneficial, and many studies suggestthat red wine has the greatest protective effects.However, in general, it appears that the consist-ent effects are attributable to the alcohol per se,rather than additional constituents particular toa specific beverage. However, antioxidants in redwine, most notably resveratrol, may contributean additional protective benefit.

Some concern has been expressed by healtheducationists about the desirability of promot-ing alcohol consumption as a means of prevent-ing heart disease because of the implications for health of alcohol in amounts greater than‘moderate’.

Fibre (non-starch polysaccharides)Sources of soluble fibre, especially from oats,have been shown to reduce serum cholesterol

levels, although the effects are not large. Insolublefibre does not appear to have a similar effect oncholesterol. Nevertheless, a significant inverserelationship between fibre intake and myocar-dial infarction and coronary mortality has beendemonstrated in two prospective studies, inFinland and the USA, in large cohorts of men.The relationship was strongest for cereal fibreand persisted when confounding variables weretaken into account. It has been suggested thatthe effects occur due to the satiating effect offibre-rich foods that results in a lowered fatintake and possibly a reduced total energy intake.

However, soluble fibre may increase sterolexcretion from the body, thereby lowering cholesterol levels. High fibre intake has been asso-ciated with a decrease in the level of insulin and increased insulin sensitivity, thus improvingmetabolic function. Additionally, a high-fibre dietalso affects the clotting factors and may be asso-ciated with a lower blood pressure. Overall, it islikely that the effects of fibre on heart disease arenot mediated through a single mechanism andno adverse harmful effects have been reportedfrom increased sources of fibre in the diet.

AntioxidantsThe inability of the lipid hypothesis to explain thelink between diet and heart disease fully, andthe completion of studies that show inconsistentor contrary results have led over the years to asearch for other influencing factors. Severalstudies demonstrated that levels of antioxidantsin both diet and serum exhibit good correlationswith heart disease incidence – often higher levelsof correlation than are seen in the same studiesfor fat indices. In particular, the MONICA study(Gey et al., 1991) has shown inverse relationshipsbetween heart disease mortality and intakes of beta-carotene, vitamin C and vitamin E. Thestrongest correlations (p 0.001) were seen withalpha-tocopherol, vitamin C and beta-carotenein food supplies and the rate of coronary heartdisease. Correlations also existed with the dietarysources of these nutrients, most notably vege-tables, vegetable oils, sunflower seed oil, seeds,nuts and fruit. In the USA, two large prospectivestudies (of male health professionals and femalenurses) found a lower incidence of coronary heart

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disease in the subjects who consumed vitamin Esupplements.

However, these results were not replicated ina series of intervention studies in various coun-tries, in which supplements of the major antioxi-dants, mainly vitamin E and beta-carotene, wereassigned to subjects. In general, these studiesshowed either no beneficial effect of supple-mentation with these antioxidants or an adverseeffect of supplementation, with a higher rate ofcoronary heart disease or cancer than the controlgroups. It is suggested that antioxidant nutrientscan act as pro-oxidants in certain conditions,which may include the administration of largeamounts of a single antioxidant.

Thus, it is likely that antioxidants worktogether to produce the effects seen in wholediet studies, and that advice should be targetedtowards fruit and vegetable consumption. It ispossible that fruit and vegetables contain othersubstances that have not yet been taken intoaccount and that have even more effect on heartdisease development. There is interest in otherfactors found in fruit and vegetables, such aspolyphenols or flavonoids. The recommendationof the WHO is to eat five servings of fruit andvegetables per day.

There are good grounds for believing that theantioxidant nutrients do play a preventive role inthe formation of fibrous plaques. It is appropriateat this point to summarize all of the functions ofantioxidants in protection against free radicals.

Mechanisms of action of antioxidantsFree radicals are produced by most of the oxida-tive reactions in the body. The most importantof these radicals are:■ the hydroxyl radical. OH■ superoxide radical. O2

■ singlet oxygen. 1O2

■ nitric oxide. NO.Also included are the peroxyl radical, hydrogenperoxide and hydroperoxyl. All share the com-mon property of having an exceedingly shortlifespan and, therefore, are very unstable. Theycan attack vital cell components, inactivateenzymes and damage genetic material. It is,therefore, reasonable to assume they play a partin degenerative diseases.

The body has a complex antioxidant defencesystem to counteract these radicals. This is madeup of endogenous and exogenous components.■ Endogenous antioxidants are mainly enzymes

that catalyse radical quenching reactions(many of these are dependent on dietary min-erals for activation) or bind pro-oxidants,which might catalyse free-radical reactions.

■ Exogenous antioxidants are mainly vita-mins that quench free radicals.

Endogenous antioxidantsThe antioxidant enzymes include:■ superoxide dismutase (SOD), which neutral-

izes the superoxide radical and which requireszinc and copper, or manganese for activation;

■ catalase, which is specific for hydrogen per-oxide and requires iron for its activity; and

■ glutathione peroxidase, which removes per-oxides and is a selenium-requiring enzyme.

Many minerals are clearly involved in activatingthese enzymes. However, copper and iron can alsoact as pro-oxidants when freely present. Thisexplains why there are binding proteins presentto prevent this happening, most notably caeru-loplasmin and albumin to bind copper, andtransferrin and ferritin to bind iron.

Exogenous antioxidantsThe most important of these are vitamins C and E,and the carotenoids. Plant flavonoids are pos-sible members of this group.

Vitamins C and E quench free radicals byproviding H atoms to pair up with unpairedelectrons on free radicals. This inactivates thevitamins, which then need to be regenerated.Glutathione is believed to regenerate vitamin Cand vitamin C can regenerate vitamin E (Figure14.7). In its turn, vitamin E may promote theantioxidant activity of beta-carotene againstlipid peroxidation. It is suggested that vitamin Cis the primary antioxidant in the plasma and is consumed first in destroying free radicals.Vitamin E is the major antioxidant in the lipidparts of membranes. Lipid peroxidation does notbegin until after the vitamin C has been used. It is important that regeneration can take place,however, so that a continued supply of the vita-mins is available. These interactions highlight


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the importance of maintaining a balance betweenthe different exogenous antioxidants suppliedto the body.

In conclusion, the theories about antioxidantsallow some of the other factors discussed earlierto be linked together. It has been suggested thatthe desire for weight loss, which preoccupies somany women and which encourages them to eatlow-calorie fruits and vegetables, helps to protectthem from heart disease by adding more antioxi-dants to their diet. Smokers, who have a greatlyincreased risk of heart disease, are recorded ashaving very low intakes of fruit and vegetablesand consequently poor vitamin C status. Whenlinked to the increased burden of free radicals,this may explain their greater risk. Finally, alco-holic beverages, most notably wines, containphenolic substances that also act as antioxidants.This may explain why there are lower rates ofcoronary heart disease among populations inwine-drinking countries.

HomocysteineIt has been known since the late 1960s that raisedlevels of homocysteine in the blood are associ-ated with severe arteriosclerosis. Initially, this wasconsidered to be a problem in individuals with

inborn errors in the metabolism of homocysteine.However, in recent years, it has been found thatraised homocysteine levels are an independentrisk factor for vascular disease, and the effect isgraded. The evidence for this comes from a rangeof different studies, including retrospective case-control, cross-sectional and prospective studies.The metabolism of homocysteine is linked to thatof methionine and cysteine, and utilizes a numberof B vitamins as cofactors. These include folate,pyridoxine, riboflavin and vitamin B12. Deficien-cies in the metabolism of homocysteine, withresultant elevated plasma levels, are associatedwith mutations in one of the enzymes (methylenetetrahydrofolate reductase; MTHFR) involved inthe metabolic pathway (see Chapter 9 for moredetails). Lower activity levels of the enzyme havebeen identified in approximately 30 per cent ofthe population, with a smaller percentage beinghomozygous for the mutation. The referencerange of homocysteine in the plasma is stilldebated, but the following are generally accepted:

5–15 �mol/L normal range15–30 �mol/L moderate elevation

30–100 �mol/L intermediate elevation100 �mol/L severe elevation

It has been proposed that homocysteine maybe directly toxic to endothelial cells, through amechanism involving nitric oxide that normallycauses endothelial relaxation. This would facili-tate monocyte adhesion and promote the processof fatty streak formation. A further possiblemechanism is through an increased coagulationtendency, by an inhibition of the normal fibri-nolytic mechanisms that disperse blood clots.However, neither of these mechanisms has yetbeen conclusively proven and much remains tobe discovered about the relationship of homo-cysteine to the processes of vascular disease.

Dietary interventions can lower homocysteinelevels. Most importantly, folate status is inverselyassociated with homocysteine levels, with as lit-tle as 200 �g/day of folate causing a reductionin plasma homocysteine levels. Evidence is lessconclusive for supplementation with riboflavin,pyridoxine or vitamin B12, although a combi-nation of these may be beneficial. It should alsobe remembered that folate is provided by fruit and

Figure 14.7 Interactions between glutathione, vitamin C and vitamin E during antioxidant activity.R• free radical.


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vegetables in the diet, so that an increase in thesefoods in line with other aspects of dietary inter-vention will also help to increase folate status.Fortification of grain products with folic acid, ata rate of 1.4 �g/g of product has been introducedin the USA since 1999. Early indications arethat, in the first year after this was introduced,there was a 3.4 per cent reduction in mortalityfrom stroke and heart attack. Mean homocysteinelevels have fallen, and mean plasma concentra-tions of folate have increased.

More controlled studies in this field are stillrequired.

Future directions

There is still a huge amount to learn about coron-ary heart disease. Developments in molecularbiology and the human genome project may inthe future allow research to identify the inter-action between risk factors and particular genes.Animal models with specific genetic modificationsare already being used to study mechanisms tounderstand existing knowledge. Improved tar-geting of dietary intervention and drug therapymay be a consequence.

1 The role of diet in the aetiology of coronary heart disease is complex.2 Early hypotheses about links with fat have been discovered to explain only part of the relationship.3 New findings about the roles of other fats, such as monounsaturated fatty acids, n-3 fats and trans fatty

acids have modified the original lipid hypothesis.4 The importance of other dietary factors, in particular the antioxidants, provides opportunities to link

some of the earlier findings together.5 Dietary guidelines promoting lower fat, and increased fruit and vegetables intakes address many of the

postulated mechanisms relating to coronary heart disease. Weight control and promotion of physicalactivity remain important preventive factors.

SUMMARY

1 Distinguish between atherogenesis and thrombogenesis, and describe the mechanisms that are currently offered as explanations of these processes.

2 Which dietary factors are thought to beinvolved in:a atherogenesisb thrombogenesis?

3 What are the main tenets of the lipid hypothesisand what changes to it have been suggested inrecent years?

4 a Explain what you understand by theantioxidant nutrients.

b Produce a diagram to show how they mightplay a part in protecting against heart disease.

5 Discuss with a colleague how you believe thetheories about the dietary links with heartdisease are reflected in current dietaryguidelines. Can you explain all of the guidelineson a scientific basis?

6 Produce a poster or leaflet to summarize themain aspects of dietary advice for theprevention of coronary heart disease. Make theinformation as practical as possible.

STUDY QUESTIONS


Appel, L.J., Moore, T.G., Obarzanek, R. et al. 1997: A clinical trial of effects of dietary patterns onblood pressure. New England Journal of Medicine 336, 1117–24.

Ashwell, M. (ed.) 1996: Diet and heart disease: a round table of factors, 2nd edn. London: Chapman & Hall.


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Bellizzi, M.C. 1995: Wine and vegetable oils: the French paradox revisited. British NutritionFoundation Nutrition Bulletin 20, 256–65.

Brown, A.A., Hu, F.B. 2001: Dietary modulation of endothelial function: implications for cardiovas-cular disease. American Journal of Clinical Nutrition 73, 673–86.

Burr, M.L. 1993: Fish and ischaemic heart disease. World Review of Nutrition and Dietetics 72, 49–60.Burr, M.L., Fehily, A.M., Gilbert, J.F. et al. 1989: Effects of changes in fat, fish and fibre intakes on

death and myocardial infarction: Diet and Reinfarction Trial (DART). Lancet ii, 757–61.Caggiula, A.W., Mustad, V.A. 1997: Effects of dietary fat and fatty acids on coronary artery disease

risk and total and lipoprotein cholesterol concentrations: epidemiologic studies. AmericanJournal of Clinical Nutrition 65(Suppl.), 159–610S.

De Lorgeril, M., Renaud, S., Mamelle, N. et al. 1994: Mediterranean alpha-linolenic acid-rich diet insecondary prevention of coronary heart disease. Lancet 343, 1454–9.

DoH (UK Department of Health) 1992: The health of the nation: a strategy for health in England.London: HMSO.

De Lorgeril, M., Salen, P., Martin, J.L. et al. 1998: Mediterranean dietary pattern in a randomised trial.Prolonged survival and possible reduced cancer rate. Archives of Internal Medicine 158, 1181–7.

DoH (UK Department of Health) 1994: Nutritional aspects of cardiovascular disease. Report onHealth and Social Subjects No. 46. Report of the Cardiovascular Review Group of the Committeeon Medical Aspects of Food Policy. London: HMSO.

DoH (UK Department of Health) 1999: Saving lives – our healthier nation. London: The StationeryOffice.

Erens, B., Primatesta, P. (eds) 1999: Health survey for England: cardiovascular disease ’98. Volume1: Findings. London: The Stationery Office.

EURODIET 2001: Report and proceedings. Public Health Nutrition 4, 2(A).Gey, K.F., Puska, P., Jordan, P. et al. 1991: Inverse correlation between plasma vitamin E and mortal-

ity from ischaemic heart disease in cross-cultural epidemiology. American Journal of ClinicalNutrition 53, 3265–345.

GISSI Prevenzione Investigators, 1999: Dietary supplementation with n-3 polyunsaturated fattyacids and vitamin E after myocardial infarction, results of the GISSI Prevenzione trial. Lancet354, 447–53.

Grundy, S.M. 1988: Cholesterol and heart disease: a new era. Journal of the American MedicalAssociation 256, 2849–58.

Halliwell, B. 1994: Free radicals, antioxidants and human disease: curiosity, cause or consequence?Lancet 344, 721–4.

Hardman, A.E. 1999: Physical activity and cardiovascular risk. Review in depth. Journal ofCardiovascular Risk 2, 285–329.

Hegsted, D.M., Ansman, L.M., Johnson, J.A. et al. 1993: Dietary fat and serum lipids: an evaluationof the experimental data. American Journal of Clinical Nutrition 57, 875–83.

Hu, H., Stampfer, M.J., Manson, J.E. et al. 1997: Dietary fat intake and the risk of coronary heart dis-ease in women. New England Journal of Medicine 337, 1491–9.

Hulshof, K.F.A.M., van Erp-Baart, M.A., Anttolainen, M. et al. 1999: Intake of fatty acids in WesternEurope with emphasis on trans fatty acids. The TRANSFAIR study. European Journal of ClinicalNutrition 53, 143–57.

Jacob, R.A. 1995: The integrated antioxidant system. Nutrition Research 15(5), 755–66.Keys, A. (ed.) 1970: Coronary heart disease in seven countries. Circulation 41(Suppl.), 11–211.Kinane, D.F., Lowe, G.D.O. 2000: How periodontal disease may contribute to cardiovascular disease.

Periodontology 23, 121–6.Kromhout, D. 2001: Epidemiology of cardiovascular disease in Europe. Public Health Nutrition

4(2B), 441–57.


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Law, M.R., Wald, N.J., Thompson, S.G. 1994: By how much and how quickly does reduction inserum cholesterol concentration lower risk of ischaemic heart disease? British Medical Journal308, 367–72.

Martin, M.J., Halley, S.B., Browner, W.S. et al. 1986: Serum cholesterol, blood pressure and mortal-ity: implications from a cohort of 361 622 men. Lancet ii, 933–36.

McKinley, M.C. 2000: Nutritional aspects and possible pathological mechanisms of hyperhomocys-teinaemia: an independent risk factor for vascular disease. Proceedings of the Nutrition Society59, 221–37.

Mensink, R.P., Katan, M.B. 1992: Effect of dietary fatty acids on serum lipids and lipoproteins – ameta-analysis of 27 trials. Atherosclerosis and Thrombosis 12, 911–19.

Renaud, S., Lanzmann-Petithory, D. 2001: Coronary heart disease: dietary links and pathogenesis.Public Health Nutrition 4(2B), 459–74.

Rimm, E.B., Klatsky, A., Grobbee, D. et al. 1996: Review of moderate alcohol consumption andreduced risk of coronary heart disease: is the effect due to beer, wine or spirits? British MedicalJournal 312, 731–6.

Scandinavian Simvastatin Study Group 1994: Randomised trial of cholesterol lowering in 4444patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (45). Lancet344, 1383–9.

Schaefer, E.J. 2002: Lipoproteins, nutrition and heart disease. American Journal of Clinical Nutrition75, 191–212.

Shaper, A.G., Wannamethee, G. 1991: Physical activity and ischaemic heart disease in middle-agedBritish men. British Heart Journal 66, 384–94.

Slavin, J., Martin, M.C., Jacobs, D.R. et al. 1999: Plausible mechanisms for the protectiveness ofwhole grains. American Journal of Clinical Nutrition 70, 459S–63S.

Troisi, R., Willett, W.C., Weiss, S.T. 1992: Trans fatty acid intake in relation to serum lipid concen-trations in adult men. American Journal of Clinical Nutrition 56, 1019–24.

Truswell, A.S. 1994: Review of dietary intervention studies: effects on coronary events and on totalmortality. Australia and New Zealand Journal of Medicine 24, 98–106.

Various authors 2000: Symposium on reducing cardiovascular disease risk: today’s achievements,tomorrow’s opportunities. Proceedings of the Nutrition Society 59, 415–40.

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Diet and cancer


❏ describe what is meant by cancer;❏ discuss the ways in which the relationship between diet and cancer is studied;❏ identify the main relationships that have been indicated;❏ describe the guidelines on healthy eating for the reduction of cancer risk.


❏ discuss the links between certain specific cancers and dietary patterns and explain the suggested mechanisms,where appropriate;

❏ discuss some of the problems inherent in studies on diet and cancer;❏ advise the practical changes needed in a Western diet to reduce the risk of cancer.

Cancer affects one in three people in the UK atsome time in their life, and is responsible forapproximately one-quarter of all deaths, num-bering some 160000 cases per year. Lung canceraccounts for almost one-quarter of all cancerdeaths and it is the leading type of cancer in men,followed by cancer of the prostate. In women,breast cancer causes most deaths, followed bylung cancer. In both men and women, cancer ofthe colon and rectum is the third major type ofcancer.

More people now die from cancer than wasthe case 100 years ago. However, this is a reflec-tion of a longer life expectancy and larger num-bers of elderly people in the population. Becauserisk increases with age, the majority of cancerdeaths occur in people aged over 65 years.Different cancers show different trends, however.Deaths from lung cancer are clearly linked tosmoking and these have followed trends insmoking throughout the century. Melanoma, acancer of the skin, has increased in recent years,probably as a result of increased exposure to thesun as more people take holidays abroad. On the

other hand, stomach cancer rates have declineddramatically since the 1950s. Several explan-ations may be offered for this, including dietarychanges. However, a major factor recently discovered is the role of Helicobacter pylori inthe development of the disease. Antibodies tothis bacterium are much more common among people brought up in overcrowded housing con-ditions, who then have a higher risk of stomachcancer. Improvements in housing provision mayhave had the added benefit of reducing exposureto this bacterium and, consequently, contributedto reduced rates of stomach cancer. This exampleillustrates the often multifactorial nature of theaetiology of cancer, and the consequent difficul-ties of study.

Other factors that need to be taken intoaccount in studying statistics on cancer are theimprovements in detection and diagnosis, andadvances in treatment, both of which mayincrease figures for the apparent incidence ofthe disease. Thus, we are not working with astatic baseline from which to explore trends. Itis also important to note that changes in the

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environment and lifestyle factors may impacton cancer statistics, and these must be continu-ously studied to give more clues about the aeti-ology of cancer at various sites.

According to the statistics, there have beenno marked changes in cancer incidence ratesthat could be attributed to toxic hazards, such aspesticides and pollution at average levels ofexposure. However, when groups of individualsare exposed to abnormal levels, for example ofradiation, as happened after the nuclear accidentin Chernobyl in 1986, then higher rates of par-ticular cancers are found. Unusual occurrencesof cancer in a community are always suspicious,since they may be coincidental or linked to aparticular environmental event. Finding ananswer can help to further our understanding ofthe development of the disease.

Around the world there are also differencesin the occurrence of particular cancers. InAfrica, Asia and Latin America, there tends tobe a higher rate of cancers of the upper respira-tory and digestive systems (aerodigestive sys-tem) (mouth, pharynx, larynx and oesophagus),the stomach, liver and cervix. Conversely, can-cers of the breast, endometrium, prostate, colonand rectum are more common in Europe, NorthAmerica and Australia. Cancers of this lattergroup are now increasing in the urbanized areasof the developing countries. Lung cancer is thecommonest cancer worldwide. Migration fromone type of community to another is often asso-ciated with a change in the pattern of cancersseen in the migrants.

What is cancer?

Cancer is now accepted as a genetic disorder ofsomatic cells, in which an accumulation ofgenetic changes causes a normal cell to give riseto one which is abnormal in form or function.Generally, several changes have to occur for can-cer to develop, varying between different typesof cancer. The fundamental change occurs withinthe genetic material and may be inherited or, inthe great majority of cases, occurs sporadically.

The resulting abnormal cells fail to respondto some or all of the regulatory signals that control division, growth, differentiation and

programmed cell death (apoptosis). In addition,the affected genes may malfunction in theirrole, for example, as tumour suppressors, ‘proofreaders’ of encoded material or repair genes.There are many types of cancers. They have dif-ferent characteristics, probably originate invarying ways, occur in different parts of thebody, have different courses of development;and require various treatments.

The developing tumour causes damage to itshost by interfering with the normal functioningof the tissue or organ where it grows. It alsodraws on the host for nutrients to support itsgrowth. Some cancers produce factors, whichcause increased catabolism of the body’s owntissues, resulting in a state of rapid weight lossand deterioration.

Although the process of development of cancer (or carcinogenesis) is not fully under-stood, it is clear that there are several stages thattake place over a period of time (Table 15.1). Theboundaries between the stages may not be asclear as implied here, but they provide a usefulframework. The exact duration of each stage isunknown, but opportunities may arise for theprocess to be stopped, and possibly reversed,before it reaches the later stages.

Studying the relationshipbetween diet and cancer

In 1997, the World Cancer Research Fund(WCRF) and the American Institute for CancerResearch (IARC) published a report in whichstudies relating to diet and cancer from the pre-vious 15 years were reviewed and their scien-tific evidence assessed in a consistent manner.Such a systematic review is an important toolfor exploring existing research findings. Thisevidence was used as the basis for recommenda-tions. Various approaches to the study of cancerexist and new evidence is continually emerging.The WCRF are currently developing a system-atic methodology for the identification, assess-ment and recording of information from thescientific literature to form the basis of a newreview. Worldwide, the occurrence of cancer isgreater in the industrialized than in the devel-oping countries, with up to 30-fold differences

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in rates of particular cancers. This suggests thatthere may be important environmental factorsinvolved in the aetiology. Many of these havebeen investigated in observational studies com-paring different communities, groups withincommunities and migrant groups moving fromone community to another. However, such studies do not provide evidence of causality orinformation about biological mechanisms, andmust be supported by experimental findings.Developments in identification and measure-ment of biological markers and rapid gains ininformation about human genetics will provideopportunities to link observational data withmolecular mechanisms.

Much of the current evidence is based onmany epidemiological studies, whose resultsallow researchers to calculate the relative risk,or odds ratio of disease, resulting from exposureto a particular factor. It is on the basis of suchdata that risk factors for the development ofvarious cancers can be proposed.

Ecological or correlational studies

These aim to show an association between theincidence of cancer in a population with a high or

low occurrence of a particular environmental fac-tor. This type of evidence can only point to theneed for further, more detailed studies as the exist-ence of a correlation does not imply causality.Changes over time in either the diet or the inci-dence of the cancer may provide further clues.

Case-control studies

These attempt to identify individuals with cancerand closely match each one with a control indi-vidual without disease. Comparison of environ-mental factors, including diet, can then be made,with the objective of identifying differences thatmay have contributed to the development of thecancer. In addition to the difficulties of obtain-ing accurate measurements of dietary intake,there are a number of other drawbacks to thisapproach.■ Studies that rely on information about

dietary intake several years ago are impre-cise. This is particularly true for a personwho has recently been given a diagnosis ofcancer, which tends to be a devastatingevent. In addition, the development of sym-ptoms associated with the disease may havealready resulted in dietary changes.

Summary of stages in cancer developmentTABLE 15.1Stage of development Associated changeInitiation Exposure to harmful agent (e.g. chemical carcinogen, virus, free radical,

radiation) or error in transcription: may permanently alter the DNA materialThe cell may remain in this state for a long periodIt is also possible for the DNA damage to be repaired, or the damaged cell to be

destroyed by the body’s normal regulatory systemsMolecular biology research suggests that there are genes that can both

promote and suppress these changes. This may explain the increased risk ofcertain cancers in families

Promotion Substances that increase the rate of cell division may cause the damaged DNA to replicate before it has been repaired or destroyed

This may not happen for 10–30 years after the first stepPromoters are believed to include oestrogens, dietary fat, alcoholThere may also be inhibitory agents, including antioxidants, dietary fibre,

calcium, other constituents in plant foods, additivesProgression The cells undergo further development and begin to grow in an uncontrolled

manner, producing a tumour

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■ Cancer is believed to develop over a longperiod of time; differences in diet a shorttime before the diagnosis may not reflectdifferences when the cancer was initiated orpromoted.

Prospective cohort studies

These offer the most promising approach. Theyinvolve the recruitment of a large cross-sectionof the population and follow up the sample overa number of years, thus monitoring developmentof disease. Data about diet and lifestyle factors,together with biochemical measurements aretaken initially and at intervals. The use of bio-markers, for example, biological function tests,blood or urine levels of substances, carries lessrisk of measurement error. Thus, if and when dis-ease does occur, data will be available that coverthe period when the disease was developing. A study of this type – the European ProspectiveInvestigation into Cancer and Nutrition (EPIC) –is currently taking place in ten countries inEurope. Recruitment started in 1992, with a tar-get of 500000 subjects and first results werereported in 2001. The study will continue to col-lect data for a further 10 years. The major disad-vantage of this type of study is the need for verylarge numbers of subjects. Research on ‘fetal pro-gramming’ and evidence from studies on growththat point to relationships with later disease, mayindicate that even a prospective study over 10 or15 years may be of insufficient duration to iden-tify factors that may trigger the cancer process.

Meta-analysis

Data from separate studies can be reanalysed by‘meta-analysis’. By cooperating with the investi-gators, it is possible to record all the outcomes ofa number of studies in a similar way and thusincrease the power of the analysis. In this way, itmay become possible to quantify the relationshipbetween exposure to a hazard and the risk of aparticular disease obtained by epidemiologicalstudy, even when that risk is only moderate. It isimportant that only those studies that have simi-lar methodologies are used, and that all relevantstudies are included, irrespective of their results,

for the analysis to be unbiased and worthwhile.More such analyses will no doubt be carried outin the future.

Environmental causes ofcancer

Various attempts have been made over the last20 years to evaluate the environmental contri-bution to the development of cancer; some esti-mates suggest that this may be up to 80 percent. Of these, the most important factors are:■ diet, which may account for an average of

one-third of cancer deaths (although the sug-gested range for different cancers is between10 and 70 per cent);

■ smoking, which is causal in 30 per cent ofcancer deaths (range between 25 and 40 per cent);

■ physical activity, which contributes tomaintenance of a normal body weight, pre-vention of excessive adiposity and is animportant protective factor.

In comparison, other factors believed to beimportant causes of cancer, such as food addi-tives, pollutants, industrial products and geo-physical factors, taken together probably accountfor 6 per cent of all known cancer deaths (range0–13 per cent). It should be noted that some foodadditives, like antioxidants and preservatives,may actually be protective against cancer.

In looking at the above data, it is not sur-prising that there is a growing interest andurgency in modifying diets and lifestyles in anattempt to reduce cancer risk. The World CancerResearch Fund estimated that attention to diet,smoking and physical activity could reducecancer incidence by 30–40 per cent, preventing3–4 million cases of cancer worldwide annually.

Role of diet

Food or nutrients may contribute to the devel-opment of cancer in a number of ways, broadlyclassified as follows.■ Foods may be a source of pre-formed (or

precursors of) carcinogens.■ Nutrients may affect the formation, transport,

deactivation or excretion of carcinogens.

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■ Nutrients may affect the body’s resistance tocarcinogens and, therefore, be importantprotective factors.Diets are extremely complex and their meas-

urement is subject to error. This is particularly aproblem in a population whose diets are rela-tively similar. If the error is not consistent and isgreater than the variation in intakes, it can resultin misclassification of individuals and a miscal-culation of risk. Random errors can also reducethe power of studies to detect relationshipsbetween intake and disease, but these errors can be minimized by repeated measurements orthe use of large cohorts. Other difficulties arisebecause of the co-variation in particular nutri-ents. For example, fat intakes and energy intakesmay change simultaneously, meat intakes mayreflect the protein content of the diet, fruit andvegetables in the diet affect the overall intake ofnon-starch polysaccharide (NSP). Finally, there isgood evidence from many studies that subjectstend to underreport their dietary intake, and thisdoes not happen in a systematic manner withsome nutrients more likely to be underreported,in particular protein, sugars and fat missed froma diet record. Again, this can be taken intoaccount in large prospective studies, if they are well designed. Despite these difficulties, epi-demiological evidence from the last 15 years has identified a number of consistent trends inthe relationship between diet and some cancers.Detailed mechanisms underlying these associa-tions remain to be elucidated.

Possible promoting factors

Total energy intakeRestricting the food intake of mice without modi-fying the proportion of the individual nutrientshas long been known to halve the incidence ofspontaneous tumours of the mammary gland andlung and to reduce susceptibility to known car-cinogens. This effect of restricted energy intakeappears to be independent of any reduction in fatcontent of the diet. In mice, increased activitywas as effective at reducing tumour developmentas restricted energy intake. Increased exercisemay promote activity of the immune system,thereby increasing resistance.

In humans, rapid growth in childhood, andespecially growth in height may also, in ways asyet unknown, contribute to a higher risk of can-cer. Data from the National Health and NutritionExamination Survey (NHANES) 1 study found apositive correlation with height and a number ofcancers, including colorectal cancer. Follow-upof children under 16 years, first studied by BoydOrr in 1937–39, has also shown a significant posi-tive association, with a 20 per cent increased riskof all cancers not associated with smoking, forevery 1MJ greater daily energy intake (Frankel et al., 1998). Potential confounding variables,such as social class and household size, weretaken into consideration in the analysis.

High energy intakes also contribute to riskby leading to greater adiposity and thereforeoverweight, if not accompanied by increasedenergy expenditure. Therefore, restriction ofenergy intake and avoidance of overweight areprobably important at key stages of life. Inwomen, being overweight at puberty and afterthe menopause appears to be linked to increasedbreast cancer risks, but pre-menopausal over-weight may be protective. These findings arelinked to pre-sensitization of breast tissue tooestrogens in the young adolescent, and unop-posed production of oestrogens by adipose tis-sue after the menopause. Both may promote thedevelopment of oestrogen-dependent tumours.Levels of ovarian hormones appear to be influ-enced by nutritional status; thus, a high caloricintake may increase production and thereby riskof breast cancer. A correlation between breastcancer risks, sex hormone levels and energyintakes has been found in countries across theworld. Sex hormones produced or modified byadipose tissue may also play a part in cancer ofthe endometrium in women and possibly theprostate in men.

A review of data on energy intake and can-cers also indicates a positive relationship withlarge bowel cancer. This may reflect greaterexposure to carcinogens with the greater foodintake but more evidence is needed in this area.

Fat intakesFat has been described as a promoter of carcino-genesis, although the effect of dietary fat is often


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difficult to distinguish from that of energy intake,as fat obviously contributes to the total energycontent of the diet. Associations with fat intakehave been reported for cancers of the breast,colon and prostate, as well as weak relationshipsfor cancer of the ovary, kidneys and pancreas.

In the case of breast cancer, there is still con-siderable controversy. Estimated fat consumptionin different countries of the world shows a strongpositive correlation with age-adjusted death ratesfrom breast cancer. In the USA, the Nurses HealthStudy (Willett et al., 1992) found no associationbetween total fat intake or intake of fibre and the incidence of breast cancer in both pre- andpost-menopausal women. It is possible that theprevailing higher fat intakes lead to earliermenarche in girls, thereby prolonging the expos-ure of breast tissue to circulating oestrogens andincreasing risk. This has not, however, been fullyinvestigated. Although in animals there is evi-dence of a promoting effect of n-6 fatty acidsand an inhibitory effect of n-3 fatty acids onmammary tumour growth, this effect has notbeen demonstrated in humans. It has been sug-gested that n-6 fatty acid intakes may already beabove the threshold of this promoting effect,after which no further increase is seen. This mayexplain the absence of evidence in women.Nevertheless, it is probably prudent to limit fatintakes, even if this simply reduces total energyintake, and thereby provides some protection.

Dietary changes in Japan in the last 40 yearshave included a dramatic increase in fat intake,paralleled by a reduction in complex carbohy-drates. Associated with these dietary changeshas been an increase in colon cancer, suggestinga link. Evidence for the involvement of fatintake is stronger in the case of colon cancer,particularly in relation to fat of animal origin,cholesterol and red meat consumption. Furtherevidence from the US Nurses Health Study hasshown a 2.5-fold increase in risk of colon cancerin women consuming beef, pork and lamb daily,compared with those eating these meats lessthan monthly. Association with chicken and fishwas negative, and there was no association withcholesterol intakes. It has been proposed thatdietary fat causes a greater secretion of bileacids; these may be fermented by anaerobic

bacteria in the colon to produce mutagenic com-pounds, leading to abnormal cell proliferation inthe colon. However, other dietary factors maymodify this process, most notably NSPs and pro-tective factors in fruit and vegetables. The low-ered pH of the bowel as a result of soluble NSPfermentation may be protective.

Prostate cancer has also been weakly associ-ated with a high fat intake, but more evidence isneeded to support this. Overall, it remains prob-lematic to separate the effects of higher fatintakes from those of a high energy intake andoverweight.

AlcoholThere is an association between consumption ofalcohol and cancers of the aerodigestive tract(mouth, throat and oesophagus), as well as theliver. The EPIC study has confirmed that the riskof these cancers is nine times greater in thosedrinking 60 g ethanol or more (7–8 units) a daycompared with those drinking 30 g or less. Theeffects of alcohol as a causative agent arepotentiated by smoking, with those smokingmore than 20 cigarettes a day having a 50-foldgreater risk than non-smoking, moderate alco-hol drinkers. The risks of oral and pharyngealcancers can be offset to some extent with a highintake of fruit and vegetables.

Oesophageal cancer has been increasing sincethe early 1970s in the UK, which parallels theincrease in alcohol consumption, with a latencyof 15–20 years. It is not clear if the relationship issimply with the amount of alcohol consumed;some evidence suggests that spirits are moreharmful than beer and wine. Oesophageal canceralso occurs in parts of the world where alcoholconsumption is low. In these cases, it is thought tobe related to micronutrient deficiencies in the diet.

Alcohol consumption, above a moderatelevel, has also been shown in the EPIC study to beassociated with a rise in breast cancer, althoughthere was no evidence of a dose–response rela-tionship with wine consumption.

SaltSalt has been suggested as a causative factor instomach cancer because it was noted that mortal-ity from this cancer was closely related to the

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incidence of stroke in communities. This wasfound to be true between countries, between dif-ferent regions of the same country and differentsubgroups of the population. Salt has highosmotic activity and has been reported to causegastritis in animals, resulting in early damage tothe mucosa. Other factors are also important, mostnotably the presence of Helicobacter pylori, whichis now known to be a major cause of chronicatrophic gastritis and which must be taken intoaccount in future studies on the exact role of saltas a factor in causation of stomach cancer.

In addition to sodium chloride, other formsof preservation using nitrates and nitrites aswell as pickling have been associated withstomach cancers. Nitrates occur in the diet aspreservatives in foods, such as ham, bacon andsausages, in beer, and are naturally present invegetables as well as in the drinking water, par-ticularly in agricultural areas owing to contam-ination from fertilizers. Dietary nitrates may notcause cancer per se, but it has been proposedthat the conversion to nitrites and subsequentlyto carcinogenic nitrosamines is more likely inthe presence of low gastric acidity. Both H. pyloriinfection and a high salt intake are thought tocause low gastric acidity and this may completethe link with nitrites.

The decline in both stroke mortality andgastric cancer over the last 20–30 years may beexplained by decreases in salt intake withadvances in food preservation. Refrigerationand deep freezing have reduced the use of saltas a preservative for meat, fish and vegetables.In addition, there has been much greater all yearround availability of fruit and vegetables. Thevitamin C content of these inhibits the forma-tion of nitrosamines in the stomach, and may bean important protective factor. Conversely,nitrosamine formation is promoted by thio-cyanates from cigarette smoke and smokershave been shown to have higher rates of gastriccancer. The decline in smoking may also havehad an effect on the incidence of this disease.

Meat and fishNitrogenous residues from meat digestion, aswell as other proteins, may be metabolized in thelarge bowel to produce ammonia and the amount

produced increases with meat consumption.Ammonia has been shown to induce cell prolif-eration in human colonic cells and to produceadenocarcinomas in rats. Other products frommeat ingestion that may contribute to the promo-tion of colon cancer are N-nitrosocompounds,which increase with red meat (but not whitemeat or fish) intake, and heterocyclic amines.The latter are formed during the cooking ofmeat, and are dependent on temperature, dura-tion and amount and type of fat in the meat.High-temperature cooking, for example, grilling,barbecuing and frying, also produces polycyclichydrocarbons and has been associated withhigher cancer risk. Molecular biology has identi-fied ‘fast’ and ‘slow’ acetylators among humansubjects. The conversion of heterocyclic aminesto carcinogenic products in ‘fast acetylators’appears to increase their risk of developing ade-nomatous polyps, which are considered to bepre-cancerous. Subjects who are slow acetyla-tors appear to be much less at risk.

Processed meats, including ham, sausages,bacon, have also been linked to moderatelyincreased risk of colon cancer, which has beenshown in the EPIC study to be 50 per centgreater in those subjects consuming 60 g/day ofprocessed meat than in those consuming none.Early results from the EPIC study have not,however, shown a significant increase in coloncancer with red meat intake, but some protect-ive effect was indicated from white meat andfish intakes, and further results are awaited. A number of other cancers have been linked insome studies with meat consumption. Theseinclude cancer of the breast, lung, prostate andpancreas, but in all cases the evidence for anassociation is weak. There is some evidence thatstomach cancer may be linked with consump-tion of processed meat (see ‘Salt’ section above).The great variety of ways in which people pre-serve and cook meat across the world, makesthis a particularly challenging area for study.

Other promoters of cancerA number of other dietary factors have beenlinked with the promotion of cancers (Table 15.2),although the data so far are equivocal and no firmconnections have been proved. In most cases, it is


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difficult to separate the effect of the proposed fac-tor from that of associated dietary components.

Possible protective factors

Non-starch polysaccharides (dietary fibre)Early observations, such as those of Burkitt et al. (1972), found a low incidence of diseasesof the bowel in communities that had a largeconsumption of plant foods. This was developedinto a theory about the protective effects ofdietary fibre in a number of diseases, as dis-cussed in Chapter 6. Knowledge about this frac-tion, now called ‘non-starch polysaccharides’ inthe UK, is currently much more extensive. It isbelieved that NSPs may protect against coloncancer by three possible mechanisms.■ High levels of NSP in the diet lead to increased

bulk, mainly due to an increase in colonicbacteria, and, therefore, faster transit timethrough the colon. As a result, potentiallyharmful carcinogenic substances are presentin a more dilute form and are in contact withthe colonic mucosa for a shorter time.

■ Fermentation of soluble NSP (as well asresistant starch) in the colon yields a number

of short-chain fatty acids, which influenceepithelial cell function. Most notable isbutyric acid, which has been shown to be anantiproliferative and differentiating agent,able to induce apoptosis (programmed celldeath) in the large bowel epithelium.

■ As a result of the formation of the short-chainfatty acids, NSP in the diet reduces the pH ofthe bowel. This allows primary bile acids tobind to calcium, preventing them from beingconverted to mutagenic secondary bile acids.The lower pH also increases the number of aerobic bacteria, which do not produce carcinogenic products from bile acids. More ofthe bile acids are excreted, bound to compon-ents such as lignin. Studies in which subjectswere supplemented with wheat bran showed areduced mutagenicity in stool samples.Problems with interpreting studies on intakes

of ‘fibre’ and the incidence of cancer arise becauseof confusion over the definition of the fractions offibre in the diet and the lack of detailed food com-position data on this. Controversy over whichfractions of fibre intake are more important inprevention of colon cancer continues, with somestudies supporting a role for fruit and vegetables,

Some proposed links between dietary components and cancersTABLE 15.2Dietary component Suggested link with Mechanism/interpretation

cancer siteMoulds: aflatoxin Liver Grows on peanuts: important cause of cancer in

some countries in AfricaCaffeine Bladder, pancreas Relationship very weak, at normal levels of

consumptionMay be protective in colon cancer

Iron Colon and rectum Relates to tissue levels of iron, not dietary intakes; may represent a breakdown of iron regulatory mechanisms

High levels of maternal Testicular cancer Endocrine environment of developing fetus nutrition/adiposity affected, predisposes both to undescended

testes and cancerCalcium Colon and rectum Weak relationship; possible action through binding of

intestinal fats and thus reduces bile acid secretionVitamin D Colon and rectum May control cell growth and differentiation; weak

associationFolate Colon and rectum Inverse relationship between plasma levels and

colorectal polyps; aggravated by high alcohol intake

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and others for cereal fibre. Further difficultiesarise from the effects of a change of NSP contentin the diet on its other constituents, which mayalso be involved in cancer development.

It is also possible that a high intake of vege-tables and fruit, and perhaps cereals, indicatesan increased intake of other substances, such asantioxidants or flavonoids, which may be pro-tective, rather than just the NSP they contain.The EPIC study has reported a 40 per cent lowerincidence of colon cancer in subjects eating ahigh-fibre diet (32.5 g), compared with thoseeating only 12 g of fibre.

In the case of breast cancer, women consum-ing ‘high-fibre’ diets have been found to excretemore inactivated conjugated oestrogen in the fae-ces, with resultant lower plasma levels. However,evidence that high-fibre diets are protectiveagainst breast cancer is weak. Recent evidencesuggests that soya products may offer some pro-tection against breast and prostate cancer becauseof the presence of phyto-oestrogens. These arebelieved to increase the synthesis of oestrogen-binding proteins, and thereby reduce the levels ofthese hormones in both men and women. Relatedcompounds called lignans may be found in wholecereals, seeds and fruit, and may in part accountfor some of the findings attributed to ‘dietaryfibre’ in protection against breast cancer.

Fruit and vegetablesOne of the most consistent findings in all of theliterature on diet and cancer is that incidence islower where fruit and vegetable intakes are high.Conversely, there is no recorded increased risk ofany cancer associated with fruit and vegetableconsumption. The initial understanding of themechanisms involved was that the antioxidantnutrients present in fruit and vegetables wereresponsible for the protective effect. The sug-gested mechanism links the antioxidant nutrientsto the prevention of oxidative damage to theDNA by free radicals, and hence the initiation ofdamage. These nutrients also protect lipids incellular membranes and may contribute to thestabilization of cells (see Chapter 14). Fruit and vegetables are also a source of NSPs andmany other nutrients, which may play a rolethrough different mechanisms. In addition, fruit

and vegetables contain a wide variety of otherchemically active substances that may play animportant role in the overall effect, and researchin this area is still relatively new (see Chapter 17).A problem associated with studies of fruit andvegetables is the inconsistency of definition ofterms used. For example, potatoes or pulses mayor may not be included in the vegetables group.Tomatoes may be included as either fruit or veg-etables and in some studies, fruit and vegetablesare subdivided into smaller groups by colour. Inreviews of evidence, therefore, the whole groupof fruit and/or vegetables may be considered ingeneral.

There is moderately strong evidence thatcolorectal and stomach cancers are fewer inincidence in communities where there is a highlevel of intake of fruit and vegetables (above500 g/day). These findings have been confirmedby early data from the EPIC study. There is alsosome evidence for a protective effect againstbreast, lung and oesophageal cancers. Finally,although there are too few data at present todraw any firm conclusions, there is also a prob-able protective effect against prostate, cervical,pancreatic and bladder cancers.

Antioxidant nutrientsFruit and vegetables provide the three moststudied antioxidants, namely vitamin A (andcarotenoids), C and E. Proposed mechanisms ofaction for a protective effect have been explored,but no firm conclusions have been possible.

Retinoids (vitamin A family) regulate epithe-lial cell differentiation and could, therefore,influence tumour growth in tissues. Carotenoidsare powerful quenchers of singlet oxygen and,therefore, act as antioxidants to minimize dam-age. It has also been postulated that the role ofcarotenoids may be mediated through potentia-tion of immune system activity.

Initial epidemiological studies had suggestedthat vitamin A (as retinol) was protective againstlung cancer. More recent data have shown a consistent inverse relationship between the inci-dence of lung cancer and intakes of variouscarotenoids (precursors of vitamin A) as well ashigh plasma levels of beta-carotene. Nevertheless,results of supplementation trials have not been


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encouraging. Supplementation of 30000 Finnishmale smokers with either beta-carotene and/orvitamin E or placebo resulted in an increasedmortality from lung cancer and coronary diseasein the carotene group (Alpha-tocopherol, Beta-carotene Cancer Prevention Study Group, 1994).Similar results have occurred in at least two othertrials. Studies on lung cancer are often difficult tointerpret because of the strong confounding effectof smoking. However, excessive amounts of any single antioxidant are undesirable, since animbalance can promote some pro-oxidant activ-ity. Supplementation with beta-carotene has alsobeen associated with an increased risk of coloncancer in two studies.

The Nurses Health Study in the USA found a20 per cent rise in breast cancer rates betweenthe highest and lowest intakes of vitamin A andcarotenoids. Among women with the lowestdietary intake of vitamin A, the use of a supple-ment reduced the risk of breast cancer. Resultsfor stomach and prostate cancers, however, donot show a consistent trend.

Vitamin C may also be an important pro-tective factor against cancers of the oesophagus,stomach and pancreas. This role may be linked toits antioxidant properties, especially in associationwith vitamin E. It also has a protective role for themixed function oxidase systems in the liver, whichare important for destroying foreign and harmfulsubstances. The most researched function of vita-min C is its role in inhibiting nitrosamine forma-tion in the stomach, thereby reducing the risks ofstomach cancer. Levels of vitamin C in the stom-ach are reduced by H. pylori infection, whichresults in a loss of gastric acid secretion and con-sequent increase in stomach pH. This situationfavours bacterial colonization and increased for-mation of nitrites and nitroso-compounds.

Results of studies into the relationshipbetween vitamin E and cancers at various sites are inconclusive, with better results obtained insmokers than non-smokers. Results are compli-cated by the interaction of vitamin E with sele-nium status and plasma cholesterol levels. Asupplementation study with various combinationsof nutrients in a poorly nourished population inLinxian, China, achieved a significant reductionin mortality from stomach cancer in those

subjects receiving vitamin E, beta-carotene andselenium (Blot et al., 1993). It is likely that ini-tial intakes were low, thus contributing to thepositive finding.

Most of the findings described above relate tofruit and vegetable intakes as part of the wholediet. It is perhaps unsurprising, therefore, thatattempts to replicate the results with single con-stituents of these foods have been unsuccessful.What is more concerning is that unexpectedadverse effects have occurred. This emphasizesonce again the need for a balance of nutrients inthe diet, to provide appropriate amounts for theirmetabolic role at cellular level.

Other chemically active constituentsA number of phenolic compounds are found infruit and vegetables. These include flavonoids,such as quercetin and catechins, which act asantioxidants and may have roles in gene block-ing or suppression. However, no convincingevidence exists at present of a protective role in cancer. Phyto-oestrogens are also a class ofphenolic compounds, the most important exam-ples are isoflavones, found in soya, and lignans,which occur in linseed, lentils, asparagus, broc-coli and leeks. These compounds can act asoestrogen agonists (promote or mimic theaction) and antagonists (oppose the action),depending on the receptors to which they bind.It is this potential to prevent a normal oestrogenresponse that may offer protection against hormone-dependent tumours, such as breast andprostate. However, the evidence base to supportthis proposal is weak at present.

Members of the brassica vegetable family(cabbage, broccoli, cauliflower, Brussels sprouts)are particularly rich in glucosinolates, whichhave been shown to have blocking and sup-pressing properties in the development of cancers.However, large amounts may also be potentiallytoxic, so a cautious approach and more researchare needed. Garlic, onions and leeks, all ofwhich belong to the Allium family, also havepotential blocking and suppressing properties,which have been demonstrated in rats to suppress the formation of gastric cancer.Epidemiological studies suggest a possible pro-tective role in humans.

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Further research is needed, however, todemonstrate if the positive effects of fruit andvegetables in the prevention of cancer may beattributed to any of these constituents.

CalciumIn recent years, a number of studies have indi-cated an inverse relationship between the intakeof calcium, particularly in the form of dairy prod-ucts, and colon cancer. It is suggested that cal-cium binds fatty acids and bile acids in the colon,preventing them from causing damage to themucosa. It is possible that calcium itself has anantiproliferative action on the colonic cells, thuspreventing tumour formation. In addition, a rolefor vitamin D in prevention of colon cancer hasalso been proposed, linked to its function in con-trol of cell proliferation. Milk may produce bene-fits in other ways. Whey proteins are rich incysteine, which is a precursor of the antioxidantglutathione. In addition, milk contains lactoferrin,which can bind iron in the digestive tract, makingit less available to act as a pro-oxidant.

Supplementation studies have again producedequivocal results, once more indicating thatattention to foods rather than individual nutrientsmay be the key to prevention. Figure 15.1 sum-marizes possible promoting and preventive effectsof nutrients.

Prevention of cancer

In the UK, healthy eating policy is embodied in the ‘Eight Guidelines for a Healthy Diet’, theDepartment of Health Dietary Reference Values(DoH, 1991) and the Balance of Good Health. Allof these give advice about a diet that aims toreduce the intake of foods containing fats andsugars and to increase the intakes of starchy carbohydrates, fruit and vegetables. Ensuring amoderate intake of sources of protein, from meat,fish, dairy products and their alternatives forvegetarians, will also provide other minerals and vitamins. Maintaining a normal body weightthrough adequate, but not excessive energyintakes and exercise is also important.

Figure 15.1 Possible promoting and protective factors in the diet in relation to cancer development.

Summary of diet and health recommendations (WCRF, 1997)TABLE 15.3Factor Public health goal Advice to individualsFood supply and eating Populations to consume nutritionally adequate and Choose predominantly plant-based diets rich in a variety of

varied diets based primarily on foods of plant origin vegetables and fruits, pulses and minimally processed starchy staple foods

Maintaining body weight Population average BMI throughout adult life to be Avoid being underweight or overweight, and limit weightwithin the range 21–23, in order that individual BMI gain during adulthood to less than 5 kgbe maintained between 18.5 and 25

Maintaining physical activity Populations to maintain throughout life, an active If occupational activity is low or moderate, take an hour’s lifestyle, equivalent to a PAL of at least 1.75, with brisk walk or similar exercise daily and also exercise opportunities for vigorous physical activity vigorously for a total of at least 1 hour each week

Vegetables and fruit Promote year-round consumption of a variety of Eat 400–800 g or five or more portions a day of a variety of vegetables and fruit, providing 7% or more vegetables and fruit, all year roundof total energy

Other plant foods A variety of starch or protein-rich foods of plant origin, Eat 600–800 g or more than seven portions of a variety of preferably minimally processed, to provide 45–60% cereals, pulses, roots, tubers and plantains. Prefer minimally total energy. Refined sugar to provide less than processed foods. Limit consumption of refined sugar10% total energy

Alcoholic drinks Consumption of alcohol is not recommended and Alcohol consumption is not recommended. If consumed, excessive consumption is to be discouraged. For those limit drinks to less than two drinks per day for men and who drink alcohol, restrict it to less than 5% total one per day for womenenergy for men and 2.5% for women

Meat If eaten at all, red meat to provide less than 10% If eaten at all, limit intake of red meat to less than 80 g total energy daily. Choose fish, poultry or meat from non-domesticated

animals in place of red meatTotal fats and oils Total fats and oils to provide 15% to no more than 30% Limit consumption of fatty foods, particularly those of

total energy animal origin. Choose modest amounts of appropriate vegetable oils

Salt and salting Salt from all sources should amount to less than Limit consumption of salted foods and use of cooking and 6 g/day for adults table salt. Use herbs and spices to season foods

BMI, body mass index; PAL, physical activity level.

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In 1998, the Department of Health Report onNutritional Aspects of the Development of Cancerpublished a number of specific recommendationsin this area. In essence, they do not differ from thebroader guidelines on healthy eating.

They are:■ to maintain a healthy body weight within

the body mass index (BMI) range 20–25 andnot to increase it during adult life;

■ to increase intakes of a wide variety of fruitand vegetables;

■ to increase intakes of non-starch polysac-charides (dietary fibre) from a variety offood sources;

■ for adults, individuals’ consumption of redand processed meat should not rise; higherconsumers should consider a reduction and,as a consequence of this the populationaverage will fall.These recommendations should be followed

in the context of the Committee on MedicalAspects of Food Policy (COMA)’s wider recom-mendations for a balanced diet rich in cereals,fruits and vegetables. In addition, it was recom-mended that:■ beta-carotene supplements as a means of

avoiding cancer should not be used;■ caution should be exercised in the use of

high doses of purified supplements of othermicronutrients, as they cannot be assumedto be without risk.The World Cancer Research Fund has identi-

fied the ‘five-star’ foods for cancer prevention:■ foods rich in beta-carotene – spinach, car-

rots, broccoli and tomatoes;■ foods rich in vitamin C – citrus fruits,

berries, melons, green vegetables, tomatoes,cauliflowers and green peppers;

■ foods rich in selenium – bran, wheat germ,tuna fish, onion, garlic and mushrooms;

■ foods rich in vitamin E – wholegrain cereals,wheat germ, soya beans and leafy greens;

■ foods rich in complex carbohydrates –bread, cereals, beans and peas.

These foods should be eaten in place of fattieritems and can help to reduce overweight. Theymay also contain other important substancesthat may help the body’s resistance to cancer.

The World Cancer Research Fund Report,published in 1997, took a global perspective onthe prevention of cancer and made recommen-dations that were also consistent with the pre-vention of other diseases. They contain policygoals and advice for individuals. It was, how-ever, intended by the report that the relativeimportance of the different recommendationswould vary in different parts of the world, for their populations. They are summarized inTable 15.3.

In addition to the recommendations detailedabove, the WCRF also identified safe storage,preservation and preparation of foods as well asthe presence of additives and residues as impor-tant areas for public health policy. Recom-mendations were also made against the use ofdietary supplements and tobacco use. Overall,the recommendations shown in Table 15.3 gofurther than those of the UK in recommending amove to a more plant-based diet. Many of thesechanges would be difficult to implement for themajority of people in the UK. However, selectinga diet from the Balance of Good Health in theproportions recommended will provide a goodbalance of the nutrients needed. What is alsoneeded is the motivation and the desire to be healthy! Although much research is stillrequired to further elucidate the role of dietaryfactors in certain cancers, we already have suf-ficient information to make recommendationsthat can significantly reduce the risk.

1 Diet may play a major role in the development of cancer.2 Particular aspects of the diet that may be involved as promoters and protective factors have been identified.3 Dietary guidelines for the prevention of cancer have been proposed. These include a high intake of fruit

and vegetables and avoidance of excess intakes of fat and energy. Protein intake, especially from meatsources, should also be moderated. Lifestyle changes, including regular physical activity are needed tosupport the dietary adjustments.

SUMMARY


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1 Why is it difficult to study the relationshipbetween nutrition and cancer?

2 a In what ways have dietary fats been linkedwith the development of cancers?

b Why is it difficult to distinguish the effects offats from those of total energy intake incancer causation?

3 List the reasons why an increase in non-starchpolysaccharides (dietary fibre) intake mightprotect against some cancers.

4 How does the advice on diet for cancerprevention compare with general healthy eatingguidelines?

5 a In what ways might the antioxidant nutrientsbe useful in the prevention of cancers?

b Does the scientific evidence currentlysupport this theory?

STUDY QUESTIONS


Alpha-tocopherol, Beta-carotene Cancer Prevention Study Group 1994: The effect of vitamin E andbeta-carotene on the incidence of lung cancer and other cancers in male smokers. New EnglandJournal of Medicine 330(15), 1029–35.

Bingham, S.A. 1999: High meat diets and cancer risk. Proceedings of the Nutrition Society 58,243–8.

Blot, W.J. Li, J.-Y., Taylor, P.R. et al., 1993: Nutrition intervention trials in Linxian, China: supple-mentation with specific vitamin/mineral combinations, cancer incidence and disease specificmortality in general population. Journal of the National Cancer Institute 85, 1483–92.

Burkitt, D.P., Walker, A.R.P., Painter, N.S. 1972: Effect of dietary fibre on stools and transit times andits role in the causation of disease. Lancet ii, 1408–12.

Burr, M.L. 1994: Antioxidants and cancer. Journal of Human Nutrition and Dietetics 7, 409–16.DoH (UK Department of Health) 1991: Dietary reference values for food energy and nutrients for the


DoH (UK Department of Health) 1998: Nutritional aspects of the development of cancer. Report onHealth and Social Subjects 48. London: The Stationery Office.

Frankel, S., Gunnell, D.J., Peters, T.J. et al. 1998: Childhood energy intake and adult mortality fromcancer: the Boyd Orr cohort study. British Medical Journal 316, 499–504.

Key, T. 1994: Micronutrients and cancer aetiology: the epidemiological evidence. Proceedings of theNutrition Society 53, 605–14.

National Dairy Council (NDC) 1995: Nutrition and cancer. Fact File 12. London: NDC.Riboli, E. 1991: Nutrition and cancer: background and rationale of the European prospective inves-

tigation into cancer and nutrition (EPIC). Annals of Oncology 3, 783–91.Riboli, E., Norat, T. 2001: Cancer prevention and diet: opportunities in Europe. Public Health

Nutrition 4(2B), 475–84.Willett, W.C., Hunter, D.J., Stampfer, M.J. et al. 1992: Dietary fat and fibre in relation to role in

breast cancer. Journal of the American Medical Association 268, 2037–44.Williams, C.M. 1996: Nutrition and breast cancer: facts and controversies. In Buttriss, J., Hyman, K.

(eds) Focus on women: nutrition and health. London: National Dairy Council.World Cancer Research Fund 1997: Food, nutrition and the prevention of cancer: a global

perspective. Washington, DC: World Cancer Research Fund and American Institute for CancerResearch.

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Challenges tonutritional status

The aim of this chapter is to:

❏ identify situations that provide an additional challenge to the maintenance of the nutritional status. This may beas a result of obstacles to food intake, difficulties in digestion and absorption, or altered metabolic states thataffect what the body can obtain from the food ingested.


❏ identify a number of conditions or situations that impose an additional challenge to nutritional status;❏ use the framework of nutrient ‘intake–processing–utilization’ to explain how each of the situations creates

a threat to nutrition;❏ provide some practical solutions to help people in these situations.

In considering challenges to nutrition, it is use-ful to consider the stages through which foodhas to travel to achieve its purpose of providingour bodies with the necessary nutrients. A use-ful framework is that of ‘intake–processing–utilization’, which summarizes this pathway fromfood in the marketplace or kitchen to metab-olism at the cell level. Obstacles or problems atany of the stages of this pathway will affect theultimate achievement of satisfying nutritionalrequirements. This framework will be used inthe following discussions.

Adverse reactions to food

Since the 1980s there has been a considerablegrowth of public interest in adverse reactions tofood, all of which are often (mistakenly) groupedtogether as ‘food allergy’. The extent of theseproblems is difficult to ascertain precisely, as levels of self-reporting are invariably greaterthan can be confirmed by rigorous testing.

It is useful to start with some definitions ofterms that are consistent with current practice inthe UK. It should be noted, however, that there

are variations in these classifications withinEurope and the USA.

Adverse reactions to food may be of threetypes:■ food poisoning – includes reactions resulting

from contaminants within the food;■ food aversion – includes psychological reac-

tions, which may not be reproduced oncovert introduction of the food;

■ food intolerance – includes reproducibleadverse reactions to food.The first of these occurs as a result of triggers

from outside the individual and is believed to be the most commonly occurring of the adversereactions. The remaining two types relate toresponses that are initiated within the individualin response to the food eaten and are consideredto be less common.

Food poisoning

This occurs as a result of the consumption ofcontaminated food or water that results in dis-ease of an infectious or toxic nature. In the UKand Europe, the causative agents are most likely

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to be microorganisms. However, in other partsof the world, food poisoning may occur as aresult of chemical contamination, parasites ortoxins naturally present in the food or acquiredwithin the food. Bacterial food poisoning occur-ring in the UK includes that caused by Campylo-bacter, Salmonella spp. and Escherichia coli.Some bacteria produce toxins, which cause thesymptoms; these include Staphylococcus aureus,Bacillus cereus and Clostridium botulinum. Foodsthat may be contaminated include eggs, poultry,cold meats, rice and spices. Among the viralcauses of food poisoning, the most widespreadare highly infectious, small round structuredviruses (SRSVs), which may contaminate shell-fish, but more probably are introduced into foodfrom infected food handlers. Consumers in semi-closed communities, such as hospitals, hotels andschools are particularly vulnerable.

Contamination of food can occur, for example,from use of dirty water, sewerage overspill, andagricultural chemicals. Some plant foods maycontain toxins, for example, uncooked red kidneybeans or some fungi, or may be contaminatedwith moulds, for example, aflatoxins, which affectgroundnuts (peanuts).

Most commonly, food poisoning causes rapidvomiting and diarrhoea, although a few of theagents can cause serious damage to the liver, kidneys, nervous system and may even be fatal.The young, sick and elderly are the most vulner-able to serious consequences from bacterial foodpoisoning.

Food aversion

Many people may be able to list foods that theyavoid, generally because of a sensory preferenceor dislike. This may be taken to an extreme avoid-ance of almost all foods in the case of anorexianervosa. In some cases, an individual believesthat the food causes them unpleasant symptoms,perhaps as a result of an experience in the pastwhere the food was temporally associated withsickness or gastrointestinal upset. In this case, thefood is avoided because of an aversion to it andan associated psychological belief that the food is harmful. When tested blind, however, it is generally not possible to reproduce any alleged

symptoms, and the conclusion must be drawn thatthis is a psychosomatic adverse reaction ratherthan one that has a true physiological basis.

Aversion may also be applied to foods thatare believed to affect other aspects of health, for example, tiredness, sleep problems, palpita-tions, bloatedness and flatulence. The individualexcludes particular foods to correct these symp-toms, although double-blind testing generallyfails to find any scientific basis for this practice.To date, in most of these cases, there is no evi-dence to support a link between the food andthe symptoms.

Food intolerance

This is the only group of adverse reactions tofood for which reproducible responses can beproduced on challenge. Precise figures for preva-lence are difficult to obtain because:■ questionnaires are unreliable because of bias

from respondents;■ diagnosis is time consuming (e.g. use of

elimination diets followed by challenge);■ there are no simple reliable tests and these

also may not be particularly sensitive;■ there is an almost limitless number of food-

stuffs and additives that can provoke aresponse;

■ reactions vary between individuals and, espe-cially in children, may change over time;

■ responses may occur immediately or after aconsiderable period after ingestion; these arepoorly understood and difficult to diagnose.Although many studies have attempted to

quantify the extent of food intolerance, a lack ofconsensus over definitions and methodologieshas made it difficult to arrive at reliable resultson prevalence.

In 1994, a study in the UK found that, in a sample of over 18000 people, 20 per cent com-plained of food intolerance, commonly citingeight different foods (Young et al., 1994). Whentested with a controlled challenge, food intoler-ance was confirmed in only 1.4–1.8 per cent of the total. This is in line with the generallyaccepted figure of 1–2 per cent of the adult popu-lation exhibiting food intolerance, with a higherprevalence in children of perhaps 5–8 per cent.

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Food intolerance may be further subdividedinto:■ allergic reactions – immunoglobulin E (IgE)-

mediated and non-IgE-mediated;■ pharmacological reactions;■ enzyme reactions.

The clinical presentation of food intolerancemay be immediate or delayed onset, and is likelyto affect the following tissues and systems (seeFigure 16.1 for a summary).■ Gastrointestinal system. Symptoms include

mouth tingling or swelling, abdominal pain,bloating of the abdomen, vomiting and diar-rhoea or constipation. In chronic intolerance,there can be bleeding or loss of plasma pro-tein into the gut lumen, with damage to thegut mucosa.

■ Skin. Dermatitis, urticaria, angio-oedema andeczema are common consequences.

■ Respiratory system. Rhinitis, laryngeal oedemaand asthma (including wheezing, breathless-ness) may occur.

■ Central nervous system. Symptoms includemigraine and possibly some behaviouralabnormalities (including hyperactivity anddepression), although the evidence for theseis controversial.Food allergy is a form of specific food intoler-

ance that causes reproducible symptoms andincludes an abnormal reaction by the immunesystem. Our diet contains a variety of substances

that can stimulate immune responses. They areusually proteins or simple chemicals bound toproteins and are termed allergens. Usually theseallergens are prevented from being absorbed bysecretory immunoglobulin A (IgA) lining the gut.However, IgA is absent in the first months of life,so that allergens can be absorbed. Breast milkcontains IgA, and may offer some protection.Avoidance of contact with potential allergens isimportant at this age, especially where there is a family history of allergy, although completeprotection is unlikely. However, in general ourimmune system has evolved responses that allowit to be tolerant to the antigen burden repre-sented by ingested food. This is known as oraltolerance. In some cases, these allergens inducean immune response, usually producing anti-bodies, which can be detected in the serum, butwhich are not pathogenic – known as immuno-logical acceptance.

In a minority of individuals, however, thisresponse is abnormal and results in pathologicalchanges when the allergen is ingested, resultingin a food allergy. The immune system respondsinappropriately against the allergen to stimulateIgE antibodies sensitized to the particular aller-gen. These are mainly attached to mast cells and on stimulation cause immediate degranula-tion of the mast cells and the release of a rangeof chemical mediators. These include histamineand prostaglandins, which have potent effects.

Figure 16.1 Symptoms of foodintolerance.


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The consequent reaction depends on the size ofthe dose, the speed of absorption and the distri-bution of the allergen in the body.

The response to the release of histamine andprostaglandins generally includes some or all ofthe following:■ dilation of small blood vessels (redness);■ increased permeability of blood vessels

(swelling/oedema);■ contraction of smooth muscle in the airways

(breathing difficulties) or intestines (causingabdominal pain); and

■ stimulation of nerve endings in the skin(itching and pain).

Reactions may be seen in the following:■ the mouth, immediately following ingestion;■ the gastrointestinal tract, when the allergen

reaches this area;■ one of many other sites, including the skin

and respiratory system, including the noseand airways;

■ several other sites, causing a widespread and possibly life-threatening reaction (seeFigure 16.2).The severity of the reaction varies between

individuals and may range from mild to lifethreatening (anaphylactic shock), resulting froma severe fall of blood pressure and possibly

Figure 16.2 IgE-mediated food allergy.


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difficulties in breathing. Immediate help in theform of an adrenaline injection is required foranyone suffering from such a major allergic reac-tion. Fortunately, most are not so extreme andrecovery follows, resulting from the body’s ownhomeostatic mechanisms, which cause endoge-nous adrenaline release.

Why do individuals develop food allergy?Genetic predisposition is an important deter-minant of susceptibility to allergic disease, alsocalled atopy. The susceptibility is more likely tobe inherited from the mother than the father but,with two atopic parents, the likelihood is greatlyincreased. However, although the susceptibilityis inherited, the actual allergens to which a childis sensitive are not necessarily the same as its parents. Babies that are born small for gestationalage are more at risk of developing allergies in their first year. This suggests that growth fal-tering in the womb may play a role in poorerimmunocompetence.

Studies suggest that the risk of atopy in achild can be reduced by avoidance of potentialallergens in the mother’s diet from very earlypregnancy. In addition, breastfeeding for morethan 4 months can reduce the development ofatopic disease. Delaying the introduction ofsolids until after 4 months is also recommended,as well as the use of low allergen foods, such asbaby rice, potatoes, fruit and vegetables.

There has been a general increase in the inci-dence of food and other allergies over the last 30 years. An explanation that is gaining accept-ance is that modern children are exposed tofewer infectious diseases and live in a generallyclean environment. This does not challenge theimmune system, which is less well developed asa result, and reacts inappropriately when pre-sented with harmless antigens, resulting in anallergic reaction.

A further explanation offered for the risingincidence of allergy is the change in balancebetween n-6 and n-3 fatty acids in our diets. Then-6 fatty acids are more predominant and fewern-3 acids are consumed. The former are associ-ated with more pro-inflammatory eicosanoids,including prostaglandins, which have an import-ant role in allergic responses.

Foods associated with allergic reactionsAlmost any food can produce an allergic reac-tion but some are much more likely to causeproblems than others.

In children, the most common causes of foodallergy are cows’ milk, eggs, peanuts, fish, wheat,tree nuts, soya beans, soya products, vegetablesor fruits. Milk allergy has been reported in 2–3 per cent of infants in Western countries,although in the majority (about 80 per cent), theallergy disappears by the age of 3 years. This isnot surprising, as milk forms the basis of theinfant’s diet and cows’ milk protein is often thefirst foreign protein to be introduced. Childrenwith persistent milk allergy may develop hyper-sensitivities to other foods, especially egg, soya,peanuts, citrus, fish, tomato and cereals, as theseare introduced into their diet. It is estimated thatthe prevalence of true food allergy in young chil-dren is about 1.4 per cent (range 0.5–3.8 per centin the literature). Although children may growout of some allergies, those to peanuts, tree nuts,fish and shellfish may persist into adult life.

Apart from the foods listed above for children,adults may experience cross-reactions betweensimilar proteins in different foods. For example,tree and grass pollens can provoke reactions tofruits and vegetables. Clusters of hypersensitivi-ties to members of the same botanical family canoccur. Reports exist of allergy to apple and pear,kiwi fruit and avocado, potato and carrot, celery,cucumber, carrot and watermelon. These rarelycause anaphylactic reactions, although some havebeen reported.

Of great concern is the growing prevalence ofpeanut and tree nut allergy, both of which areassociated with severe life-threatening reactionsmore commonly than the more traditional foodsassociated with allergies. In some individuals,sensitivity to peanuts is so great that as little as100 �g of peanut protein can provoke symptoms.At present, the exact prevalence is unknown, buta prevalence of 0.5 per cent among UK children in1996 was reported. The UK Department of Health(1997) has recommended that pregnant womenwith any history of atopy in the family shouldavoid eating peanuts during pregnancy.

The increased prevalence is reportedly linkedto the increased exposure of young children to


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peanut proteins in peanut butter, cereals, con-fectionery and baked goods. Cold pressed peanutoil used in cooking may contain peanut protein.Many children appear to have become sensitizedat a very young age, possibly from peanut oils ininfant foods. There have been reported deathsfrom peanut allergy, resulting from rapid anaphyl-axis affecting the larynx. Avoidance of peanuts isvital, as well as other pulses (or legumes) and othernuts. The use of adrenaline syringes in emergencyis essential.

Non-IgE-mediated reactionsAdverse responses to food may not alwaysinvolve IgE, and mast cells and other parts of the immune system may be involved, such as T-lymphocytes and scavenger cells. The reactionis generally delayed and may take several hoursor even days to develop. In addition, the reactionsto trigger foods may involve one system or sev-eral and may, therefore, imitate the reactions toIgE-mediated allergy described above. It is verydifficult to identify and confirm the relationshipbetween particular foods and an adverse reac-tion that occurs some time later and that alsomay be initiated by a number of different foodsand possibly also environmental conditions.

The best defined example in this group isgluten sensitivity, whereby the immune systemof genetically susceptible individuals reacts inappropriately to dietary gluten, causing a vari-ety of problems. In coeliac disease, the targetorgan is the gastrointestinal tract, predominantlythe region of the small intestine, in which a vari-ety of changes are seen, resulting in malabsorp-tion of nutrients. The skin may be affected, withan itchy blistering rash on the knees, thighs andelbows. There have also been reports of neuro-logical manifestations of gluten sensitivity,although the evidence of this is not scientificallystrong, and these disorders may be a result ofnutritional deficiency consequent on malabsorp-tion. Diagnosis of coeliac disease has classicallybeen by small-bowel biopsy, but serological testsfor antibodies found in the circulation are nowalso used. Exclusion of gluten from the dietresolves the changes affecting both the gut andthe skin. A gluten-free diet should be maintainedfor life and lists of permitted foods are provided

by the UK Coeliac Society. It is estimated that theprevalence of gluten sensitivity is 1 in 300 inEurope, with a 10 per cent risk of the condition infirst-degree relatives of those already diagnosed.Although often identified in young children, thecondition may be ‘silent’ and not diagnosed untiladulthood. In this case, there may already be a number of existing nutritional deficiencies,such as folate or iron deficiency leading toanaemia, or inadequate calcium absorptionresulting in poor bone development.

Other conditions for which a non-IgE-mediated allergic response has been investigated,but not confirmed include:■ urticaria and dermatitis;■ infantile colic;■ irritable bowel syndrome;■ asthma;■ migraine;■ hyperactivity and attention deficit hyper-

activity disorder (ADHD);■ rheumatoid arthritis.In all of the above, where there is an apparentlystrong history of food intolerance in the individ-ual, it is important to test thoroughly with appro-priate scientific techniques, if specific foods arecausing the symptoms of illness. It is likely that,in some of these conditions, food is one of a num-ber of triggers for the symptoms, which makes thediagnosis very difficult. Once identified, if a foodhas to be eliminated, this should be done withqualified professional advice to ensure the main-tenance of adequate nutritional intake.

Pharmacological reactionsSome foods contain pharmacologically activeagents or may cause the production of suchagents in the body. Usually these are harmlessunless ingested in relatively large amounts. Evenwhen released in the body, the amounts neededare much larger than those involved in the IgE-mediated allergic reaction discussed earlier.For example, foods such as cheese (Roquefort,Parmesan, mature Cheddar), wine (and other fer-mented products), bananas, yeast extract, avo-cados, chocolate, oranges and some fish products(e.g. pickled fish) contain biogenic amines, suchas histamine, tyramine, phenylethylamine andoctopamine. Other foods may directly cause the


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release of histamine from mast cells; this hasbeen shown to occur with chocolate, tomatoesand strawberries. Caffeine is another agent thatcan produce this type of intolerance, resultingin tachycardia (increased heart rate), irritability,sleep disturbances and intestinal colic. The doseat which this occurs may be as little as two cupsof coffee or three cups of tea. Prunes containhydroxyphenylisatin, which is a stimulant ofintestinal motor activity and can produce rapidtransit through the gut. Sodium nitrite presentin preserved meats can cause intolerance symp-toms, including flushing, headaches, urticariaand abdominal symptoms.

Food additivesMany people believe themselves to be sensitiveto food additives. Mentioned most often in thiscontext are■ colouring agents, such as tartrazine;■ preservatives, such as benzoic acid and

benzoates;■ antioxidants, such as butylated hydroxy-

toluene (BHT) and butylated hydroxyanisole(BHA).

The diagnosis of these reactions is very difficult,as no immunological effect is involved. More-over, additives are rarely consumed singly, soindividual reactions are difficult to identify. How-ever, concern has been expressed that, for theirsize, children who eat a large amount of pro-cessed foods containing additives may be con-suming an unacceptably high level of additive‘cocktail’, which could have adverse effects. Often,where apparent sensitivity exists to food addi-tives in children, it accompanies other allergicconditions, such as eczema, and may exacerbatetheir symptoms.

Sulphite used in preservation of wine, otheracidic drinks or fruit and vegetables may liber-ate sulphur dioxide, which may aggravate asth-matic reactions. Some people believe they aresensitive to monosodium glutamate, which isused as a flavour enhancer in many foods and is present in large amounts in some Chinesedishes. Responses described include tachycardia,flushing and wheezing, but blind trials have failedto show a consistent link with a specific array ofsymptoms.

Food safety requires that some additives areused in food preservation but it is important thattheir safety for humans is reviewed regularly, and their use controlled. Without additives, foodswould be hazardous, owing to bacterial contamin-ants and deterioration, and food-transmittedinfections actually already cause more reactionsin people than any effects of food additives.

Enzyme defectsThe most common of these is the inability todigest lactose in milk, generally due to the disap-pearance of lactase after infancy (this is discussedin Chapter 6). Congenital lactase deficiency, whenactive lactase is absent from birth, is rare. Otherdisaccharidase enzyme activities in the gut maybe compromised, for example, by some drug therapies and in chronic or binge alcohol con-sumption. In all of these cases, symptoms of intolerance occur when sugars are consumed.These result from the bacterial fermentation oflactose (or more rarely other sugars) in thecolon and the resulting osmotic effects, causingbloating and diarrhoea.

Other enzyme defects that occur may beinborn and have systemic effects when metabolicpathways cannot be completed. Examples includealcohol dehydrogenase deficiency, which affectsmetabolism of alcohol, or fructose intolerancewhere fructose metabolism is incomplete andresults in hypoglycaemia. In addition, there are a number of inherited disorders of amino-acidmetabolism that require lifelong dietary modifi-cation to prevent serious consequences.

Diagnosis

To obtain a reliable diagnosis, strict criteria mustbe adhered to. An adverse reaction to a food canonly be confirmed if the symptoms disappearwhen the food is removed from the diet and reappear when it is re-introduced. Great care mustbe taken if there is any risk of anaphylaxis, andpatients who believe they are at risk may refuseto undergo testing. Because of the risk of a severereaction on re-introduction, this should be car-ried out under supervision. A careful history ofdiet and symptoms needs to be taken to identifypossible triggers. The testing procedure should be

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performed by a double-blind technique, so thatneither the clinician nor the subject knows whenthe suspect food is introduced, within a range offood testing. If several foods are involved and ifthe reaction is delayed, the procedure may takemany weeks to complete. Where there is a sus-pected allergy, skin prick tests or assay of IgElevels – radioallergosorbent test (RAST) method –may be used as laboratory tests. Even with these,failure to obtain a positive result may not neces-sarily indicate the absence of hypersensitivity.Intestinal biopsy or intestinal permeability mayalso be measured in the clinical setting, if this isconsidered appropriate (see Figure 16.3).

A large number of other tests are availabledirectly to the public. Most of these have not beenscientifically validated and, therefore, are notconsidered to be of value in the diagnosis of foodallergy. They are potentially dangerous as theyare likely to result in misdiagnosis of food allergyand potential harm from restricted diets. Evenwithout testing, individuals may be tempted touse self-diagnosis and elimination of foods fromthe diet. This can readily result in omission of keyfoods and nutrients, which can produce deficien-cies and is particularly hazardous in children.Dietary manipulation should only be undertakenunder the supervision of a dietitian.

Nutrition and the immunesystem

There are close links between the nutritional status of the individual and the effectiveness of

the immune system in providing an appropriateresponse in the event of challenge. It has beenrecognized for many centuries that infectious dis-ease was more common in undernourished popu-lations and that famines were associated withepidemics. The understanding of the two-wayrelationship between nutrition and immunity is now much greater as new challenges haveemerged that demonstrate their interdependence(see Figure 16.4). The inappropriate response tofood components that leads to adverse reactionshas been discussed above. The appearance ofhuman immunodeficiency virus (HIV) infectionsand the acquired immunodeficiency syndrome(AIDS) has provided a further example of howimmune status and nutrition are related. Othernutritional challenges have an impact on immunefunction, for example, in chronic disease, in thevery young and the elderly.

A brief outline of the role of nutrition inimmunity is given here.

Effect of infection on nutritional status

The presence of infection has a potential impact on nutritional state. This can be as aconsequence of:■ loss of appetite and poor dietary intake;■ failure to digest or absorb nutrients, either

through loss by vomiting or diarrhoea, or lossof digesting/absorbing ability through lack ofenzymes, damage to the mucosa of the gut orintestinal hurry caused by infestation withparasites;

Figure 16.3 Diagnosis of food intolerance.


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■ increased requirements owing to raised meta-bolic rate consequent on fever, increased util-ization of certain nutrients, such as aminoacids and antioxidants, or a redistribution ofnutrients between different body compart-ments as part of the immune response.

Therefore, nutritional state may decline duringan infection and compromise the body’s abilityto combat it and recover. This is one of the reasons for a higher mortality from infections in poorly nourished individuals, compared tothose with better nutritional status.

Effect of nutritional status on immunity

The most studied aspect of this relationship is thatbetween protein energy malnutrition and immunefunction. Almost all aspects of the immune sys-tem depend on adequate protein status. Thisincludes the organs of the immune system, suchas the thymus, spleen and lymph nodes, whichproduce phagocytic white blood cells. In addition,the biologically active proteins, such as immuno-globulins, acute-phase proteins and cytokines aredependent on adequate protein status. Cytokinesare a large and diverse group of proteins secretedby cells for the purpose of altering its own func-tion or that of adjacent cells; cytokines may have

multiple activities, and include tumour necrosisfactor and interleukins. It is, therefore, not sur-prising that protein deficiency makes the individ-ual vulnerable to almost all infections. Specificamino acids have also been identified as particu-larly important in sustaining an immune responseduring acute infections, and following trauma orsurgery. These are the sulphur-containing aminoacids (methionine and cysteine), arginine and glu-tamine. Some enteral feeds have been developedcontaining these amino acids for use in hospitalpatients.

The role of dietary fat in immune functionhas received considerable interest. In experimen-tal studies, a reduction of total dietary fat intake,from 40 to 30 per cent of energy, resulted inimproved immune activity in a variety of sub-jects. This has led to the suggestion that high-fatdiets may have a suppressing effect on humanimmune function. Polyunsaturated fatty acids(PUFAs) of the n-6 series, when consumed inamounts typical of the Western diet, have noclear effects on immune function. However, n-3PUFAs, such as those found in fish oils and lin-seed oil, have been reported to have a suppress-ing effect on immune responses. For this reason,there is interest in their role as potential anti-inflammatory agents for use in conditions where

Figure 16.4 The relationshipbetween infection and nutrition.

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the immune system is responding inappropriatelyto triggers and causing chronic disease states.These include rheumatoid arthritis, Crohn’s dis-ease, ulcerative colitis and psoriasis. Results oftrials to date are inconclusive and further workis still needed.

Among the micronutrients, both vitamins andminerals are important in immune function.

Vitamin A deficiency is closely linked withsusceptibility to infection, especially of the respiratory system in malnourished children. Therole of vitamin A appears to be widespread, inmaintaining the integrity of epithelial surfacesas well as in the production and function of bothcellular and humoral aspects of the immune sys-tem. Other vitamins that have been proposedand studied with regard to an immune functionrole are vitamins B6 and B12, folic acid, and vitamins C and E.

The most important mineral in relation toimmune function is zinc and subjects who aredeficient have immune impairment. Supplementa-tion with zinc of malnourished children decreasesthe risk of diarrhoea and increases the numberof T lymphocytes. In small for gestational ageinfants, a supplement of zinc (5 mg/day), givenfor 6 months increased immune function. How-ever, it should also be noted that excess intakes ofzinc (300mg/day) can impair immune function.

Iron deficiency has also been associated with impaired immune function. However, excessiron may inhibit immune function, although themechanisms are unclear. Selenium is concen-trated in tissues involved in the immune system,such as lymph nodes, spleen and liver, and vari-ous components of the immune system havebeen shown to be impaired in selenium defi-ciency. The bactericidal activity of phagocytes isimpaired. There have been reports also of bene-fits of selenium supplementation in HIV-infectedsubjects.

Overall, it is clear that adequate nutritionalstatus is needed for correct immune function.Supplementation with multi-nutrient mixturescan improve immune function in those individ-uals whose previous intakes were poor. However,there is little evidence to support enhancementof immune function by the use of supplementsin those who are adequately nourished. Indeed,

there is a possibility that for some nutrients an excess intake may result in suppression ofimmune action. More research is needed in thisarea.

Nutrition in HIV infectionand AIDS

Nutritional status is an important considerationin patients with HIV infection, and improve-ments or maintenance of nutritional adequacymay have important implications for survival. A major advance in the management of patientswith HIV infection has been the development of highly active antiretroviral drugs, which havebeen able to significantly improve the prognosis.Many patients with HIV, however, have no accessto these drugs and, for this group, attention tonutrition can make a difference. Malnutritioncan affect the length of survival by:■ reducing immune responsiveness;■ causing organ damage;■ reducing the effectiveness of therapies;■ contributing to progressive debility.

Body weight

One of the most readily available markers ofnutritional status is body weight. Weight loss isreported as a major clinical sign in HIV infection,and has for some time been considered inevitableand irreversible. There is now a better under-standing of the variations in weight as more of the components of the weight change havebeen studied. Survival appears to be increased inpatients with a higher body mass index (BMI; inthe range 25–30), although deliberate overeatingand development of obesity is not encouraged.The composition of this body weight is probablyalso important, with a higher lean body massbeing more advantageous than increased fatstores. An exercise programme may help to boostthe amount of lean tissue.

Weight loss can occur at all stages of the HIVinfection and is not constant, but rather occursintermittently, suggesting that it is not simplycaused by the underlying HIV infection. The initial loss is of fat but, in later stages, may be predominantly of lean body mass. There can


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be periods of weight stability and significantweight gain is also possible.

Several factors are thought to be responsiblefor weight loss in HIV infection:■ increased resting energy expenditure, owing

to the ‘hypermetabolism of the disease’;■ concurrent infections;■ reduced food intake – this may arise for a

number of reasons, including difficulties ofobtaining and/or eating food, and loss ofappetite;

■ malabsorption.

Increased metabolismAlthough the metabolism may be increased, by approximately 10 per cent in patients withHIV infection, and perhaps up to 30 per cent during periods of opportunistic infections, it isnow thought not to be the main cause of weightloss. Careful studies have demonstrated that theincrease in resting energy expenditure is morethan outweighed by the reduction in physicalactivity. In addition, and especially during periodsof infection, there is a marked reduction in foodintake that contributes to the negative energy bal-ance and weight loss. To maintain body weight,the periods of reduced food intake need to becompensated by increases following recoveryfrom infection. It is proposed that these periodswould be an ideal time for aggressive nutritionalsupport to help re-establish body weight. This canbe by enteral or even parenteral feeding, if neces-sary and appropriate. It is also important thatother nutrients are provided at this time and thatthe aim is not simply to gain weight.

Patients with HIV infections appear to loseprotein during weight-loss episodes. Usually,when food intake is low, the physiologicalresponse after the first 3 days is for protein to bespared and for fat stores to be predominantlyused for energy. In HIV infection, however, theresponse is similar to that seen in trauma orphysiological stress, with the breakdown of bodyprotein and negative nitrogen balance. Reversingthis loss should aim at optimizing the anabolicprocesses, perhaps by the use of hormones, aswell as the use of appetite stimulation. Resistanceexercise can help increase lean body mass inthese cases.

Patients with HIV infection have also beenfound to have abnormal lipid metabolism, withraised plasma triglycerides, which becomes moreelevated as HIV progresses to symptomatic AIDS.Conversely, cholesterol and phospholipid levelsare lower in HIV-infected subjects. Treatmentwith antiretroviral drugs has also been found tolead to a metabolic syndrome, termed lipodystro-phy, with abnormal lipid levels, reduced glucosetolerance and insulin sensitivity. In addition, thereis a redistribution of body fat, with a loss of sub-cutaneous fat, including the legs, arms and face,and increased abdominal adiposity and depos-ition of fat across the back (buffalo hump) and onthe breasts. The development of this condition inpatients treated successfully for HIV infection isa paradox, and raised future health problems,which are similar to those seen in obese individ-uals, who are at risk of coronary heart disease,diabetes and pancreatitis. The causes of this meta-bolic syndrome are unexplained but may be dueto a delay in clearance of lipids from the circula-tion, with resulting consequences of raised circu-lating lipids. Low-fat diets, exercise and drugs toreduce plasma lipids may be a way forward.

Concurrent infectionOpportunistic infections and cancer are causesof major, rapid weight loss in patients withAIDS. Treatment of the infection can reverse theweight loss. The management of these hasbecome better as knowledge has increased.

Reduced food intakeThis may arise for a number of reasons, including:■ a loss of desire to eat due to anxiety or

depression;■ a deliberate desire to lose weight;■ an inability to obtain food or afford to buy

food;■ problems with eating, owing to painful mouth

or throat infections, or side-effects of drugtherapy;

■ the consequences of eating, with nausea,gastric pains, and diarrhoea.

MalabsorptionAbnormal function of the gastrointestinal tractis a fairly common aspect of AIDS, although itmay only affect nutritional status in later stages

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of the disease. Common features include fat mal-absorption together with episodes of diarrhoea,which may be linked to malabsorption of bilesalts. Where malabsorption is an important fea-ture, there is chronic progressive weight loss.Pathogens may be present in the gut, dependingon the degree of immunosuppression of thepatient. They may interfere with all aspects of gutfunctioning, including chewing and swallowing,cause gastric pain and consequent reluctance toeat, reduce absorption, cause nausea and vomit-ing, general malaise and anorexia.

As with any condition where the body is facedwith a reduced food intake and increased needs,maintaining good nutrition whenever possible isimportant. Food provides not only nutritionalsupport, but also psychological support and socialactivity, and this should be recognized in anynutrition therapy.

Studies have shown that low plasma vitaminA levels are associated with accelerated pro-gression of HIV and increased risk of mortality.Vitamin A supplementation has significantlyreduced mortality and morbidity in HIV-infectedchildren. Other studies have shown that low serumvitamin B12, vitamin E, selenium and zinc levelsare associated with increased risk of progressionto AIDS. Multivitamin supplementation of preg-nant women, improves the survival chances oftheir babies with fewer low birthweight and pre-term deliveries.

Although as a general principle an optimaldiet may well prolong a person’s survival, it ispossible for someone in this vulnerable state tofall prey to nutritional misinformation, and per-haps end up consuming a very unbalanced diet.Many supposedly beneficial diets have been pro-posed, including supplementation with very largedoses of vitamin C, use of ‘live’ yogurt, macro-biotic diets or herbal supplements. At present,there is no evidence that any one feature of thesediets will be especially beneficial in HIV infection.However, a patient’s desire to help themselvesthrough the diet is important to respect and mayencourage them to take an interest in other aspectsof their food intake. It is important that adequatelevels of all nutrients are provided and not com-promised. The development of antiretroviral drugshas brought a new approach to the management

of patients with HIV infection, with better sur-vival, but with new complications resulting frommetabolic disturbances that increase risks of otherdiseases.

Drug–nutrient interactions

Drugs used in medical treatment may affectnutritional status by influencing food intake ormetabolism; similarly, their action and effective-ness may be altered by a person’s pre-existingnutritional state.

These interactions between drugs and nutri-ents have been a focus of interest only in the lasttwo decades. They can occur within the gastro-intestinal tract, in the blood or at the cellular siteof action of the drug. The consequence of anyinteraction will vary with the drug, its formula-tion, the timing of food intake, and the nutri-tional status and disease state of the individualconcerned.

Effects of diet on drugs

Most drugs are taken into the body by mouthand, therefore, are processed by the gastro-intestinal tract. Many drugs have to be solubi-lized by the digestive secretions before they canbe absorbed. In a fasted subject, drugs will passquickly through the stomach, reaching the smallintestine within minutes. Drugs taken with foodor after meals are likely to be more slowlyabsorbed than those taken following a period offasting. The presence of food and fluid also facili-tates the solubilization of solid drugs. Theincreased flow of blood in the splanchnic circu-lation associated with eating may enhance thebioavailability of some drugs, for example, someof the beta blockers.

Nevertheless, there are some drugs that arebetter absorbed in the fasting state, such as peni-cillin and tetracycline. In particular, tetracyclineis less well absorbed when taken with foods con-taining calcium, magnesium, iron or zinc, andshould, therefore, not be taken within 2 hours of food containing dairy produce or protein. The presence of protein in the meal reduces theabsorption of L-dopa, but a low-fat diet enhances


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the effectiveness of the lipid-lowering agentlovastatin. Unpleasant flushing can occur whenchlorpropamide is taken with alcohol or nifedip-ine (a calcium-channel blocking agent) with ahigh-fat meal. A high-fibre diet can bind somedrugs; this may be of benefit, protecting againstharmful effects, or a disadvantage, if absorptionis too slow.

Dietary factors affecting drug metabolismAdequate protein intake is required for normaldrug metabolism and a low protein status may belinked with prolonged drug action. Fat-free dietsmay also reduce the activity of drug-metabolizingenzymes. Vitamin C is required for hepatic cyto-chrome P450, a key component of the micro-somal oxidizing system, which metabolizes drugs.Many of the other enzymes involved in the phase I (oxidation, hydroxylation, reduction orhydrolysis) reactions, which alter the functionalgroups on the drug molecules, require vitamins,especially the B complex, and minerals to act ascofactors. Dietary factors are also needed to supplythe groups needed to conjugate drugs in phase IIreactions. These include glucuronate, glutathione,acetate and sulphate, all of which facilitate thesolubilization and excretion of drugs.

This presents a potential problem for indi-viduals with a chronic disease. If the diseaseaffects their food intake, yet is treated by drugs,the effectiveness of the drugs and their potentialside-effects may be significantly influenced bythe nutritional status. In other words, those whorequire the drug therapy may well be in themost nutritionally vulnerable state and leastable to metabolize the drugs.

Dietary factors affecting drug excretionA low-protein diet may alter urinary pH, decreaserenal blood flow and reduce the excretion of cer-tain drugs. Some drugs are preferentially excretedin acidic conditions and reabsorbed when the pH of the urine becomes more alkaline. Lowerclearance via the kidney may increase levels inthe blood, resulting in side-effects. This hasbeen reported in patients with gout, who aretaking allopurinol and a low-protein diet. Whenseveral drugs are taken, there may be competition

between drugs for renal excretion, with higherlevels remaining in the blood.

Effects of drugs on nutrition

Food intakeOne of the most important influences of manydrugs is their effect on appetite. In some cases, thismay be the declared aim of using the drug, whenweight loss is required. However, other drugs mayinduce nausea or cause oral ulceration, whichmakes food intake painful. A notable example of this group of drugs are those used in cancerchemotherapy. Effects further along the gastro-intestinal tract, such as abdominal pain, bloatingor diarrhoea, may also reduce the desire to eat.

Some drugs can increase appetite as anunwanted side-effect. Major examples are thebenzodiazepine tranquillizers and lithium usedin manic depressive illness. Cyproheptadine isan antihistamine drug that has been used toencourage individuals with a wasting conditionto increase their food intake.

Gastrointestinal functionDrugs may affect absorption from the digestivetract. Examples of such effects include:■ an alteration in pH (by antacids) and thus a

change in the solubility of minerals forabsorption;

■ inhibition of folate deconjugating enzymesby sulphasalazine, which is used in inflam-matory bowel disease, thus preventing liber-ation of folate from foods or competitionwith carrier molecules for folate transport;

■ induction of catabolism of 25-OH vitamin Dby anticonvulsants, reducing circulating levels and interfering with calcium absorption;

■ binding of fat-soluble vitamins to mineraloil laxatives;

■ destruction by long-acting antibiotics, suchas neomycin, of gut flora that synthesizesome vitamins;

■ reduced vitamin B12 absorption owing tointeraction with peptic ulcer drugs (H2antagonists);

■ damage to mucosal surfaces of the gut andsmall intestinal enzymes by excessive intakesof alcohol.

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Metabolic effects of drugs on nutrientsSome drugs may be specific antagonists of themetabolic role of vitamins and may result inalterations in mineral status by specific effects onexcretion. Specific vitamin antagonists includethose that are intended to inhibit the vitamin orthose that affect the vitamin as a side-effect.The most important of the specific antagonistsare those for folic acid, which are used in can-cer chemotherapy, against Pneumocystis carniiinfection in AIDS, and as antimalarial and anti-inflammatory agents. Coumarin derivatives, usedas anticlotting agents, are vitamin K antagonists.

Nitrous oxide used as an anaesthetic and theantituberculosis drug isoniazid, however, haveunwanted side-effects, interfering with B12 andB6, respectively.

Drugs may also lead to excessively high levelsof sodium, potassium, calcium and magnesium byinterfering with normal regulatory mechanisms.This may be a particular problem with drugs usedin cardiac patients receiving diuretic therapies orwhen several drugs are used together. Diureticscan also result in mineral depletion. In both thesecases, the mineral intake of the diet may need tobe monitored.

The group in the population most at risk fromthese many interactions are the elderly. It hasbeen reported that nursing home residents con-sume on average eight different medications perday. This may also be seen in elderly people liv-ing elsewhere, who may take a range of both pre-scribed and non-prescribed drugs. Interactionsbetween the pharmacological effects of thesesubstances are inevitable. If, at the same time, thephysiological processes to cope with the metab-olism of the drugs are beginning to be less effi-cient and maybe the nutritional intake is not asgood as it could be, there is potential for undesir-able side-effects. These may take the form ofexcessively large or inadequate therapeuticeffects, both of which have medical implications.

Nutrition and the athlete

High levels of energy expenditure impose unusualphysiological demands on the body. There is anincreased need for energy and associated nutri-ents for increased metabolism as well as adequate

fluids to maintain body temperature in the face oflarge amounts of heat production in exercisingmuscles. Exercise generates large amounts of freeradicals because of the increase in oxidativeprocesses. Thus, there is an increased need forantioxidant factors in the body and these shouldbe plentiful in the diet.

To enable the body to make the most of itsnutrient supplies, regular training facilitates thedevelopment of a more profuse blood supply inthe muscle and shifts metabolism to more energysparing pathways. In addition, physical activityconfers a number of health advantages. A largefollow-up study of 1800 British male civil ser-vants showed that those who took vigorous exer-cise in their leisure time had less than a quarter ofthe fatal heart attacks seen in the inactive group.

In addition, exercise promotes a sense ofwell-being, believed to be related to altered levelsof neurotransmitters in the brain. There is gener-ally less body fat and more lean body mass thanin comparable non-exercisers and a healthierblood lipid profile, with higher levels of high-density lipoproteins (HDLs). Those who exercisecan consume more fat in their diet withoutincreasing their adipose tissue levels. People whoexercise regularly may also adopt other aspectsof a healthier lifestyle, particularly not smoking.

The dietary needs of the athlete are, inessence, very similar to those of the average indi-vidual. Differences may arise, however, becauseof increased energy needs, the timing of meals toensure an adequate intake around a busy sched-ule, and the importance of maintaining a highintake of carbohydrate during training and aftercompetition. Fluid balance is also important.

Athletes can be very vulnerable to sugges-tions about their diet and may follow a successionof dietary fads and ideas, often spending a hugeamount of money on pills and potions. Whendietary advice is proposed, they may be reluctantto change what they believe to be a ‘winning’diet, even if this is not nutritionally sound. If anathlete can be persuaded to adopt a sound healthydiet, it could remove a whole area of worry fromthe training programme and allow the focus to be concentrated on the physical training regime.In addition, careful attention to nutrition canmake the difference between winning and coming


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second. It is the responsibility of the nutritionistto work with the athlete, to identify specific nutri-tional goals that are achievable and to providestrategies that match individual circumstances.

Energy needs in sport

The key consideration in any sports perform-ance is the need for energy that is additional tothat required for maintaining normal metab-olism and everyday physical activity. Not allindividuals undertaking sport have high energyrequirements: in some sports, energy expend-iture may be little more than is found in a mod-erately active person. Total amount of energyused is also dependent on body size, so a light-weight athlete will use less energy than onewith a large body size. Exercising intensively onan energy-restricted diet can cause increasedprotein breakdown and may cause physiologicalstress. This, in turn, can result in a suppressionof immune function. It is also very important toremember at this point that energy needed for

growth must also be met. In teenage athletes,high levels of activity and inadequate intakeswill compromise growth. Thus, adequate levelsof energy must be provided.

Provision of energy for sport (Figure 16.5)At the cellular level, the muscles use adenosinetriphosphate (ATP) in their contraction. A con-stant supply of this must, therefore, be main-tained. In the first moments of exercise, the bodywill use its store of ATP, contained in the muscles,but after 3 seconds this has been exhausted. Thenext source is generation of ATP from creatinephosphate, also stored in the muscle, which canprovide about 15 seconds’ worth of ATP. Thismay be enough for a short burst of activity, suchas a single jump, throw or lift. After this, ATPmust come from other metabolic substrates,namely carbohydrates, proteins and fats. All ofthese can be transported to the muscle cell andbroken down for energy; however, they are notused in equal amounts. Proteins do not usuallycontribute much to total energy expenditure in

Figure 16.5 The provision of energy in sport.


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exercise except in very prolonged, enduranceevents or in very intense exercise, when theymay supply about 10 per cent of the total energy.The major supply comes from fats and carbohy-drates. The choice of fuel is made on the basis ofseveral aspects of the exercise, of which the mostimportant is the intensity.

At rest, almost all the body’s energy is sup-plied from fat oxidation. This is the most effi-cient source of energy, providing 80–200 unitsof ATP per molecule. Its main drawback, how-ever, is that it is a slow producer of energy anduses more oxygen than carbohydrate metab-olism does. Energy obtained from fat has beenlikened to a steam engine – it can use up fuel forlong periods of time and maintain a steady pace.Even at low rates of exercise, the body has to usea small amount of carbohydrate to complete theoxidation of fats. Thus, stores of carbohydrate inthe form of glycogen are important.

As exercise intensity increases, ATP must beproduced more quickly to maintain energy sup-plies. This can be achieved by using increasinglymore carbohydrate, which can produce 38 unitsof ATP per molecule of glucose as long as theoxygen supply is adequate, that is, under aerobicconditions. If the intensity of exercise becomes sogreat that the production of energy outstrips thesupply of oxygen, glucose can still be brokendown, albeit very inefficiently (no other substratecan be broken down in this way), but will onlyproduce 2 units of ATP per molecule of glucose,by anaerobic metabolism. Such a burst of energycan be harnessed for a short and intense exercise,such as a 100-m race or a power lift. However, it is an incomplete metabolic process and lacticacid is produced. This has several consequences,particularly in the production of fatigue. A build-up of lactic acid reduces the pH in the muscle tothe point where contraction can no longer occur.This terminates the exercise, so anaerobic exer-cise is of necessity of short duration (a maximumof about 90 seconds). The body’s tolerance to lactic acid also increases with training, increas-ing the length of time the exercise can continue.Once the need for a rapid energy supply stops,oxygen can once again meet the needs of themetabolic pathways and the ‘incomplete’ oxida-tions can be brought to a conclusion, with the

further oxidation of lactic acid into pyruvic acid,and thence via the Krebs cycle. This has beentermed ‘repaying the oxygen debt’.

To maintain muscle contraction at a rapidrate, the following two conditions must be met.■ The oxygen supply must be as great as pos-

sible. This is improved by training, whichallows a greater utilization per minute ofoxygen, as lung capacity increases.

■ There must be adequate supplies of glycogen.This is also improved by training, since theability to use fat as fuel increases in a trainedathlete and, therefore, extends the period ofavailability of carbohydrate.In summary, whatever the intensity of the

exercise, both fat and carbohydrate are generallyused. At low levels, the balance is mostly infavour of fats, with little carbohydrate used. Athigh intensity, the exercise is fuelled mostly bycarbohydrates, unless it is at maximal intensityand proceeds anaerobically, when carbohydrate isthe sole fuel. Most exercise will predominantlyoccur at a level between these extremes, with per-haps only short bursts of intense action. However,the longer the duration of exercise, the greater theproportion of fat:carbohydrate used. Eventually,the supply of carbohydrate is exhausted and exercise has to stop. In addition to supplying themuscles, carbohydrate is also needed to maintainblood glucose levels, to meet the energy require-ments of the vital organs, most notably the brain.These levels are maintained by the liver, whichuses stored liver glycogen, but also manufacturesnew glucose from glycerol (from fat metabolism)and amino acid residues, in a process known as gluconeogenesis. Falling blood glucose levelscontribute to fatigue. Low blood glucose levelsalso cause physiological stress, which results inrelease of hormones, such as cortisol, which inturn have a negative effect on immunity.

From the above it can be seen that maintain-ing a high level of stored glycogen in the muscleis important to extend duration of exercise.Many studies on exercising subjects, first carriedout in the 1930s, have shown that exercise timeto exhaustion can be lengthened in subjects consuming a diet containing a high proportion ofcarbohydrate. This increases exercise times com-pared with times achieved by subjects on normal


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diets, which in turn are greater than those in sub-jects fed a high fat/protein diet with low levels ofcarbohydrate. It has subsequently been shownthat exercised muscle is capable of taking up carbohydrate in increased amounts in the first1–2 hours after activity, which helps to replenishstores and permits exercise to be repeated on the following day (Figure 16.6). This increasedcapacity to store carbohydrate is believed to be atleast partly the result of increased blood flow tomuscles in the post-exercise period. Cell volume,influenced by osmotic changes is also a deter-minant of carbohydrate synthesis after exercise.These two findings highlight the importance ofcarbohydrate in the diet of the athlete.

During trainingIn practical terms, the diet during trainingshould be based on carbohydrates, ideally sup-plying 55–60 per cent of the energy. This meansthat, if levels of protein are 10–15 per cent ofenergy, the amount of fat is 25–35 per cent. Thisis clearly very close to the general healthy eat-ing guidelines. The carbohydrate should be amixture of both simple and complex sources. In reality, an athlete who has very high energy

needs would find it very difficult to consumethe volume of complex carbohydrate this wouldrepresent. This would be exacerbated by theusual lack of time for eating, which is commonamong amateur athletes. Nevertheless, adequateintake of carbohydrate is essential if daily exer-cise is taken (Figure 16.7). A daily requirementof 8–10 g carbohydrate/kg body weight is rec-ommended during periods of hard training. Fortraining sessions that last for more than 60 min-utes, it is also important to take carbohydrate atintervals starting after the first 30 minutes. Thishelps to maintain circulating blood glucose levels and prevents depletion of liver glycogenstores. Once these have been depleted, they can-not be replaced until exercise has stopped.

After exerciseWhen exercise stops, the muscles need to berefilled as quickly as possible with glycogen.The first priority after exercise is thus to con-sume some carbohydrate-containing food,which will be readily absorbed and deliver itsglucose content to the muscles. The food chosenshould have a high glycaemic index, which willcause a quick rise in blood sugar. During thistime, it is recommended that at least 50–100 gcarbohydrate is consumed (1–2 g/kg) within thefirst hour. (Foods grouped according to gly-caemic index are given in Table 16.1.)

Figure 16.6 Effects of different amounts of carbohydratein the diet on the refuelling of muscle glycogen in the24–48 hours after exercise. (From Wootton, 1988.Reproduced with kind permission of Simon & Schuster,London.)

Figure 16.7 Effects of different amounts of carbohydratein the diet on muscle glycogen levels during threeconsecutive periods of exercise over 72 hours. (FromWootton, 1988. Reproduced with kind permission ofSimon & Schuster, London.)


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Many athletes find that they do not want toeat immediately after exercise; in this case, acarbohydrate-containing drink is useful. Thishelps to achieve the goal of replenishment ofcarbohydrate stores, as well as providing somerehydration. Small carbohydrate-containingsnacks eaten at frequent intervals are also help-ful. It should be remembered, however, that toomany high-sugar foods may pose problems fordental hygiene and appropriate advice shouldalso be given on this. Where possible, a meal orlarge snack high in carbohydrate should be con-sumed within 2 hours.

Later on, foods with a lower glycaemic indexare acceptable, as they cause a slower but moresustained increase in blood glucose levels, whichcan enter the muscles over a longer period of timeto maintain the refuelling process. Protein supplyis also important at this time to ensure sufficientlevels of amino acids in the circulation for tissuerepair and protein synthesis. This does not need tocome from special protein supplements, but canreadily be supplied from normal foods, such as asandwich with cheese, lean meat or fish, a bakedpotato with beans, or a pasta dish with a meat- or cheese-based sauce. All of these provide acombination of protein and carbohydrate.

Protein needs

Many athletes believe that, to make full use oftheir muscles in exercise, they require a high

protein intake. This stems from the idea thatmuscles are used up in some way in exercise and,therefore, require extra protein to restore them.

Protein makes a very small contribution toenergy supply in exercise and is hardly used up at all. However, an exercising muscle doesincrease in mass over a period of time, so thatwhen a person first starts to take regular exercise,more protein will initially be retained by thebody. However, when equilibrium is reached, the additional food consumed to meet the energyneeds should provide more than enough proteinto meet the needs of the muscles for repair.Recommended levels for protein intake are in theregion of 1.5 (1.2–1.7 ) g protein/kg body weight.There is no advantage in exceeding more than

Grouping of some commonly eaten foods according to glycaemic indexTABLE 16.1Foods with high Foods with moderate Foods with lowglycaemic index (above 85) glycaemic index (60–85) glycaemic index (less than 60)Bread (white or wholemeal) Pasta and noodles Apples, grapefruit, peaches, plumsRice Porridge BeansBreakfast cereals (e.g. cornflakes, Grapes, oranges Milk, yogurt and ice creammuesli, Weetabix) Crisps Fructose

Raisins, bananas Biscuits Tomato soupPotato, sweetcornGlucose, sucrose, honeySoft drinksMaltodextrin drink (20%)

Adapted from Williams and Devlin, 1992. Reproduced with the kind permission of the publisher.

An athlete requires a daily intake of approximately21 MJ (5000 Calories). Calculate the amount of car-bohydrate this would represent according to theabove guidelines.

Devise a day’s menu to supply this amount ofcarbohydrate:■ using predominantly sources of complex car-

bohydrate■ including some simple carbohydrate.Repeat the calculation using a target energyintake of 10.5 MJ (2500 Calories).

Compare the practicalities of consuming thetwo diets.

Activity 16.1


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2g/kg, and such a high level may compromisethe carbohydrate intake. Consequently, there willbe insufficient glycogen for the muscles to exer-cise in training and any potential benefit of theextra protein will be lost anyway. The proteinshould always be balanced by an adequate energyintake, equal to 170kJ (40Calories) per gram ofprotein. There are many successful vegetarianathletes whose protein intakes are derived onlyfrom plant foods, and also athletes whose proteinintakes do not exceed 10 per cent of the energyintake. It is the training that increases musclesize, strength and exercise capacity, and not theincreased protein intake. Many athletes fromdeveloping countries do not have access to suchhigh levels of protein, yet compete effectively onthe world stage.

Dietary supplements

Athletes use a wide range of supplements, andsurveys from various countries indicate thatover 90 per cent of athletes studied are currentlyusing, or have used dietary supplements in thepast. Usage varies with the particular sport,level of competition and gender of the athlete.

Very few of the supplements used by athleteshave been scientifically evaluated for efficacy to enhance performance, although, if the diet isinadequate, there may be a valid case for usingthe supplement.

Vitamin and mineral supplementsThere is little evidence that vitamin supplementsare of any benefit in an adequately nourishedathlete. Studies that have claimed to show animprovement often give no indication of the ini-tial nutritional status of the athlete and, there-fore, their findings prove little.

The following two points are, however,important:■ Athletes who consume very little food in

an attempt to maintain a low body weightappropriate to their particular sport may notmeet their nutritional requirements for allmicronutrients. A supplement may be indi-cated in this case.

■ Intense physical activity produces free rad-icals, which may represent a health risk to the

individual, if insufficient levels of antioxidantnutrients are present. Attention should bepaid particularly to vitamin E and C intakes toensure adequate status. There is some evi-dence that immune status is poorer in athleteswho undertake heavy training. This may belinked to low levels of certain micronutrientsneeded for the components of the immuneresponse, although stress responses may alsobe an important factor.Mineral status is of concern in terms of cal-

cium and iron, especially in female athletes, whomay consume diets deficient in both of thesenutrients. Low calcium status in young women,together with a low body weight, which resultsin amenorrhoea (loss of menstrual periods), maycompromise bone density and lead to fracturesand early osteoporosis. This condition has beendescribed as ‘fit but fragile’. The drive to main-tain a low body weight may be so intense that atype of anorexic behaviour is seen, with obses-sive avoidance of food that might cause weightgain, compulsive exercise, and amenorrhoea withresulting low bone density that may lead to frequent fractures. This is sometimes describedas the female athlete triad. When competitivesport participation stops, normal menstrual activ-ity is likely to return but it is possible that bonedensity does not recover to that expected for age.Most at risk are young females in whom high levels of exercise delay menarche and disrupt thephase of most rapid bone mass accretion.

Iron needs are higher in women because ofmenstrual losses; low-weight female athletesmay cease to menstruate and thereby conservesome iron. However, evidence exists of a higherturnover of iron in athletes, possibly owing toincreased destruction of red blood cells. This mayresult in increased needs and, if these are notmet, then stores will decline and anaemia candevelop, which will affect performance.

CreatineCreatine phosphate is an important energy sourcefor muscles during intense exercise. However, thecontent in muscle is limited. Creatine is obtainedfrom the diet, predominantly in meat and animalproducts, but is also synthesized in the bodyfrom amino acid precursors, such as glycine and

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arginine. Vegetarian athletes have to rely onendogenous synthesis, which can provide enoughcreatine. However, since the early 1990s, creatinesupplements have been available, which havebeen shown to enhance the content in muscle by up to 50 per cent. The scientific evidence supports a positive effect of creatine supplemen-tation in repeated short bursts of intense activity.It does not enhance duration of prolonged effort.Creatine supplementation can result in an initialgain in muscle bulk of 1–2kg after a loading dose(4 � 5g doses daily) for 4–5 days. This is prop-bably due to swelling of cells, which may beaccompanied by increased protein synthesis. Amaintenance dose of 1–2g daily is recommended.Subjectively, heaviness of muscles may be areported side-effect. No clinically significant neg-ative effects have been reported to date.

There are many other dietary supplementswhich are used by athletes. Some of these arementioned in Chapter 17.

Fluid

Fluid is also an important consideration for athletes. Sweating is essential to lose heat andmaintain body temperature. The sweat containselectrolytes, most notably sodium, potassium andchloride ions, derived from the plasma. However,the concentration of electrolytes in the sweat isdifferent from that in the plasma, with the resultthat the remaining plasma may actually havehigher concentrations of some electrolytes at theend of the exercise. Consequently, the top priorityfor replacement after exercise is water, to restorenormal concentrations in plasma.

The issue is complicated by the observationthat the best way to increase water absorptionfrom the gut is to include some electrolytes insolution. This enhances water uptake and speedsrehydration. Many rehydrating solutions areavailable; most of them contain electrolytes (atless than 2.6g/dL), together with varying amountsof carbohydrate. The carbohydrate is present inamounts that may be:■ lower than concentrations in body fluids

(hypotonic solutions);

■ the same as body fluids (isotonic solutions); or■ greater than body fluids (hypertonic solutions).Absorption of these is most rapid from thehypotonic solution and slowest from the hyper-tonic solution. Drinking a hypertonic solutionwill not provide rapid rehydration and mayactually aggravate matters, as fluid from thebody is drawn into the digestive tract. However,hypotonic and isotonic solutions are useful inproviding quick rehydration. The added benefitof the carbohydrate content when taken at theend of exercise is its contribution to refuellingthe glucose stores. These solutions are also useful during prolonged exercise, when theyhelp to maintain blood glucose levels and pre-vent dehydration, thus enabling performance tocontinue at an optimal level. Solutions thatcontain glucose polymers are now available;this enables more glucose to be contained in the drink without compromising the tonicityand, therefore, provide more potential energy inthe drink.

Overall, many athletes do not consume a dietthat is appropriate to optimize their sportingperformance. This may be due to a variety offactors, including a lack of practical knowledgeand time as well as a reluctance to take advice.More education about diet and nutritional needsof both athletes and those who have responsibil-ity for their training is needed.

Alcohol abuse

Moderate amounts of alcohol (e.g. taken withinthe UK recommended limits of 2–3 units or 3–4units per day for women and men, respectively)are believed to be beneficial to cardiovascularhealth, as described in Chapter 14. One unit ofalcohol, as defined in the UK contains 8 g ofalcohol, and is usually interpreted as the amountof alcohol in one standard drink (a half pint ofregular beer, one glass of wine or one measure ofspirits). However, amounts in excess of this takenover a period of time are likely to result in harmand to compromise health. The exact level ofintake that may cause harm is difficult to define,as it is variable between individuals and dependson genetic predisposition. However, chronicintake of over 55 units per week for men and


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35 units per week for women is defined as‘unlikely not to cause harm’.

It is very difficult to obtain a true assess-ment of the number of people whose health is damaged by alcohol. In Britain, figures quotedsuggest that there are 250 000 people dependenton alcohol and a further one million at risk of dependence. The diagnosis may be difficultbecause so many people with an alcohol prob-lem conceal this from those around them, oftencontinuing to work and maintaining an exter-nal appearance of normality. It is only through alcohol-related disease, such as liver disease orencephalopathy (brain disease), that alcoholismmay be diagnosed. In addition, alcohol taken inexcess contributes to other diseases, such ascardiovascular disease and hypertension, ulcers,cancer and mental illness, as well as accidentsand violence.

The pattern of alcohol abuse has changed inthe last decade in Britain, with a rapidly increas-ing incidence in women. This reflects both theincreased economic independence of women aswell as the increased access to alcoholic drinks.Drinking among women has possible implica-tions for the health of the fetus, if it is continuedthroughout pregnancy. High levels of alcoholingestion may result in ‘fetal alcohol syndrome’,characterized by developmental abnormalities ofthe face, brain, heart and kidneys.

Young people are also drinking more, particu-larly in a ‘binge’ drinking pattern, when largeamounts of alcohol are consumed in a relativelyshort space of time. Such high intakes may accel-erate the damage caused.

The elderly, especially if affected by loneli-ness, are also recognized as a group at increasedrisk of excessive drinking. This may go unnoticedby primary health care staff until there is a crisis, such as a fall.

Nutritional implications

Food intakeFood intake can be affected by alcohol consump-tion in various ways, including the following.■ There is likely to be a reduced appetite or an

overall lack of interest in food as a result of apreoccupation with alcohol. Inflammation of

the stomach lining (gastritis) may result inpain on eating or cause vomiting.

■ Access to food may be difficult, especially ifthe alcoholic has left home. Cafe or take-away food may form a large proportion ofthe diet; this may not be particularly healthyor nutrient rich.

■ Money available to buy food may be scarceand be preferentially spent on drink.

Digestion and absorptionAlcohol is an irritant to living tissue, resultingin a permanent state of inflammation along thedigestive tract, and leading to vomiting anddiarrhoea. Gut contents tend to be moved alongrapidly and enzyme production may be impaired.This is particularly the case for the enzymesproduced in the wall of the small intestine, whichcomplete carbohydrate and protein digestion.The villi may be flattened and absorptive areasreduced. There may be secondary intolerance tosugars, which remain undigested and ferment inthe large intestine.

Metabolic changesLiver damage is recognized as one of the main consequences of alcohol abuse. The liveris also the site of activation, storage and metab-olism of many of the nutrients in the body.These will be adversely affected. Some nutrientsare specifically needed to metabolize and detox-ify the alcohol, and requirements for these willincrease.

Alcohol is a diuretic agent, increasing urineproduction. This will cause the loss of morewater-soluble nutrients from the body. The pan-creas may be inflamed, resulting in pancreatitis.Although this predominantly affects the pro-duction of digestive enzymes, there may also beimplications for insulin release and therebycontrol of blood sugar levels.

Energy balanceThere is controversy about the utilization of theenergy content of alcohol. The theoretical energyyield is 29kJ (7Calories) per gram of ethanol.However, individuals consuming large amountsof alcohol in addition to a moderate food intakedo not exhibit the weight gain one might expect

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from the excessive energy intake. This has led tothe proposal that some of the potential energyfrom alcohol is liberated as heat rather than beingconverted into usable ATP. Some alcohol ismetabolized via the microsomal ethanol oxidiz-ing system (MEOS), which becomes more activeat higher levels of alcohol intake. It is possiblethat this oxidation does not yield usable ATP, andconstitutes a ‘drain’ for the excess energy. Alco-holics may, in fact, be underweight or overweight,and which of these occurs appears to depend onthe total intake of food, rather more than theamount of alcohol consumed.

Abnormal findingsFat metabolism by the liver becomes abnormal.The production of NADPH by alcohol metab-olism drives fat synthesis, with large amountsaccumulating in the liver. Circulating lipid levels, especially the very low density lipopro-tein (VLDL) fraction, are elevated, increasing therisk of heart disease.

Control of blood glucose levels becomes lessprecise. This is partly the result of a failing pro-duction of insulin in the pancreas, but alsobecause of reduced gluconeogenesis by theliver. There may be periods of hypoglycaemia(low blood sugar), with feelings of dizziness andfaintness, and possibly blackouts.

The liver is one of the main sites for proteinsynthesis and degradation. In the liver of analcoholic, protein degradation may continue ata relatively normal rate, but protein synthesisand, therefore, tissue repair declines. Levels ofessential proteins will gradually decline, forexample, the plasma proteins in the blood or theproteins that function as digestive enzymes.

Among the water-soluble vitamins, it is theB complex that is most affected. Multiple defi-ciency states may exist, involving niacin,riboflavin and pyridoxine, and resulting in soremouth, diarrhoea, dermatitis and psychologicaldisturbances. Megaloblastic anaemia is likely asa result of folate malabsorption. Thiamin defi-ciency is likely, as it is required for the metab-olism of alcohol, and may, in addition, be lost invomiting and diarrhoea. This deficiency willresult in neuropathy, affecting hands and feet,making walking difficult. In its severe form,

psychological disturbances with loss of memoryand psychosis (Korsakoff’s syndrome) maydevelop. Poor vitamin C status owing to a poordiet is also possible.

Absorption of fat-soluble vitamins may alsobe affected, especially if the production of bilefrom the liver is reduced. Particularly at risk isvitamin K, as there are generally small stores ofthis vitamin. Low vitamin D status has also beenreported; it is believed that the breakdown ofactive vitamin D is induced by the alcohol.

Among the minerals, zinc is important, as itforms an essential part of the alcohol dehydro-genase enzyme. Levels may become depleted,affecting alcohol metabolism, wound healing,sense of taste and immune function. Electrolyteimbalances may arise because of vomiting anddiarrhoea, and can lead to changes in musclefunction. Iron status may be either high or low,depending on the beverages drunk. Spirits pro-vide no iron (or any other nutrients), but somewines and beers may contain iron. However,blood loss due to intestinal irritation may causeiron depletion, and the alcoholic may becomedeficient despite an apparently adequate intake(see Figure 16.8).

Influence of disability onnutrition

The term ‘disability’ is used to cover a very widerange of physical or mental conditions that mayinfluence the ability of an individual to func-tion in the able-bodied world. The disabilitymay be present from birth, or may have affectedthe person as a result of an accident or disease(such as Parkinson’s disease, multiple sclerosisor stroke). The degree of disablement will bereflected in the extent to which functions arecompromised. The disability may be progressiveand deteriorating, or there may be gradualimprovement. The perception of change mayinfluence the person’s willingness to look afterthemselves, and take an interest in their healthand possible rehabilitation.

Some disabilities will have very little impacton nutrition; others may have profound effects.Those having the greatest effects will be those


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that affect food intake, digestion and absorp-tion, and metabolic needs.

Impact of disability on food intake

This is probably the largest area of potential dif-ficulties. Food intake may be influenced by:■ factors affecting appetite;■ factors affecting the ability to obtain and

prepare the food; or■ factors affecting the ability to ingest, chew

and swallow the food.

AppetiteAppetite will be influenced by mental state, andthus can be affected by anxiety or depression.Physiological factors will also have an influence;for example, dulled sensation of taste, nausea,constipation or pain after eating will reduceappetite. A common side-effect of drug therapy isa dry mouth, which makes food ingestion difficult

and unpleasant, and depresses the appetite foreating. Physical factors, such as lack of exerciseand immobility, may also mean that the individ-ual does not feel hungry.

Environmental factors, including monot-onous menu presentation, especially if the diethas to be soft or puréed, and unpleasant sur-roundings may be off-putting. Eating snacks orsweets between meals may also be a major factorcontributing to lack of appetite at mealtimes.

In a non-verbal individual affected by anyof these factors, their unwillingness to eat andthe carer’s desire to provide food for eating mayresult in conflict and frustration.

Ability to obtain and prepare foodIn the situation where the individual is respon-sible for his/her own food supply, both the men-tal and physical capabilities are important.Understanding what to buy to produce a meal isessential. The process of going out and buying

Figure 16.8 Nutritionalimplications of alcohol abuse.

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the food may be compromised in many ways,including mobility, ability to communicate, tosee/hear and to carry the food. All of these willdetermine the range of foods that are actuallyavailable to eat. Cooking skills and capabilitiesare also important.

Where a carer is responsible for all of thesefunctions, the autonomy of the individual mustbe taken into account. The question of whetherthe food that is being prepared is actually whatis desired needs to be addressed. Food is a verypersonal issue and another person’s choice maynot be our own.

Ability to ingest, chew and swallow foodIngestion, biting, chewing and swallowing offood may be difficult in some disabilities. Theremay be tongue thrusting, spitting out, chokingand dribbling. These may be linked, for example,to a lack of coordination, involuntary move-ments, lack of lip closure or cleft lip and palate.Careful techniques are required to provide usefulnutrition. Appropriate modification of texturemay be needed, with the use of thickeners toimprove the appearance of meals and make themeasier to eat. If the individual is responsible forhis/her own feeding, hand to mouth coordinationis needed.

Appropriate positioning is essential to facili-tate swallowing and prevent regurgitation.Special feeding utensils are available to help the process; occupational therapists can help todevelop skills required for feeding and adviseon modified equipment. Becoming an independ-ent feeder can lead to marked improvements innutritional status.

Impact on digestion and absorption

Some individuals with disabilities may tend toregurgitate or ruminate food. Food that hasbeen swallowed may later be brought back intothe mouth and spat out. If this is continuousand severe, nutritional status will be threatened.

Drugs used to manage an underlying con-dition, such as tranquillizers, anticonvulsants,antibiotics, analgesics and antihypertensive drugs,may all affect the digestion and absorption offood from the gut. It is important that potential

drug–nutrient interactions are anticipated andavoided by suitable timing of drugs and meals,wherever possible.

Laxatives may be used to treat constipation.A form of laxative that has no impact on nutri-ent absorption should be chosen and, if pos-sible, dietary fibre and fluid intakes should beincreased.

Impact on metabolism

Nutritional needs may be altered by increased orreduced energy expenditure, drug-induced alter-ations in metabolism and specific nutritionalrequirements related to the underlying condition.It is, therefore, important to monitor the nutrientneeds of each individual. In children, growthshould be monitored regularly, including heightand weight; in adults, weight can be a useful indi-cator of adequate energy intake. However, otherassessments of nutritional status may be required,particularly micronutrient status.

Nutritional consequences

If total food intake is small, there is a risk of mal-nutrition, resulting in poor physical and mentalwell-being, increased risk of infection and, inchildren, delayed growth. More often, however,sufficient food is eaten, but it may be low innutrient density, perhaps because of the foodschosen or if it is diluted during purée production.Attention should also be paid to nutrient reten-tion during preparation. Foods that are kept hotfor periods of time lose vitamin content, andmodification of texture may result in significantlosses of water-soluble vitamins. If specificgroups of food are omitted entirely, the individ-ual may be left vulnerable to deficiencies; forexample, if few fruit and vegetables are included,they may lack trace elements and folate. Consti-pation may be a problem if non-starch polysac-charide (NSP) intake is low. Laxative use, on theother hand, may deplete the body of fat-solublevitamins.

Infection and the associated physiologicalstress will increase nutritional needs, especiallyfor B vitamins and vitamin C, zinc and protein.


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Involuntary muscle spasms may increaseenergy expenditure and result in weight loss, ifthis is not met. This is particularly common inchildren with athetoid cerebral palsy and autism,and with oral defects.

Specific drug–nutrient interactions shouldbe anticipated by adjusting food intake. Ifappetite is very poor, a nutritional supplementmay be needed to improve well-being to a point

where adequate nutrition can be obtained throughthe diet.

In summary, there are many threats to thenutritional status of a person experiencing somedisability. If these can be identified and antici-pated, they should not result in nutritional defi-ciency. However, the most important criterion isto judge each case in the context of the specificcircumstances.

1 Several situations that provide an additional threat to nutritional status have been reviewed.2 People suffering from food intolerance may need a modified diet. However, this should be devised with

appropriate consultation with a dietitian, so that nutritional content is maintained.3 In people with HIV infection or AIDS, nutrition can contribute to health, and every effort should be made

to maintain nutritional status during periods of infection and debility.4 Drugs that are used therapeutically can influence nutritional state. However, poor status with respect to

nutrition in the patient may in its turn affect the metabolism of drugs and perhaps produce unexpectedreactions.

5 Athletes have additional nutritional needs. These can be met from increases in food intake. A particularemphasis should be made on the carbohydrate content of the diet.

6 Disability may have short- or long-term implications for food intake. People affected by disability shouldhave access to various aids and modifications that can improve their nutritional intake. Monitoring ofhealth and weight is important.

SUMMARY

1 a Think about the examples of challenges tonutritional status discussed in this chapter.Construct a table to identify which part of thefood path (intake–processing–utilization) isactually affected in each of the cases.

b Suggest other challenges to nutrition thatcould be analysed this way.

2 a What are the characteristic features of a foodallergy?

b Why is allergy to peanuts currently ofconcern?

3 Identify the main focus of nutritional advice tobe given to HIV-positive subjects.

4 a In what ways does nutritional status affectdrug utilization?

b What are the possible implications of this inpeople who are ill and are receiving drugtreatments?

5 a What do you consider to be the maindifficulties encountered by an athlete thatmight prevent the consumption of anadequate diet?

b How can some of these difficulties be tackledand overcome?

6 Prepare an article to appear in a newsletter forparents of children with disability, givingpractical help about diet.

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British Nutrition Foundation 2001: Nutrition and sport. Briefing Paper. London: British NutritionFoundation.

Buttriss, J. (ed.) 2002: Adverse reactions to food. The report of a British Nutrition Foundation TaskForce. Oxford: Blackwell Science.

DoH (UK Department of Health) 1995: Sensible drinking. The Report of an InterdepartmentalWorking Group. Wetherby: Department of Health.

DoH (UK Department of Health) 1997: Peanut allergy. Committee on Toxicity of Chemicals,Consumer Products and the Environment. London: Department of Health.

Gowland, M.H. 2002: Food allergen avoidance: risk assessment for life. Proceedings of the NutritionSociety 61, 39–43.

Grimble, R.F. 2001: Nutritional modulation of immune function. Proceedings of the NutritionSociety 60, 389–97.

Hughes, D.A. 2000: Dietary antioxidants and human immune function. British Nutrition FoundationNutrition Bulletin 25, 35–41.

Maughan, R. 2002: The athlete’s diet: nutritional goals and dietary strategies. Proceedings of theNutrition Society 61, 87–96.

Prentice, A.M., Stock, M.J. 1996: Do calories from alcohol contribute to obesity? British NutritionFoundation Nutrition Bulletin 21, 45–53.

Saarinen, U.M., Kajosaari, M. 1995: Breast feeding as prophylaxis against atopic disease: prospect-ive follow-up study until 17 years old. Lancet 356, 1065–9.

Salomon, J., De Truchis, P., Melchior, J.-C. 2001: Nutrition and HIV infection. British Journal ofNutrition 87(Suppl. 1), S111–19.

Semba, R.D., Tang, A.M. 1999: Micronutrients and the pathogenesis of human immunodeficiencyvirus infection. British Journal of Nutrition 81, 181–9.

Terho, E.O., Savolainen, J. 1996: Review: diagnosis of food hypersensitivity. European Journal ofClinical Nutrition 50, 1–5.

Thomas, J.A. 1995: Drug–nutrient interactions. Nutrition Reviews 53(10), 271–82.Ware, L.J., Wootton, S.A., Morlese, J.M. et al. 2002: The paradox of improved antiretroviral therapy

in HIV: potential for nutritional modulation? Proceedings of the Nutrition Society 61, 131–6.Williams, C., Devlin, J.T. (eds) 1992: Foods, nutrition and sports performance. London: E & F Spon.Wootton, S. 1988: Nutrition in sport. London: Simon & Schuster.Young, E., Stoneham, M.D., Petruckevitch, A. et al. 1994: A population study of food intolerance.

Lancet 343, 1127–30.

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Optimizing nutrition


❏ discuss the concept of optimal nutrition;❏ describe some of the foods that are available to the consumer that may be used to optimize health;❏ describe the evidence to support the use of these foods.


❏ explain what is meant by functional foods;❏ evaluate the evidence for the role of non-nutritional factors in human health;❏ debate the advantages and disadvantages of using designed food products to optimize health.

In the last few decades, the developed world haswitnessed a shift in perception about the possibleroles of food and nutrition. The fundamentalrole of food is to supply the basic nutrients forthe maintenance of physiological function (andgrowth) in the body and fulfilment of social activ-ity, while at the same time satisfying sensoryneeds. From this understanding come concepts,such as nutritional requirement and dietary ref-erence values, which are discussed in Chapter 2.As our knowledge of the role of nutrients in thebody and possible interactions with the preven-tion or development of diseases has developed, afurther role for food has become apparent. Thisis the recognition that components of food,which may or may not have specific nutritionalroles, may be beneficial to health. Thus, therehas been a shift from discussing ‘adequate’nutrition to considering ‘optimal’ nutrition.

This presents a challenge to nutritional sci-entists to decide, where relevant:■ how much is enough (to minimize deficiency);■ how much is best (to meet biochemical,

physiological and other functions for normalhealth);

■ how much can provide other benefits innon-nutritional ways;

■ how much is too much and causes harmfuleffects.Suitable indices are required in order to be

able to define these limits, and this brings con-siderable methodological, practical and ethicalchallenges.

Traditional approaches have included bal-ance studies, tissue saturation studies, measure-ment of body stores and functional studies.Many of these methods have been used to deter-mine minimal requirements for nutrients.

The function of a nutrient within a specifictarget tissue or pathway can be used to deter-mine its level of activity, and to explore theeffects on this of changes in intake or blood levelof the nutrient. Generally, it would be expectedthat increases in intake, or blood levels, up to acertain level would cause a dose–responsechange in activity of the measured function. Atthe point where activity ceases to increase, it canbe assumed that maximal physiological (or opti-mal) function has been achieved.

With the current state of knowledge, the roleof a nutrient is likely to be assessed in a rathergeneral way, for example, in terms of its effect onantioxidant status, muscle strength or blood clot-ting. This is because, in most cases, the exact first

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biochemical point at which a particular nutrientis involved and at which it becomes limiting indeficiency may not be known. However, withdevelopments in molecular biology, it may bepossible in the future to explore the effects ofnutrients on gene expression and determine theirrole precisely. A general function is also likely tobe used to assess possible health benefits of anutrient, perhaps in amounts greater than meetthe functional needs.

There are many difficulties, however, intranslating results obtained at the laboratorylevel into guidelines or targets for the intake ofa particular nutrient. These can include:■ interactions between nutrients and other

chemical components in food;■ uncertainties about the bioavailability of

nutrients at the gut level;■ efficiency of transport to the target site;■ inter-individual variation;■ potential interaction between nutrients at

different stages in the life cycle.For all of the above reasons, research on opti-mal levels for the majority of nutrients is still at an early stage. The Food Standards Agency in the UK has an Optimal Nutritional StatusResearch programme, which has a number ofobjectives.

The first objective is the need to understandthe links between optimal nutrition status andthe maintenance of good health. This will explorethe potential interactions between micronutrientsat different life stages in the reduction of specificdisease.

The second objective is to develop accuratemeasures of bioavailability of nutrients fromfoods. This will explore the processing of nutri-ents at the gut level and their transport to cellu-lar sites. There are a number of subissues withinthis objective that have been identified:■ to measure the fraction of an ingested nutri-

ent that meets functional demand at the target tissues;

■ to develop functional markers of status for each micronutrient or group of micro-nutrients;

■ to use human intervention studies to deter-mine dose–response relationships of tissuefunction;

■ to understand the extent of inter-individualvariation in order to identify optimal nutri-tional intakes for the whole population and,therefore, provide advice that could reducemorbidity and mortality from chronic disease.

Foods, food componentsand health claims

The growth of interest in the use of food to pro-mote a state of health and well-being, andreduce the risk of disease has led to the rapiddevelopment of an industry that produces foodsthat claim to possess these characteristics. Ahealth claim describes a positive relationshipbetween a food substance in the diet and a dis-ease or other health-related condition. This mayinclude a lessening of the condition or a reduc-tion in the risk of that condition.

Early research on these foods started inJapan in the 1980s, with the purpose of develop-ing foods for specific health use (FOSHU). Thesewere defined as ‘processed foods containingingredients that aid specific bodily functions inaddition to nutrition’. Legislation allowed claimsto be made about specific health effects of foodsin certain categories. In the USA, the NutritionLabelling and Education Act, enforced in 1994,allowed health claims to be made for ingredientsfor which there was recognized evidence of acorrelation between intake and cure or preven-tion of certain diseases, although this does notnecessarily mean that the evidence can beapplied to the food itself.

The promotion of foods with health claims ismuch more restricted in the UK, where the lawseparates foods and medicines so that foods can-not be described as providing a medical healthbenefit. Therefore, foods cannot be labelled as‘preventing’ or ‘curing’ a specific disease. As aresult of growing concern about the unregulatedmarket in the UK, the Food Advisory Committeeproduced a set of guidelines. These have beendeveloped into a Code of Practice by the Joint Health Claims Initiative (JHCI), a panel ofrepresentatives from consumer, food industryand enforcement groups. This aims to help thefood industry to make health claims that arewithin current legislative constraints. An expert

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committee is to review all claims to ensure thatthey are supported by scientific evidence, withthe aim of producing a list of approved generichealth claims for use by food manufacturerswhose products meet the criteria. New submis-sions for products will also be considered. It isanticipated that this will allow consumers toreceive information about health benefits with-out infringing current UK legislation.

There is a relatively high degree of publicsuspicion of processed foods in the UK, relatedto a number of food-related health scares inrecent years. A meeting with consumers by theForesight Task Force, set up by the Governmentin the UK in 2001, indicated that there is cyni-cism among consumers about the need for newproducts developed by the food industry, and thereasons for their development. It is evident,therefore, that products that might be valuableto optimize nutrition need to be clear in theirpresentation to the consumer.

This puts the onus on the food industry tofollow the principles of scientific research andon regulatory authorities to ensure that systemsare in place to protect the consumer.

The following points summarize stages inthe process of developing such products or foodcomponents.■ Fundamental research techniques can iden-

tify possible interactions between a foodcomponent and a function relevant tohealth, thus generating hypotheses for study.Appropriate markers of this function need tobe developed for the assessment. This is aproblematic area, as few such markers exist.

■ The hypothetical effect needs to be tested inappropriate models, including human stud-ies, and safety assessments carried out. Trialsshould be carried out in a manner similar todrug testing, with the potential to demon-strate a dose–response relationship, and anypotential risk be evaluated. The cost–benefitof the use of the food component should beanalysed.

■ The food component being studied shouldbe able to be included in a variety of normaldiets, in amounts sufficient to produce thedesired effects, that is, they should remain‘foods’.

■ Possible adverse effect of an excess intake ofthe component must also be examined (e.g.if the same component is included in a num-ber of products, will this still be safe?).

■ The differential effects of the component inpeople of different ages and states of healthshould be considered.

■ The evidence relating to the product must beevaluated by an independent authority, whichis empowered to approve the use of the prod-uct, and which can determine the nature andcontent of the health claim being made. Thisis a fundamental part of any food safety andlabelling regulations that exist in a country.

■ The information to the consumer about theproduct must be both clear and informative. It should include information about the tar-get group or condition (if this is specific),the benefit claimed and the amount to beconsumed.

TerminologyThere is a confusing range of terms given tofoods that have been specifically developed bythe food industry to meet the demand forhealthier foods.

Smart foods

This is a term that is being used in schools in theUK as part of the Design and Technology cur-riculum. The food industry uses the term ‘mod-ern’ or ‘novel’ food materials. These are foodsthat have been developed through new orimproved processes, generally by human inter-vention and, therefore, not through naturallyoccurring changes. This classification includes:■ foods with novel molecular structures,

including fat substitutes and sweeteners;■ meat analogues, including novel proteins;■ foods produced by biotechnology;■ functional foods (also known as phar-

mafoods or nutraceuticals).

Foods with novel molecular structures

In relation to healthy eating initiatives, the mostimportant components in this group are fat

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replacers and sweeteners. Both are useful in reduc-ing the energy content of the diet. Fat replacerscan be derived from carbohydrate or protein, or be lipid-based. In the case of carbohydrate- orprotein-derived products, these can be used tosubstitute fat in the production of low-fat meals,and additionally act as stabilizers to preventseparation of ingredients. Lipid-based fat replac-ers are fatty acid esters with sugars, which arenot absorbed from the digestive tract. Thesehave the advantage of being stable at high tem-peratures and can, therefore, be used in fried orbaked products, such as crisps and biscuits. Anexample of this group is Olestra, licensed for usein the USA.

Sweeteners are a well-established item in thediet of people wishing to reduce their energyintake. The main products used in the UK are sac-charin, aspartame, acesulfame and cyclamate. Allthe intense sweeteners provide the sensation ofsweetness in very small amounts because of theirmolecular structure and can, therefore, mimic theeffect of sucrose, without supplying the associ-ated energy. Aspartame is composed of phenyl-alanine and aspartic acid and, therefore, yieldsthese amino acids when digested. However, thequantity consumed produces a negligible amountof energy. Because it contains phenylalanine,aspartame should not be used by people withphenylketonuria (PKU) who cannot metabolize it.Over 2000 products available in Europe containaspartame.

This group of smart foods also containsmodified starches, which are used in many foodproducts that need to be stabilized or thickened,

and has extended the range of ‘instant’ and‘ready to eat’ products on the market.

Meat analogues

This group of smart foods includes productsmade from soya protein (textured vegetable pro-tein, tofu) or fungal proteins (Quorn) that havebeen extruded, spun, coagulated and mouldedinto products that resemble meat in texture.Flavours and additional nutrients may be addedas part of the processing. These products areincluded in the diet of people who prefer not toeat meat, but may also be considered by some tobe a healthier alternative to meat. This may notnecessarily be the case, as levels of fat may becomparable to those in similar meat dishes andmicronutrient levels may be lower.

Foods produced by biotechnology

Plant and animal breeders have for centuriestried to breed in the best characteristics of thespecies, and breed out the least advantageousones. Biotechnology is the use of biologicalprocesses to make useful products. The use ofyeast to make bread and beer, and microorgan-isms to make yogurt and vinegar are all trad-itional examples. In recent years, developmentsin molecular biology and genetics have made itpossible to manipulate the genes of plants andanimals to an extent that specific characteristicshave been transferable. This has made it possibleto produce new varieties of certain plants havingdesirable characteristics. Disease resistance canbe enhanced by genetic modification so thatinsect or virus borne diseases no longer destroythe crop. This has been achieved for a substan-tial proportion of maize grown in the USA. Workis under way to increase disease resistance in the sweet potato, which could enhance yieldsthree-fold.

One of the most successful ‘genetically modi-fied’ (GM) plants has been the soya bean, whichcarries resistance to particular herbicides, thusallowing more effective treatment of the culti-vated land with less herbicide and hence moreefficient crop growth and less environmentaldamage. Varieties of maize and rice have also

1 Look in the supermarket for examples of‘instant’ and ‘ready to eat’ products. Identifywhich of these contain modified starch that isacting as a stabilizer or thickening agent.

2 Prepare a number of drinks (e.g. cups of tea)with different sweetening agents – try to useexamples of each chemical type, as well assugar. Test these on several volunteers tostudy any perceived differences in taste andsweetness detected.

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been developed, which have advantages in termsof nutrient composition or yield over the moretraditional varieties. For example, the proteinand vitamin A content of rice has been enhancedto improve dietary balance. It is anticipated that,in the future, more beneficial amino-acid profilesor higher meat yields can be engineered into ani-mals. Higher levels of antioxidants are beingbred into tomatoes. The removal of potentialallergens from foods, such as wheat, is anotherexciting area of research, which would help indi-viduals who are unable to consume gluten.Similarly, research on allergens in peanuts mayyield a non-allergenic product. Slower ripeningallows crops to be preserved better with fewerlosses.

There is concern that introducing alien genesinto plants may have adverse consequences forthe humans who consume these, and a consider-able amount of resistance to the introduction of foods containing GM components. Carefultesting for safety and long-term trials are neces-sary to ensure that these products are safe. Clearlabelling of products that contain GM ingredi-ents is also called for by consumers, andEuropean legislation has been reviewed in thelight of concerns and will be monitored in thefuture.

Functional foods

This is the largest category of smart foods andalso the most diverse. The functional food mar-ket in Europe was estimated to be worth $55billion in 2000, and is rapidly expanding. Afunctional food may be defined as one havinghealth-promoting benefits, and/or disease pre-venting properties over and above the usualnutritional value. This definition can cause dif-ficulties in that some common foods could beconsidered to be covered by this definition. Forexample, many vegetables provide non-nutritivephytochemicals, which are believed to havehealth-promoting benefits but do not contributeto the accepted nutritional value of the vege-table. It has been suggested that functionalfoods might be better viewed as a concept thatcan help to optimize nutrition rather than ameans to categorize them.

Nevertheless, it is useful to consider the dif-ferent types of products that could come intothis group.■ foods containing added (fortified) or reduced

levels of nutrients – these may be nutrientsthat would normally be found in the productor ones that are not typical of the food;

■ foods containing phytochemicals, that is,components with no known nutritional rolethat are promoted as such in the diet, orhave added levels of some phytochemicals;

■ foods containing added components that donot occur generally in the typical diet, withthe specific aim of producing a functionaleffect;

■ foods containing bacteria that are used topromote gastrointestinal tract function.

The following sections will consider examplesof foods/food components in each of these cate-gories and some of the evidence for their use asfunctional foods.

Fortified foodsThis group includes foods that have been forti-fied with macronutrients or micronutrients. Ona global basis, food fortification is an importantstrategy for combating specific nutrient defi-ciency that may be prevalent in a community.Notable examples of this include fortification ofsalt with iodine or the use of various vehicles asa medium for increasing iron intakes. In suchnational schemes, it is important to choose bothan appropriate food for fortification, which rep-resents a regular item in the diet, as well as thebest form of the mineral or vitamin to maintainthe stability of the food product, and maximizebioavailability of the nutrient.

There is no widespread single nutrient defi-ciency in the UK, yet there are a great numberof fortified foods available aimed at promotinghealth rather than preventing deficiency. Theseinclude white bread and flour, which are requiredlegally to have thiamin, iron and calcium addedto restore the content to that found in whole-meal flour. This was introduced to protect thehealth of the population following World War II,but has been maintained ever since, althoughthe nutritional need for this is arguable. In theUSA, folate is added to flour; but this is not the

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case in the UK, following a decision taken by theFood Standards Agency in 2002, after a wide-ranging consultation. Margarine is required bylaw to be fortified with vitamins A and D, toprovide levels of these vitamins that are com-parable to those in butter. Many of the otherspreading fats are also fortified with these vita-mins. Breakfast cereals are voluntarily fortifiedwith a wide range of nutrients; however, this isnot a legal requirement. The range of nutrientsadded, and the level of fortification variesbetween products and from time to time in thesame product (see Figure 17.1).

Infant milks and foods contain various addednutrients to enhance their nutritional value.There are guidelines on the levels of nutrientsthat should be provided in foods for infants.Other products that are fortified include instantmashed potato, bedtime drinks, yogurts, softdrinks, condensed milk and dried milk powder.The range of fortified foods available is not con-stant and it is interesting to note the informationon food labels to keep up to date with products.Most of the examples mentioned above containadded nutrients that would be found in a more‘natural’ form of the food. However, there arenow exceptions to this, with nutrients beingadded that would not be found associated withthe product. An example of this is the addition ofcalcium to orange juice. Currently, it is difficultto add some nutrients to foods because of thetechnological difficulties of dispersal, taint andstability of the products. However, micro-encap-sulation of nutrients may expand this field fur-ther in the future. One group of nutrients being

considered in this context is the n-3 fatty acids,which could be added to some foods in the futurein this way. Similarly, calcium can be added tosoya milk in an encapsulated form that avoidsprecipitation of the soya protein.

Reduced content of nutrientsThis group contains foods mostly for the weight-reduction market, with a wide range of productsthat are ‘low calorie’ and, therefore, to be used‘as part of a calorie-controlled diet ’. Theseinclude individual products, such as drinks, bis-cuits, yogurts and whole meals, available as‘ready meals’ that have been ‘calorie counted’. Afurther range of foods are ‘low-fat’ products,which represent a separate area of the market.These are not necessarily lower in energy con-tent than a corresponding regular product, asthey may contain other energy-containing con-stituents within the formulation, but do meet

Figure 17.1 Examples of fortified foods.

1 Look at some of the foods mentioned in thissection in a grocery store or supermarket.For each of the foods:a Note the added nutrients, how much is

added and how this relates to the referencenutrient intake (RNI).

b What fraction of the RNI does the food provide?

c How much of the food would need to beeaten each day to meet the RNI – is thisrealistic and feasible?

d Is there any indication on the label of thetarget consumer group for the product?

2 Try to find some examples of foods with addednutrients that would not normally be found inthe food (as in the case of orange juice men-tioned above). Why do you think these foodshave been chosen for fortification with theseparticular nutrients?

3 List the advantages and disadvantages of for-tifying foods with nutrients. If possible, thinkabout the different situation in industrializedand developing countries. Discuss your find-ings with other members of your group.

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regulations of having lower percentage fat thanthe regular product.

Specific alterations to other constituentsmay include reduced sugar or salt content. Anumber of specific dietary products are marketedto meet the demand for foods that are free froma specific component, such as gluten-free prod-ucts for people with coeliac disease. Otherexamples may include products that are freefrom lactose, sucrose, milk or egg.

Foods containing phytochemicalsVegetables and fruit have been promoted as partof a healthy diet for many years and, since the1990s, there has been specific advice to includefive portions, or 400 g, of these in the daily diet.Both fruit and vegetables contain a number ofvaluable nutrients but, in addition, it has beenrecognized that they are rich in non-nutritivesubstances, known as phytochemicals. Theseoccur in plants and products made from plantsat varying concentrations. Amounts are rela-tively low in the storage parts of plants, higherin the fruiting parts, and highest in the seeds andparts that are dried and concentrated for use asherbs and spices. The latter, however, are gener-ally used in small amounts and, therefore, maynot represent an important dietary source. Ingeneral, the phytochemicals are produced by theplant as a defence against predators, and are bit-ter, acrid or astringent in an attempt to make theplant unpalatable or toxic. As a result, humanstoo may find these substances unpleasant, andthis may be a strong disincentive to consumefoods that could be good for our health but maynot agree with our palate. A challenge to thefood industry, both in the past and future hasbeen to breed varieties of plants in which thebitter taste is reduced, while at the same timeattempting to ensure that the beneficial effectsof the phytochemicals are preserved or enhancedby selective breeding. Extracting the activeagent and adding it to other products is a pos-sible developmental step. This has already happened with the use of isoflavones from soyain some types of bread.

The interest in phytochemicals stems fromthe strong link between diets rich in plant foodsand lower rates of cancer and coronary heart

disease. The diversity of these compounds cre-ates an enormous task to study the roles of indi-vidual phytochemicals in disease prevention orrisk reduction and, at present, the evidenceoften relates to groups of related compounds.Several different mechanisms of action havebeen identified, usually by in vitro study. Theseare briefly reviewed in the following sections.

Phenolic compounds, including flavonoidsHigher concentrations of phenolic compoundsare generally found in young sprouting plantsor seedlings than in the mature plant, in linewith their role as protection against predators.Immature fruit, such as apple or grapefruit, arevery bitter because of the presence of thesecompounds.

There are over 5000 different flavonoids;many are responsible for the colour of flowers,leaves and fruit. They are generally bitter orastringent. The various flavonoids differ accord-ing to their molecular structure and occur in different sources. Flavones, include rutin andquercetin, and are found in apple skins, broccoli,grapes, olives, onions and parsley. Quercetin isthe most important contributor to the estimatedintake of flavonoids, mainly from the consump-tion of apples and onions. Flavanones, includinghesperetin, are predominantly found in citrusfruit and their peel, and contribute to the bitter-ness of these fruit. The catechins occur in greenand black tea, and red wine (from both the seedsand skins of grapes). They contribute substan-tially to the bitterness of Japanese green tea.Catechins are also thought to be responsible forthe bitter taste of chocolate. Finally in this groupare anthocyanins, which are darkly coloured andoccur in richly coloured fruit such as berries,cherries, grapes, wine and tea.

In addition, there are high-molecular-weightpolyphenols, also known as tannins, which arefound in sorghum, millet, barley, peas, dry beansand legumes, fruit, tea and wine. Tannins forminsoluble complexes with proteins and starches,and reduce the nutritional value of foods.

The most researched property of all of theflavonoids and phenolic compounds is theirantioxidant activity. This may include limitingthe production of reactive oxygen species,

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stabilizing white blood cells and scavenging freeradicals. All of these result in less low-densitylipoprotein (LDL) oxidation and potential forendothelial damage. In addition, flavonoids havebeen proposed as having other roles includinganti-inflammatory, antitumour, antithrombo-genic, and antiviral roles. However, much of thesupporting evidence is based on small studies orin vitro research, and conclusions cannot bedrawn. More research on phenolic compoundsand flavonoids is required, together with moreinformation about the bioavailability of thecompounds, and more analytical techniques formeasurement of intake and excretion levels.

In the meantime, it is important that theknown dietary sources of these compounds areencouraged in the diet, to maximize the diver-sity of intake and benefit from them.

Dietary phyto-oestrogensPhyto-oestrogens are present in plant foods; thetwo major subclasses are isoflavones and lig-nans. The majority of interest has been focusedon the isoflavones, of which the major examplesare genistein and daidzein, which are found insoya beans and products derived from themincluding textured vegetable protein, tofu andsoya milk. The richest source of lignans isflaxseed (linseed); however, many fibre-richfoods contain small amounts, including lentils,sweet potato and oat bran. More accurate ana-lytical data are needed. A more potent phyto-oestrogen has recently been discovered in hops,and more sources may yet be discovered.

Phyto-oestrogens have been shown to exert awide range of hormonal and non-hormonaleffects in animal and in vitro studies. In addition,epidemiological evidence indicates that, in Asiancountries, where the habitual daily intake ofisoflavones is between 20 and 50mg/day, there isa lower incidence in women of many hormone-dependent diseases, such as coronary heart dis-ease, menopausal symptoms, osteoporosis andbreast cancer. Women in communities wheresoya beans are eaten tend to have longer men-strual cycles, by 1–2 days. This can relate to 2 fewer years of menstruating life, less ovarianactivity and possibly reduced breast cancer risk.In Japanese men, the incidence of clinical

prostate cancer is significantly lower than inAmerican men and prostatic tumours developmore slowly. Benefits in terms of coronary heartdisease and osteoporosis also apply in men.

Interest in the phyto-oestrogens arosebecause of their structural similarity to mam-malian oestrogen. The compounds were shown toact both as oestrogen agonists (mimicking theeffects of the hormone), as well as antagonists(blocking the action of the hormone). The vary-ing effects are attributable to the existence of twodifferent oestrogen receptors in specific tissues,which result in varied responses. Target tissuesinclude breast, ovaries and uterus, brain, bone,lungs, blood vessels, kidneys, adrenals, testes and prostate. In addition to oestrogen relatedresponses, phyto-oestrogens have also beenshown to alter steroid metabolism, increase sex-hormone binding in the blood, act as anti-oxidants and reduce thrombogenesis. At present,these effects have not been fully tested in clinicalstudies, although small short-term studies havereported benefits in menopausal symptoms andbone loss. There is much to discover about thebioavailability of the phyto-oestrogens fromdietary sources, the levels achieved in the bloodand at active sites, and the amounts required toproduce a clinical effect. Studies also indicatethat there is considerable individual variation inthe metabolic fate of the compounds and thismay make recommendations about dosage verydifficult to predict. These compounds represent achallenge to the functional food market, in tryingto balance a beneficial health effect with accept-ability and safety. One of the problems with soyaproducts is their bitterness; the food industrymakes attempts to reduce this, but may at thesame time remove the beneficial isoflavones.

GlucosinolatesThese compounds occur mostly in the cruciferousvegetables (cabbage family), including broccoli,cauliflower, turnips, Brussels sprouts, cabbageand kale. In vitro studies suggest that glucosino-late compounds, such as sinigrin and progoitrin,induce enzymes that inactivate carcinogens byneutralizing their toxic properties and speedingtheir elimination from the body. In addition,products derived from glucosinolates during


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digestion, including isothiocyanates, are alsoreported to block the effects of carcinogens.Clinical studies have so far not been able to sup-port these findings. However, diets high in crucif-erous (and other) vegetables are linked inepidemiological studies with lower cancer rates,including lung and alimentary tract. One of themajor practical problems for food scientists is thebitter taste of many of the vegetables in this fam-ily. Selective breeding, genetic modification andalteration of growing conditions are all beingused to decrease bitterness and increase con-sumer acceptability, while protecting the contentof active agents.

CarotenoidsCarotenoids are fat-soluble pigments found inmany fresh fruit and vegetables. Initially, theywere of nutritional interest because of the role ofbeta-carotene as a major precursor of vitamin Ain the body; other carotenoids have lower levelsof provitamin A activity. The total amount ofcarotenoids taken up from the diet is relativelysmall and a regular intake appears to optimizeabsorption. It is now known that some 600carotenoids exist and at least 40 have been isol-ated in foods. The association between plasmalevels of beta-carotene and cardiovascular diseasehas been reported in a number of epidemiologicalstudies. However, supplementation trials usingbeta-carotene have not replicated the beneficialresults. For example, a study in smokers resultedunexpectedly in a higher incidence of lung cancerand heart disease (Omenn et al., 1996).

Although a specific physiological role forcarotenoids has not been clearly defined, theyhave been shown to possess antioxidant activityand, as such, are of interest in reduction of dis-ease risk. It should be remembered that antioxi-dants donate an electron to stabilize a free radical.In so doing the antioxidant itself becomesunstable, with the potential to become a free rad-ical and propagate a chain reaction. It is essen-tial, therefore, that there are other antioxidantsto repair and maintain the system. One suchagent is believed to be vitamin C. This illustratesthe importance of having adequate and compa-rable levels of various antioxidants in the bodyand may explain why large amounts of one of

these may be more harmful than protective (seeChapter 14 for more on antioxidants). Thus, anysupplement that provides additional carotenoidsshould also contain adequate vitamin C.

Lycopene, an acyclic form of beta-carotene,has been found to be a more potent antioxidantthan beta-carotene itself. In vitro studies sug-gest that it protects LDL against oxidation.Lycopene is one of the major carotenoids in theWestern diet, being found in tomato and tomatoproducts. Intake levels are lower in developingcountries. Other sources include pink grapefruit,watermelon, guava and apricot. An epidemi-ological association has been reported betweenlow plasma levels of lycopene and prostate can-cer in the USA. A study in Finland recentlyreported an excess incidence of acute coronaryevents and stroke in association with low levelsof lycopene.

Lutein is a major pigment in chloroplastsand, as such, is one of the five most commoncarotenoids in the diet. Together with zeaxan-thin (which is similar in structure), it is found inthe macular region of the eye, which is theregion of the highest visual discrimination, butalso the most light-sensitive area. This area is,therefore, very vulnerable to damage by freeradicals produced by light interacting with oxy-gen in the blood. Over time, this can result inmacular generation (age-related macular degen-eration; AMD) and blindness. This is the com-monest cause of blindness in Western society. Itis particularly common in smokers, in whomlevels of lutein have been shown to be lowerthan the population average. Lutein absorbs bluelight and, as an antioxidant, quenches free rad-icals. Lutein cannot be synthesized in the bodyand, therefore, a dietary intake is needed tomaintain serum levels; active transport mech-anisms concentrate lutein in the macula. Thereare high levels of lutein in breast milk. In add-ition, lutein is found in green leafy vegetablesand in orange/yellow fruit and vegetables.

All of the phytochemicals discussed abovehave potential roles in risk reduction and healthpromotion. The evidence for most of them is, atpresent, based largely on in vitro or animal stud-ies, with only a few clinical studies. However,epidemiological data support the link between

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intakes of fruit and vegetables in the preventionof a number of diseases. Food scientists candevelop varieties in which the active agents areenhanced but, in the mean time, five servings aday of fruit and vegetables remains sound nutri-tional advice.

Foods with added componentsDesigning foods with a specific health purposemay involve adding an ingredient that is notusually present in foods, or present in onlysmall amounts in the food.

Phytosterols are compounds that are struc-turally similar to cholesterol and are currentlybeing used in a range of products as cholesterol-lowering agents. Phytosterols are thought tohave been present in the diet of our ancestors inmuch greater amounts than occurs currently.Intakes of naturally occurring plant sterols arehigher in vegetarians than in omnivores. Theplant sterols currently used are extracted fromsoya bean oil or pine tree oil and are esterified toincrease solubility. The most common are sitos-terol, campesterol and stigmasterol. Productsmay contain plant sterol (unsaturated) or plantstanol (saturated) esters, and evidence showsthat both have a similar capacity to lower circu-lating total and LDL cholesterol levels. The phy-tosterols reduce the absorption of cholesterolfrom the small intestine by forming insolubleparticles with cholesterol, and by competingwith cholesterol for bile that would facilitateabsorption. Thus, a greater proportion of dietarycholesterol is excreted, although some of thephytosterol is absorbed. Absorption is estimatedas no more than 5 per cent of the phytosterol.The liver does compensate for reduced choles-terol absorption by increasing synthesis ofendogenous cholesterol, but the net effect is areduction of total cholesterol in the body.

These effects are achieved with relativelysmall doses of the phytosterols. As little as 1g/daymay have an effective lipid-lowering effect,although a dose of 1.6 g/day of plant sterol isrecommended. There appears to be a plateaueffect with no further reduction of cholesterolseen at intakes above 3 g/day. The averagereduction in cholesterol levels is in the region of 5–8 per cent from spread alone and, when

combined with other lipid-lowering measures inthe diet, or drug treatments, levels of cholesterolmay be reduced by 10–15 per cent. The dispersalof the phytosterol within the food productappears to be the key determinant of its effectiveness.

There has been some concern expressedabout the potential for reduced absorption offat-soluble vitamins, as a consequence of phy-tosterol ingestion. Lower plasma levels of vita-min E and carotenoids have been reported, butthese effects are considered to be marginal.

Although developed as an aid to the man-agement of blood lipids levels in cardiovasculardisease reduction, new evidence suggests thatthe plant sterols may also have a role in inhib-ition of tumour growth.

Plant sterols and stanols are currently mar-keted as a range of spreads, dairy goods, such asyogurt and cream cheese, and salad dressing.

Omega-enriched eggsA range of eggs is on sale in the UK from chick-ens that have been fed on a vegetarian seed-richdiet containing n-3 fatty acids. This results ineggs enriched with these fatty acids. This illus-trates how manipulation of the nutritional con-tent of a product can be achieved. The eggsform a small part of the total egg sales in theUK, but can provide up to 70 per cent of the cur-rently recommended level of n-3 fatty acids inone egg.

Clinical usageIn clinical nutrition, feeds are being producedthat contain ‘functional’ components for whichthere is believed to be an additional need in par-ticular circumstances. Glutamine is an import-ant fuel source for rapidly dividing cells, forexample, those lining the gastrointestinal tractand blood cells. Severely ill patients may be atrisk of receiving insufficient glutamine to meettheir increased demands. Supplemental glutam-ine may improve gut mucosal and immunefunctions, and reduce episodes of clinical sepsis.Trials have shown reduced mortality, lowerinfection rates and shorter hospital stay.

Arginine is also a conditionally essentialamino acid in states of trauma and sepsis, and


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arginine-containing formulas may reduce com-plications in surgical patients.

Sports productsThe sports nutrition market contains a widerange of functional foods for athletes that arepromoted as supplying specific benefits over andabove basic nutrition.

The development of sports drinks containingglucose polymers allowed more carbohydrate tobe consumed, without undesirable effects interms of sweetness and palatability as well asexcessive osmotic effects. Products, such ashigh-energy bars, also provide a large amount ofenergy in a very small volume of food, allowingenergy needs to be met. Glycerol is now includedin some sports drinks as research has suggestedthat this can promote hyperhydration, althoughthe evidence is equivocal.

A huge range of products that have poten-tial use as ergogenic aids is marketed and can beconsidered as functional foods. Some of theseare summarized in Table 17.1.

Although there is a theoretical potential for a metabolic effect for some of the functionalproducts available for athletes, the actual abilityof the substances to reach the target site and be

incorporated into the cellular or subcellular meta-bolic machinery is usually not proven. Muchmore research is needed to examine possiblebeneficial effects of putative ergogenic agents,as well as their safety.

Foods containing bacteriaThe contribution to human health of bacteria resi-dent in the gut is increasingly recognized. Morethan 500 different bacterial species inhabit thehuman gut, amounting to about 1 kg in weight.Some of these are considered to be beneficial andhealth promoting, some benign and some harm-ful or pathogenic. The balance of these bacteria isimportant and a predominance of one group overanother can alter the risk or progression of dis-ease, and the health and function of the colon.Longevity had been noticed among groups of theworld population who consumed fermented dairyproducts that were believed to reduce levels oftoxin-producing bacteria, thus suggesting thatthe dietary intake may have an influence on thehealth of the bowel and the organism.

Far from being a passive excretory route, thebowel is now understood to be a metabolicallyactive organ that provides a protective barrierfor the host through effects on the immune

Functional foods in sports nutritionTABLE 17.1Dietary constituent Suggested role Strength of evidenceAmino acids

Arginine, lysine, ornithine Promote growth hormone secretion Weakand aid muscle development

Glutamine Prevents immunodepression, Some experimental evidencereduces infections

Caffeine Promotes fatty acid release, Can be beneficial, within sparing glycogen stores legal limits

Carnitine Central role in energy production, Weakcould enhance aerobic performance

Coenzyme Q10 Needed for generation of ATP WeakCreatine Increases capacity for repeated Good

bouts of high-intensity exerciseGinseng Increase mental energy and stamina WeakSodium bicarbonate Increased alkaline reserve to May be effective in specific

buffer lactic acid produced circumstances. Gastrointestinalin anaerobic exercise effects unpleasant

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system. The protection exists at various levels,in terms of physical exclusion of the antigen,elimination of antigens that have penetrated themucosa and finally control of any antigen-specific immune reactions. In order to be able toperform these functions, the gut depends onboth appropriate nutrients as well as a benefi-cial microbial balance.

In addition, metabolism in the bowel mayprovide between 7 and 10 per cent of the dailyenergy supply through the fermentation of carbo-hydrates and proteins (to a lesser extent). Some60–80 g of the food ingested each day reachesthe colon; the microflora degrade this by fer-mentation to lactic acid and short-chain fattyacids, as well as carbon dioxide, hydrogen,methane, phenolic compounds, amines andammonia (see Figure 17.2).

In the past, there was a frequent challenge tothe gastrointestinal tract by microorganismspresent in the environment and in food, and thisprimed the immune system to function normally.Our increasingly clean and processed envir-onment, with foods containing artificial sweet-eners, preservatives and even antibiotic residuesreduces the microbial challenge and results in an underperformance of the immune system.Modern lifestyle, with poor eating habits, stressand use of antibiotics can all contribute to alter-ations in the microflora. It is believed that thismay be one of the mechanisms whereby therehas been an increase in chronic inflammatorydiseases, including eczema, asthma, allergies,Crohn’s disease, inflammatory bowel disease andulcerative colitis.

The gut of the newborn infant is sterile butbecomes colonized soon after birth. The methodof feeding determines the bacterial flora, withlactobacilli and coliform bacteria and bifidobac-teria prevailing in the breastfed infant. Formulafeeding induces a wider microflora, which additionally includes Bacteroides, clostridia andstreptococci. After weaning the microflorabecomes similar to that of the adult, with a pre-dominance of anaerobic bacteria, which die inthe presence of oxygen. Among these, the bifi-dobacteria and lactobacilli are considered to bebeneficial to health, and some, such as certainEubacterium spp., are benign but suppress thegrowth of harmful bacteria. Examples of the latter include proteolytic Bacteroides spp., manyClostridium spp. and pathogenic species ofEnterobacteriaceae. Many other microorganismsare present in the bowel, some of which have notyet been characterized, and there is moreresearch required.

Probiotics have been developed, therefore, asan aid to restore the immune function of the gutand to reduce the incidence or symptoms of asso-ciated clinical conditions. Thus, probiotics can bedescribed as products that contain live micro-organisms in fermented foods, which could pro-mote good health by establishing an improvedbalance in intestinal microflora. The main organisms currently used are various species oflactobacilli and bifidobacteria, together with anon-pathogenic yeast, Saccharomyces boulardii.

A probiotic product must fulfil several criteria including safety, ease and reproducibilityof production, and stability during storage.

Figure 17.2 How microflora areused in the bowel.


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Furthermore, the organisms should be able tosurvive in the digestive tract and colonize thebowel in adequate amounts to be able to providebenefit to the host. Although there is evidencefrom in vitro and animal experiments of benefi-cial effects of probiotics, clinical studies inhumans are still at a relatively early stage. Mostevidence exists for the reduction of diarrhoeaand prevention of gastroenteritis, especially ininfants and young children. In adults, antibiotic-induced and hospital-acquired diarrhoea hasbeen shown to be better controlled with the useof probiotics as part of the treatment. Probioticscontaining lactobacilli have also been used suc-cessfully in cases of lactose malabsorption. A study in older adults showed an improvementin several aspects of cellular immunity after 3 weeks of probiotic use, especially in those withlow immune status at baseline. Some evidenceof an immune system stabilizing effect has alsobeen found in inflammatory bowel conditionsand atopic eczema. There is still a lack of goodevidence, however, that probiotics can preventcancer, reduce plasma cholesterol levels or reducelevels of Helicobacter pylori infection in thestomach. Major advances in studying the mech-anisms of action of probiotics, and gut structureand function in vivo are needed to further clarify the potential benefits and better targetspecific organisms for particular health needs.

Microorganisms require a substrate on whichto grow and multiply. If this is not provided inthe diet, the microflora can be compromised. Thisis the basis of the use of prebiotics, which arenon-digestible food components that reach thecolon where they can selectively stimulate thegrowth of beneficial microorganisms. In manyways, this definition is similar to that for compon-ents of dietary fibre, although these do not sup-port the growth of one type of microorganismalone. Candidates for prebiotics are the oligosac-charides containing fructose (fructans). A natur-ally occurring example of this group is inulin,although other fructans are found in wheat,onions, bananas and chicory. Oligosaccharidescontaining xylose, galactose and mixtures ofthese sugars have also been studied. The mostpromising results have been obtained withfructo-oligosaccharides (FOS), which were shown

to stimulate growth of bifidobacteria in the colonand change the balance of microflora. Lactulose(containing galactose and fructose) has also beenused in a number of clinical trials and found topromote growth of lactobacilli. Prebiotics may beuseful in the management of constipation, owingto the osmotic effect associated with increasedbacterial fermentation. Increased acidity in the bowel has been suggested to be beneficial inthe absorption of a number of minerals, mostnotably calcium.

As with all of the other functional foods,however, more randomized controlled trials areneeded to confirm this effect and any associatedhealth benefits.

Prebiotics are found in a range of foods inEurope, including dairy products, infant formulaand bakery products (see Figure 17.3).

Organic food

The concept of organic food is in many ways theopposite end of the spectrum from the functionalfoods discussed above. Organic foods representmore traditional food production methods, with-out the use of man-made chemical agents topotentiate the yield or reduce pest damage.Organic farming systems rely on traditional con-cepts of crop rotation, the use of animal and plantmanures, and biological methods of pest control.The market in organic foods has increased rapidlyin the last 5–10 years, as consumers have becomeconcerned about the perceived safety of mass orintensively produced foods. Such concernsinclude the presence of pesticide, growth pro-moter and antibiotic residues. In addition, theremay be concerns about the presence of known(such as bovine spongiform encephalopathy; BSE),or unknown disease causing factors in the foods.

Although the primary concern may be one of food safety, organic food is also perceived ashaving superior sensory attributes and being‘healthier’. This is taken to mean that food pro-duced organically has a higher nutrient con-tent. Williams (2002), in reviewing the evidenceon nutritional quality of organic food, notes thatthere is no evidence in the scientific literature tosupport these claims. There are methodologicalshortcomings in most of the publications that

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report on nutritional quality of organic versusconventionally produced foods. Many cover along time period, during which there have beenmany changes in the production methods. Com-parisons of effects of feeding experiments in ani-mals produce inconsistent and conflicting results.No studies of effects on human health have beenperformed. Some data show that conventionallyproduced vegetables, especially green leafy vege-tables may have a lower vitamin C content. This isassociated with a higher water content producinga dilution effect. Conventionally grown plantsgrow more quickly and are harvested sooner thanthose grown organically, resulting in a higherwater content. Nitrate levels were also higher inthe conventionally grown leafy vegetables, prob-ably associated with fertilizer use. There is no evi-dence of a negative impact on health from thesedifferences. An area of potential interest that hasnot been studied is the level of various phyto-chemicals contained in plants. These are producedby plants as a protection against adverse condi-tions or to combat attack by potentially damagingpests or diseases. It is possible that levels may be

higher in organically grown products that are lessprotected by sprays. However, there has been nostudy of this area.

It should also be remembered that organicfood may carry a higher level of microbial con-tamination, through the application of manureor the unchecked growth of fungi or bacterialcontaminants.

Much of the organic food available for sale inthe UK is imported. This has possible implicationsfor its freshness and associated nutritional con-tent. It is also more expensive than conventionalproduce. As a result, a substantial proportion ofthe population are unable to afford organicfoods. If they choose to buy organic produce, thismay be at the expense of other items in the dietthat could have contributed more to a healthybalance. Where money is not an issue, individ-uals can buy organic produce without fear ofcompromising the balance of the rest of their diet.

In summary, it is more important to concen-trate on consuming a diet in line with healthyeating guidelines, as there is much more goodscientific evidence to support this than to worry

Figure 17.3 Probiotics and prebiotics.


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about any risk to health of conventionally pro-duced foods that might be avoided by eating‘organically’. At present, there is insufficient evidence to support any benefit to health of‘organic’ food, and more research is needed toclarify these issues.

Conclusions

The concept of optimal nutrition opens a new erain the science of nutrition. Advances in know-ledge about molecular biology and the character-ization of the human genome will make itpossible at some point in the future to studygenetic polymorphisms that are associated withparticular diseases. It is likely that these will alsocharacterize individual responses to particulardietary components. We will also have a clearerview of the molecular mechanisms of nutrientaction. An understanding of how genetic poly-morphisms affect nutrient metabolism may makeit possible to design specific dietary regimes totackle nutritional problems, or disease risk. It islikely to become the responsibility of the food

industry to develop products that help to fulfilthese goals.

Nevertheless, although progress in recentyears has been rapid, the preceding sections haveindicated how little is known in some cases aboutmechanisms at cellular and tissue level. This ishindered by a lack of biomarkers and specifictools for identification of processes, for example,within the gut mucosa. Properly controlled large-scale clinical trials need to be performed to evalu-ate the potential benefits of products, andcaution needs to be exercised when claims aremade that have not been properly evaluated andcause confusion among consumers. Safety aspectsmust also be addressed, if new products aredeveloped.

In the mean time, consuming a balanceddiet following healthy eating guidelines is ourbest guarantee of optimizing nutrition fromfood. This, after all, is what has sustained thehuman race over thousands of years, and shouldnot be forgotten in the rush for new designerfoods that offer promises of better health anddisease reduction.

1 Optimal nutrition is a concept that encompasses positive benefits of food in the promotion of health.2 Foods with altered nutritional contents have been produced to address some issues of ‘healthy eating’.3 Some of the more researched food components have been introduced into foods to produce potentially

health-promoting products.4 There are many other components of food that have no known nutritional role but may modify the risk

of disease.5 The use of bacteria to promote gut health is a novel approach to optimizing nutritional state.

SUMMARY

1 Debate with a partner what are the argumentsfor and against more development of smartfoods. You could consider:a are they useful for all people?b should they be targeted at specific groups? –

if so, give examplesc which foods should be promoted and which

allowed to disappear?d are there other smart foods that you think

might be useful?

2 You could imagine that you are an ExpertCommittee and have to decide on permissionfor the development of some new products.What would you need to know?

3 Survey a number of people in your communityto discover how many buy organic foods.a Which foods are commonly bought, and what

are the perceived benefits of choosing these?b What foods are they replacing in the diet,

and does this lead to better or poorerbalance of healthy items?

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Buttriss, J., Hughes, J., 2000: A review of the MAFF optimal nutrition programme: aims and objec-tives. British Nutrition Foundation Nutrition Bulletin 25, 79–80.

Cassidy, A., Faughnan, M. 2000: Phyto-oestrogens through the life cycle. Proceedings of the NutritionSociety 59, 489–96.

Johnson, I.T. 2001: New food components and gastrointestinal health. Proceedings of the NutritionSociety 60, 481–8.

Kolida, S., Tuohy, K., Gibson, G.R. 2000: The human gut flora in nutrition and approaches for itsdietary modification. British Nutrition Foundation Nutrition Bulletin 25, 219–22.

Marteau, P., Boutron-Ruault, M.C. 2002: Nutritional advantages of probiotics and prebiotics. BritishJournal of Nutrition 87(Suppl. 2), S153–7.

McConnon, A., Cade, J., Pearman, A. 2002: Stakeholder interactions and the development of func-tional foods. Public Health Nutrition 5(3), 469–77.

Omenn, G.S., Goodman, G.E., Thornquist, M.D. et al. 1996: Effects of a combination of beta caroteneand vitamin A on lung cancer and cardiovascular disease. New England Journal of Medicine334, 1150–5.

Rowland, I.R. 2002: Genetically modified foods, science, consumers and the media. Proceedings ofthe Nutrition Society 61, 25–9.

Schrooyen, P.M.M., van der Meer, R., De Kruif, C.G. 2001: Microencapsulation: its application innutrition. Proceedings of the Nutrition Society 60, 475–9.

Various authors 1999: Symposium on optimal nutrition. Proceedings of the Nutrition Society 58,395–512.

Williams, C.M. 2002: Nutritional quality of organic food: shades of grey or shades of green?Proceedings of the Nutrition Society 61, 19–24.

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Public health nutritionand health promotion


❏ review and link some of the issues discussed in earlier parts of the book in relation to increasing health throughimproved nutrition;

❏ consider some of the obstacles to improving nutrition that may exist;❏ describe strategies for health promotion and nutrition education that have been developed in recent years;❏ consider future directions.


❏ discuss the importance of nutrition in prevention of chronic disease;❏ recognize the stages involved in undergoing change and the barriers that may exist;❏ describe and evaluate some of the strategies that exist to promote better nutrition.

To develop and implement policies for the pre-vention of a disease, it is important at the outsetto make a realistic assessment of its prevalenceand the extent to which it impacts on morbidityand mortality statistics in the population. Further,if these policies are to relate to dietary intakeand nutritional goals, it is also important tomake an assessment of the role of the diet in theaetiology of these diseases and how much gaincan be expected from changes in the diet.

These are areas of controversy, generatingquite polarized opinions. At one extreme, it issuggested that, because we cannot be certainthat diet plays a role in a particular disease, weshould do nothing, with the implication that tochange could do more harm than good. On theother hand, others suggest changes based onvery weak evidence, coming from a small data-base. However, between these extremes there isa broad consensus on desirable dietary change,based on evidence from large numbers of stud-ies. Many of these have been re-evaluated usingthe technique of ‘meta-analysis’, which allows anumber of studies with similar research criteria

to be combined to increase the statistical powerof the results.

The World Health Organisation (WHO), sinceits formation in 1948, has been working toimprove the health of all the peoples of theworld. In the last two decades, it has becomeclear that there have been changes in patternsof morbidity and mortality in many countries.These have arisen from:■ reductions in maternal and infant mortality;■ better control of infectious diseases through

immunization and environmental improve-ments, although the spread of HIV infectionhas run counter to this trend;

■ increased population life expectancies owingto advances in medical technology andlifestyle changes;

■ improvements in diets in some areas.However, in parallel with these, there has been apersistent rise in chronic non-communicable dis-eases, such as cardiovascular disease, cancers,diabetes, chronic respiratory diseases and osteo-porosis. In the Western industrialized countries,these diseases have been well established for over

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40 years and, in many of these countries, therehave been decreases, especially in coronary heartdisease incidence. However, there has been anupward trend in the countries of Eastern Europeand, most notably, in the developing countries.

Many countries whose traditional diet andlifestyle had been associated with a low inci-dence of non-communicable disease have beenexperiencing a period of food transition. This istypified by an increased consumption of animalprotein and reduction in vegetable proteinsources, generally associated with a higher fatintake. In addition, the intake of carbohydratefrom the starchy staple, and minerals and vita-mins from vegetables may begin to decrease.This has been noted in Japan, where the preva-lence of obesity and coronary heart disease, bothpreviously relatively rare conditions, has begunto increase. Countries such as China and those in South America are also experiencing thistrend. In some of the poorer countries in theworld, the gradual transition to a more Westerndiet, accompanied by rapid increasing urbaniza-tion and lower levels of physical activity (as wellas smoking), is causing a rapid rise in chronicdiseases. Because of the greater numbers of people in these countries than in the developedcountries, mortality from chronic diseases hasnow outstripped on a numerical basis that in thedeveloped world. There is also concern aboutthe spread of overweight and obesity in thesecountries, and the potential for associated healthproblems, as has already happened in the indus-trialized world. These trends have been monitoredby the INTERHEALTH programme of WHO, whichstudies the risk of the major non-communicablediseases in a number of populations around theworld, as well as trends in diet and nutrition,and aims to promote and monitor community-based strategies for intervention.

In Europe, the WHO has been working todevelop a Food and Nutrition Policy by 2005.This aims to increase awareness of the linksbetween food growing, buying and eating, andthe effects on health and environmental sus-tainability. This reflects a new approach inher-ent in many nutrition policies that incorporatesconcepts of social justice and the importance offair access to food for all.

The European Community has also enshrinedhuman health protection as a part of all its pol-icies. This has led to the formulation of a publichealth framework, including an action pro-gramme, public health policies and legislation.The EURODIET project has been one aspect ofthis and aims to contribute towards a coord-inated European Union (EU) and member-statehealth promotion programme on nutrition, dietand healthy lifestyles. Progress has been madeon European dietary guidelines. Other objectivesof this project include:■ translating these into food-based dietary

guidelines within member states;■ promoting these to the population;■ identifying and overcoming barriers;■ a European Food Safety Authority to over-

see the food supply from its production toconsumption.Despite some improvements in the incidence

of coronary heart disease, it is estimated that,across Europe, the demand for treatment relatedto chronic diseases will continue to increase,because of the increases in the elderly popula-tion. It is, therefore, essential that changes inlifestyle and diet are introduced to reduce theincidence of these diseases, as clearly healthservices will not be able to cope with such hugeincreases in demand. There is, therefore, an eco-nomic benefit to be gained as well as the socialgain for individuals.

Measures to prevent chronic diseases areneeded and these are the goals of many strat-egies around the world. It is recognized that suchstrategies must take into account all aspects ofthe food chain:■ production policies;■ social policies determining access to the

foods;■ education policies to increase awareness;■ dietary guidelines to inform choice.

They must, therefore, involve the govern-ments as well as all those concerned with food.Policy makers also need to examine healthimpact effectiveness and cost effectiveness intheir decision-making. In addition, there needsto be a commitment to the strategy, which istranslated into action. Much has been learned inthe last decade about public health approaches

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that are likely to result in changes in attitudes,behaviour, risk factors, morbidity and mortality.Attention is needed to public health nutrition,which is the promotion of good health thoughnutrition and physical activity, and the primaryprevention of related illness in the population.

What is the basis of health-promoting policiesand what is proposed?

There exists public concern in Europe aboutpotential hazards associated with recent devel-opments in a complex food chain. This concernfocuses on new infections, such as bovinespongiform encephalopathy (BSE), E. coli 0157,novel viruses, and perceived environmental haz-ards from the use of genetically modified plantsand food. Yet this concern is out of proportion tothe effects on health from these sources, com-pared to the impact of dietary imbalances, whichaccount for at least 100-fold more prematuredeaths and considerably more ill health. Aboutone-third of all premature deaths in Europe arediet related and many are preventable. The costof this burden of ill health is in excess of thatcaused by tobacco use. Despite this, the budgetin most European countries for health promo-tion is on average, less than 1 per cent of thetotal health budget.

Dietary links

Over 100 expert reports, produced throughoutthe world over the previous 20 years, have beenin broad agreement about both the major chronicdiseases threatening health and the dietarychanges that are needed to reduce their inci-dence. The change in disease incidence over thelast 40 years has made it increasingly clear thatchanging environmental factors, including diet,are involved in their aetiology. Although we arenow discovering more about the role of genes inthe susceptibility to disease, these are rarely thesole factor in its development and, at present,are believed to play a much less important role than other environmental factors, such asactivity and diet. It is also unlikely that geneticchanges or mutations would have produced such

major changes in a relatively short time span.The dietary trends seen around the world point toalterations in the balance of nutrients in the diet,which parallel, in most countries, the changes indisease incidence. Inevitably, there are exceptionsthat need explanation. In some cases, a satisfac-tory explanation can be proposed; in others itawaits further research. Additional dietary con-cerns are also emerging, as our understanding ofdisease increases. Table 18.1 shows some of theproposed linkages between chronic disease anddietary factors.

Specific nutritional problems are also import-ant. Anaemia is increasingly recognized as aproblem among the female population, affectingadolescent girls in particular. Consumption offoods with low bioavailability of iron contributesto this problem, and can result in reduced phys-ical performance and lowered cognitive function.In addition, where it exists in pregnant women,poor iron transfer to the fetus will impact on itsearly development.

The increasing number of older adults resultsin a higher prevalence of low vitamin D status.This appears to be associated with low sunshineexposure, even in Southern European countries.Bone pain, difficulty in walking and acceleratedbone demineralization may all occur.

In Europe, there is still a problem with iodinedeficiency, affecting populations in the centralparts of the landmass and in mountainousregions. The use of iodized salt is an importantpublic health measure but education about itsneed is required. The consequences for maternalhealth and, in particular, the normal developmentof the fetus are profound, if deficiency exists.

Lifestyle and social factors

In addition, other aspects of lifestyle are import-ant. There is convincing evidence that physicalactivity is an essential component of health and interacts with dietary aspects in a numberof ways including:■ activity increases energy expenditure and

is, therefore, crucial for the maintenance ofenergy balance and normal weight;

■ activity increases physical fitness and thesense of well-being, and may be important

WHAT IS THE BASIS OF HEALTH-PROMOTING POLICIES? ❚

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in the control of blood pressure, preventionof colon cancer, regulation of blood glucoselevels and lowering of blood lipid level;

■ weight-bearing activity maintains bonehealth and limits demineralization of bonein later life;

■ activity helps to maintain muscle mass andsense of balance, which is important withincreasing age to preserve independence andprevent falls.The most prevailing social factor that

impacts on diet and health is that of poverty.This has increased substantially throughoutEurope in the last two decades, as a result of ris-ing unemployment, more insecure and low-paidwork, and pressures experienced by govern-ments in providing social security. All the evi-dence shows that the health experience of thesegroups is worse than in the better off, with anaverage of 5 years lower life expectancy. This is

attributable to many factors, including dietarychoices, lack of physical activity, access toshops and leisure facilities, stressful life experi-ences and an increased burden of illness. Manydietary goals have now recognized the need toaddress such social inequalities.

On the basis of existing evidence, theEURODIET team has put forward population goalsfor nutrients, some foods and lifestyle features,consistent with the prevention of major publichealth problems. These are based on a review ofthe scientific literature and represent the consen-sus view. These population goals are intended to form the basis for food-based dietary guide-lines to be developed, or that have already beendeveloped within individual countries, whichreflect the national diet. The population goalsfor Europe are shown in Table 18.2.

There has been debate about who should bethe target population for dietary goals. Those

Summary of chronic diseases and other health problems with possible dietary linksTABLE 18.1

Disease Dietary excess Dietary lackHeart disease Saturated fats Antioxidant nutrients

Total fats n-3 fatty acidsTrans fatty acids Dietary fibre

Folate

Hypertension Salt Calcium?Total fat PotassiumAlcohol

Diabetes (Type 2) Energy intake (via obesity)Cancers Total fat/energy Antioxidant nutrients

?Meat Fruit and vegetables? Salt Dietary fibre

?Dairy products

Gallstones Energy intake (link via obesity) Dietary fibreOsteoporosis ? Salt Calcium

?Animal protein ?Vitamin DFruit and vegetables

Dental disease Sugar FluorideDietary fibre

Arthritis Total energy (linked to obesity)Liver cirrhosis Alcohol ?General dietary deficiency

Dementia ?Folate?Vitamin C


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individuals with most risk factors and the mostsevere risk factors will be in greatest need ofintervention. However, they represent only asmall proportion of the total population and,therefore, reducing their risk will make little

impact on overall population morbidity andmortality. On the other hand, the majority of thepopulation will have moderate levels of risk.Improvement in these risk factors will have lesssuccess on an individual basis (because the

Population goals for nutrients, foods and lifestyle factors, consistent with the prevention of major public health problems in Europe (Eurodiet CoreReport, 2001)

TABLE 18.2

Component Population goal Background informationPhysical activity level (PAL) PAL 1.75 Maintenance of energy balance and

cardiovascular healthAdult body weight Body mass index An optimal individual BMI may be 20, and

(BMI) 21–22 Asians may be susceptible to weight-related diseases above BMI 23–24

Dietary fat (% energy) 30% The goal is for the prevention of overweight.Higher fat intakes up to 35% may beconsumed with high levels of physicalactivity

Fatty acids (% energy) These intakes are recommended in relationSaturated 10% to blood lipid levels. Stearic acid has littleTrans 2% effect on these. A lower ratio of n-6:n-3MUFAs 10–15% acids than at present is recommendedn-6 PUFAs 4–8%n-3 PUFAs 2 g linoleic

200 mg verylong chain

Alcohol (where consumed) 24–36 (men) The lower values are optimumg/day 12–24 (women)

Carbohydrates (% energy) 55% Rich in non-starch polysaccharides and oflow glycaemic index

Dietary fibre (g/day) 25 (or 3 g/MJ) Based on Southgate method of analysisSugary foods (occasions/day) 4 To reduce the risk of dental decay; frequency

of consumption is a major factor. Importantfor lifelong oral health

Fruit and vegetables (g/day) 400 These have many health-promoting properties,including non-nutritional components

Folate from food (�g/day) 400 Bioavailability from food is only 50% of thatof folic acid; needed for pregnancy and fornormal homocysteine levels

Sodium (as sodium chloride; 6 Population benefits are greater than thoseg/day) obtained if only hypertensive subjects adopt

the guidelineIodine (�g/day) 150 Essential for normal developmentExclusive breastfeeding About 6 months Promotes immunological responses, lower risk

of infection and atopic disease, reduced risk of breast cancer in mother

MUFAs, monounsaturated fatty acids; PUFA, polyunsaturated fatty acids.

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original risk is less) but, taken for the popula-tion as a whole, will amount to a greater reduc-tion in the population’s risk of morbidity andmortality.

Hence, many strategies, such as the Europeangoals shown here, are now targeted at the wholepopulation, because this will bring the greatestreduction in risk. It also provides more social sup-port for changes in dietary patterns. This does not,however, exclude an additional policy directed atthose most at risk, with more intensive and spe-cific targeting at this group. Of course, before thiscan happen, the problem of identifying those withgreatest risk must be overcome!

From goals to guidelines

In order to achieve the population goals, practicaladvice must be developed. It is recognized thatacross Europe there are different dietary patterns,so national guidelines must take into account theexisting culturally determined diet. Of course,there are many differences between intakes ofindividuals within any one country and these canprovide an opportunity to study which existingdietary pattern comes closer to the desirable goals.In recent years, dietary guidelines have movedfrom being nutrient based to being food based(see Chapter 3). In other words, instead of recom-mending that consumers ‘eat more fibre’ and ‘eatless fat’, foods that contain these nutrients areused in the recommendations. Clearly, this is eas-ier for the consumer to understand, as it coincideswith how we buy and select our daily food.

Many countries are now publishing food-based guidelines, with the emphasis on foods andthe numbers of servings to be eaten; these can

also be used to develop advice for populations at higher risk, such as those produced by theAmerican Heart Association in 2000. These rec-ommend the inclusion of fruits and vegetables,whole grains, low-fat dairy products, legumes,fish and low-fat meats. Achieving and maintain-ing a healthy body weight through physicalactivity is included as a guideline.

Several stages have been identified in compiling food-based dietary guidelines. Theseinclude identification of:■ the major food sources of the nutrients

recommended (e.g. from tables of food composition);

■ the foods contributing substantially to theintake of the population (e.g. from nationalfood surveys);

■ existing food patterns that show differinglevels of intake of key nutrients (e.g. fromindividual dietary intakes studies);

■ key foods that explain the major variation inintakes of specific nutrients in the diets ofhigh and low consumers.

With this information, it should be possible toidentify the most important foods or eating pat-terns that could be targeted for change in orderto move all dietary intakes towards achieve-ment of a dietary goal. If this can be done forseveral key nutrients or foods, then many goalscan be achieved. Guidelines can be formulatedto include choice of products, menu planning,portions and frequencies of eating that have asound basis within the target population. A fur-ther strategy may be to change the supply offood, by modifications to existing products (e.g.lowering the fat content, fortifying with a nutri-ent) or introducing new products.

Consideration of the population goals sug-gests some common themes. Reduction of fatintake and attention to the balance of fats with a reduction of saturated fat, and attention topolyunsaturated fats, especially those of the n-3family addresses a number of health issues. Thereduction in energy intake that will ensue may bebeneficial for weight loss but, in many people, itwill have to be counterbalanced by an increase in other energy sources. Most appropriate is anincrease in complex carbohydrates from cereals,grains, pulses, roots, vegetables and fruits. These

What common themes are apparent in Table 18.1that could form the basis for coordinated dietaryadvice?If you were presented with this group of suggestedlinks between diet and disease, what specificdietary changes might you recommend?Check these with the targets suggested in Table 18.2.

Activity 18.1


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will provide not only starch, but also intrinsicsugars, dietary fibre and a wide range ofmicronutrients. Among these will be folate, theantioxidant nutrients and other non-nutritionalfactors, such as the phytonutrients, which areconsidered to be important as protective factors(see Chapter 17). A shift in the diet to fewer, or atleast lower-fat animal products may also occuras fat intakes are reduced.

Thus, a series of nutrient goals may beachieved by the same changes in the diet. In the-ory, this should make the giving of dietary advicemore straightforward, as the basis of a ‘healthydiet’ will apply whatever the client’s needs.Clearly, there will be differences in emphasis, forexample, if weight needs to be lost, or if theappetite is small, as in older sedentary people orin young children.

In Britain, the Nutrition Task Force devisedthe National Food Guide (the Balance of GoodHealth), which has been adopted throughoutmany areas of nutrition education as the basicframework for achieving the nutrient goals (seeChapter 3).

The role of the Nutrition Task Force cannot,however, be viewed in isolation. It was part ofan overall strategy, emanating from the ‘Healthof the nation’ paper, which has involved manyin the move towards actually ‘adding years tolife’ and ‘life to years’. Since its publication,public health initiatives related to nutritionhave remained on the political agenda. TheDepartment of Health has recognized the import-ance of nutrition in a series of National ServiceFramework documents, published since 2000.These indicate the standards of service and carein relation to coronary heart disease, mentalhealth, older people and diabetes, and, in eachcase, include a role for nutrition. Most recently,the Food Standards Agency (FSA), created in2000, has become responsible for the public’shealth and consumer interests in relation tofood. One of the key aims is to secure long-termimprovements in the health of the population byworking to reduce diet-related ill health, withinthe UK Strategic Framework for Nutrition. Themain elements of this are:■ securing a sound evidence base for action to

promote a healthy diet;

■ developing appropriate means of informingthe general population;

■ identifying and addressing barriers tochanging dietary behaviour;

■ evaluating and monitoring the effectivenessof action taken.

This framework is intended to form the basis fordeveloping realistic and effective programmesfor the future.

It is possible to illustrate how this mightwork by considering the Nutrition Strategydeveloped by the Food Standards Agency Wales.The strategy aims to improve the diet of all thepeople in Wales, but certain groups have beenprioritised, owing to their poor diet and health,and, therefore, have the greatest potential gainfrom improved nutrition.

The top priority groups were identified asinfants, children and young people, and sociallydisadvantaged and vulnerable groups. The sec-ond priority groups were women of child-bearingage, especially pregnant women, and men, espe-cially middle aged men.

The main recommendations include:■ increase the uptake of a healthy balanced

diet to meet recommended levels for nutri-ents and micronutrients;

■ increase fruit and vegetable intake;■ develop and manage initiatives to prevent

and manage obesity and overweight;■ ensure that schemes and policies are in place

to assist improvement in healthy eating;■ provide information and training to key

players;■ ensure that the public is well informed about

the need for dietary improvement;■ ensure that local initiatives are in place

to tackle the main barriers to improvingnutrition;

■ develop and promote initiatives with thefood industry to improve healthy eating,especially relating to access to specific foods;

■ evaluate the impact of activities resultingfrom the strategy.Key players in delivering the strategy

will include policy and decision-makers, health,nutrition and catering professionals, practition-ers and educators at national and local levels,and the food production and the retail industry.

WHAT IS HEALTH PROMOTION? ❚

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Recruiting and training volunteers to becomeinvolved with local projects is important. Theapproach is, therefore, multi-dimensional andflexible, and able to focus on specific targetsand develop local initiatives suited to the needsof particular communities. Settings for theinterventions can be very diverse. They mayinclude schools, workplaces, health care loca-tions, the commercial sector (e.g. supermarkets),local clubs or day centres, or even street markets.

A systematic review of interventions to pro-mote healthy eating in the general populationhas shown that the most effective appear to:■ adopt an integrated, multidisciplinary com-

prehensive approach;■ involve a complementary range of actions;■ work at individual, community, environ-

mental and policy levels.Information provided by itself is insufficient

to produce change. Thus, any attempt to imple-ment food-based dietary guidelines needs tolearn from previous work and adopt the lessonsfrom other interventions. In so doing the diffi-cult challenge of changing diets to improvehealth will make progress.

What is health promotion?

The above discussion illustrates some of theprinciples of health promotion, these will nowbe considered in their own right.

The Ottawa Charter for health promotion,developed by the WHO (1986) outlines anapproach to health promotion that includes:■ building healthy public policies;■ creating supportive environments;■ developing the personal skills of the public

and practitioners;■ re-orienting health services;■ strengthening community action.It, therefore, demonstrates that health promotioninvolves more than just providing people withknowledge about the functions of the body andways of preventing illness, and thus helps themto maintain well-being. This part of the processcan be better described as health education, or ifit is carried out in the nutritional context, then itis nutrition education.

Nutrition education, in turn, has beendescribed as the process that assists the public inapplying knowledge from nutrition science, andthe relationship between diet and health to theirfood practices. Having the knowledge, however,is insufficient in itself to effect change. This canbe witnessed all around us most vividly in thecontext of smoking. Almost everyone knows thatsmoking is injurious to health, yet a substantialproportion of the population continues to smoke.For knowledge to be translated into action, theenvironment must be supportive of the changeand thereby enable it to happen. This includesthe political context, the social environment andthe individual’s personal environment. In add-ition, the person making the change must havethe desire and the belief that this is achievable,by the means available to them.

Thus, health promotion must be seen in awide context. It includes:■ having in existence the political and com-

munity structures that can make health-promoting changes possible;

■ providing the information about health-promoting measures to all interested andinvolved parties;

■ developing in the individual the desire towant to change towards a healthier set ofpractices;

■ showing the individual that they have theability to do this.

Briefly, health promotion has been described as‘making healthier choices the easier choices’.

In the context of nutritional improvements,the introduction of nutritional goals is acceptedas the responsibility of governments in mostcountries of the world. This was not always so.The first advice formulated about reducing fatintakes for the prevention of coronary heart dis-ease was developed by the American HeartAssociation. This government-led approach hadbeen perceived by some as unwarranted interfer-ence by the State in food intake, which is a purelypersonal matter. Nevertheless, without appropri-ate support from the government in establish-ing food production policies and legislation, forexample, for clear nutritional labelling, the con-sumer is left without adequate information tomake a choice.


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Health promotion incorporates a number ofrelated phases:■ planning;■ intervention;■ evaluation.

Planning

This is arguably the most important stage andcan determine the success or failure of the pro-gramme. Most importantly, the issue that is tobe addressed must be identified. In coming tothis decision, the planners balance the perceivedneeds with the possible benefits. This may be illustrated in the form of the ‘health gainrhomboid’ (shown in Figure 18.1). At the twoextremes, there are very few interventions thathave been assessed and shown definitely to pro-vide health gain, or to diminish it (i.e. at 1 or 4,respectively). Interventions classified as 2 wouldgenerally be considered worthwhile, but theremay be an equal number at 3 that have not beenfully evaluated and whose benefits to healthpromotion are uncertain. Where decisions haveto be taken about the use of a finite amount ofresources, most planners will chose interven-tions in the area 2, rather than 3.

A further element of the planning process is to identify the target group, since particular

interventions may be more appropriate and relevant to certain groups. This type of planningand consultation was undertaken in the prepar-ation of the ‘Health of the nation’ paper. During this period, a very large number of possiblegoals and targets were discussed, with support-ers of each putting forward strong arguments.Eventually, only a small number of goals wereidentified, although these were chosen becausethey were believed to be the most appropriate toachieve the maximum health gain. This has alsobeen described in the case of the Food StandardsAgency Wales Nutrition Strategy.

A further aspect of planning includes takingaccount of the nature of the problem, for example, by collecting data about morbidity andmortality statistics. Perhaps also at this stage it isimportant to consider the lifestyle aspects of thetarget community. When this is being done atnational level, the variation among communitieswithin the country makes this more difficult.

Finally, general aims and specific objectivesare formulated, taking into account the nature ofthe existing problem and the potential changeexpected. This, in turn, depends on existingknowledge, attitudes and behaviours of the target group. A very important consideration isthe readiness to change on the part of the target.This has been studied extensively and a modeldeveloped that shows change as a process com-prising several stages (Table 18.3). It will benecessary to consider what aspects of the pro-gramme will facilitate people moving from onestage to the next in the change process.

In the UK, the information about food intakesis available from National Food Survey data andfrom National Dietary and Nutrition Survey data.

Applying this in the nutrition context, the nutri-tionist or dietitian wants people to adopt healthiereating practices. Ways must be found to makethese ‘the easier choices’.■ Who will need to be involved? Think of all

the parties concerned in the food productionchain.

■ What does the consumer need to know aboutthe healthier choice?

■ How will the consumer be convinced to trythis out?

■ What might the obstacles be and how canthey be tackled?

In working through this activity, you should findyourself referring back to the key points madeabove about health promotion.

Activity 18.2

Figure 18.1 The health gain rhomboid.

WHAT IS HEALTH PROMOTION? ❚

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Intervention

An obvious but important element of this stageof the process is the decision on the methodologyto be used. This should take into account infor-mation about previous uses of this methodologyand their level of success. Constraints that mightexist must be taken into account. For example, ifthe promotional material is presented in a writtenform, this necessitates that the target group can,and wants to, read. Computer-based images maybe more appealing to young people than thewritten word. Thus, the methodology must beflexible and adaptable to meet the objectiveswith all of the targets.

The FSA Wales is employing a variety ofinterventions. Breakfast clubs have been set upin some schools, which can provide a healthystart to the day and encourage children to inter-act. Nutrition and health education activities inthe workplace are increasing awareness of thelinks between diet and cancer in middle-agedmen. Midwives working with vulnerable groupsare teaching about meal planning and budgetingto reduce the numbers of low birthweight babies.Local grocers are involved in delivering fruit toschools as part of a school tuck shop scheme.Fitness training in a local club for young peopleis being linked with some nutrition education aswell as smoking, drugs and alcohol education.

Evaluation

The process of health promotion may be seen as cyclic. The evaluation of one programme maygenerate questions and proposals for an improvedprogramme, which can start with another plan-ning stage. No programme can be brought to a

conclusion without evaluating what it hasachieved. In the case of health promotion, changesin some of the measures that were used at theplanning stages may be indicative of success.These may include morbidity data, measures ofquality of life or, in the case of nutrition pro-grammes, changes in patterns of food purchasing.On the other hand, outcomes may be programmesand policies that need to be taken up in subse-quent interventions. In its ‘Eat well II’ report, theDepartment of Health (1996) published an evalu-ation of the first 2 years of operation of the Nutri-tion Task Force initiatives. Follow-on initiativeshave since been introduced, so the original out-comes have been superseded by new interventions.

The FSA Wales Nutrition Strategy is aimingfor some quantitative outcomes, for example, interms of knowledge about portions and increasedconsumption of fruit and vegetables in prioritygroups, as well as a balance of the diet closer torecommendations by 2010.

The national progress towards a healthier dietin the UK is more difficult to follow. However, thereare indications that intakes of fat are falling,although rates of obesity are increasing. Intake offruit has increased, although vegetable intakes arestatic. There is increased knowledge about recom-mendations to increase fruit and vegetable intakeand reduce intakes of fat. Yet, generally food intakepatterns remain resistant to change. Many studiesdemonstrate that people are not making changesfor a number of reasons. These include:■ confusion over the message (e.g. what is a

portion);■ perception that the messages are frequently

changing and the professionals cannotagree;

Model for stages of changeTABLE 18.3Stage of change Associated behaviourPre-contemplation Not considering any change or need for changeContemplation Thinking about changing, but not yet prepared to start the processPreparation When the change seems possible and benefits are perceived, ready to changeAction Actually doing things differently. May need much support and reassurance; may

slip back to earlier stagesMaintenance New behaviour becomes part of the healthier lifestyle

Adapted from Prochaska et al., 1992.


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■ belief that the subject’s diet is already healthy,so the messages do not apply to them;

■ inadequate/incorrect knowledge about whichfoods contain particular nutrients;

■ concern that healthy food is unappealing;■ perceptions about the cost of healthy food;■ beliefs about the availability of healthy foods,

both in local shops and in catering venues;■ lack of interest.For all of these reasons, progress is inevitablyslower than nutritionists and other health pro-fessionals would like it to be. However, if goalsare made specific, measurable, achievable andrealistic, then after a set time some progress isgenerally found to have occurred. It is import-ant to recognize that such small steps will eventually add up to more substantial change.Trends in the incidence of chronic disease willtake longer to become apparent. Evaluation is,therefore, essential to ensure that all changesare recorded and lessons learned from them.

Health-promotioninitiatives and theindividual

Most individual consumers may know little aboutnational initiatives and are dependent on changesin their own immediate environment to providethem with opportunities to improve their nutri-tion. This section will consider what differencehealth-promotion initiatives might make to theindividual.

Information and education

The National Food Guide continues to be pub-lished as The balance of good health (FSA, 2001).It is an example of food-based dietary guidelinesand, as such, should be readily understood byconsumers. It is used widely by retailers andhealth professionals, and has been adapted foruse with groups, such as ethnic minority groupsand diabetics.

Past advice had tended to focus on singlenutrients. Thus, consumers heard the messagethat they should ‘eat more fibre’, for example.They follow this advice by buying wholemealbread and eating a wholegrain breakfast cereal,but continue as before with their previous diet.

This may still be high in fat, low in fruit andvegetables, high in salt, or even all of these, butthe consumer may believe that he/she is noweating ‘a healthy diet’.

This focus on single nutrients has also led toan enormous increase in consumption of sup-plements, with up to 30 per cent of some groupsin the population taking supplements regularly.This again reflects the message about ‘antioxi-dant nutrients’, which are being consumed intablet form rather than by amending the diet. Itis possible that it is the chemical substancesfound alongside these antioxidants that mayactually be the biologically important agents.

The balance of good health moves away fromthis approach and provides a whole diet picture.It can be used in many ways, both as an educa-tional tool in settings ranging from schools toantenatal clinics, a meal-planning guide or evena shopping list; and provides a non-verbal illus-tration of the balanced diet, which can be veryuseful in allowing each person to understand theguide in their own way.

Although we are exposed to many messagesabout nutrition and health throughout the week,some are more likely to persuade us than others.The effectiveness of a message is determined bythe wording. Messages need to be:■ reasonable (we should understand the mes-

sage, and the reason for it);■ practical (we should find the change possible);

and■ compelling (we should want to do it).

We are more likely to be influenced by messages that fit in with existing belief systems,rather than those which seem alien to us. In devis-ing messages, the health promoter must be surethat he or she understands the belief systems ofthe target group, so the messages will be under-stood and acted on. A common failing is thathealth promoters make assumptions about theirtarget group’s level of understanding; this canlead to misunderstanding of the message.

Schools

A network of ‘School Nutrition Action Groups’has been set up as school-based healthy alliancesbetween schoolchildren, staff and caterers,together with a community dietitian. These

HEALTH-PROMOTION INITIATIVES AND THE INDIVIDUAL ❚

391

groups aim to develop a health-promoting envir-onment in the school, establishing, monitoringand evaluating a consistent food policy withhealth as the main objective, and providinghealthy options on the school menu, at lunchtimeand for snacks. It allows pupils, caterers andteachers to have involvement and ownership ofschool meals provision. The existence of goodexamples of healthy food aims to serve as aneducational model. There is now more teachingof food and nutrition in schools, and computer-based packages to facilitate this have been pro-duced by the British Nutrition Foundation. Theintroduction of new guidelines on school mealsin 2001 should help to integrate the educationaland food-based messages.

The NHS and health professionals

It is recognized that the majority of people willturn to members of the primary health care teamif they want specific nutritional advice. However,many studies have indicated that doctors may beuncertain about nutritional advice and, althoughthey appreciate that it is important, often havenot included nutrition in a consultation. This maybe influenced by a number of factors, includinglack of time, inadequate teaching materials, lowconfidence and patient non-compliance. Thepractice nurse in the primary health care settingis more likely to provide nutritional advice andmay have more time to do so. The importance oftraining in nutrition for many groups of healthprofessionals is now widely recognized andincluded in the curriculum. A recent report by theRoyal College of Physicians (2002) confirmedthat nutrition of patients was a doctor’s responsi-bility and should be supported by appropriatetraining in nutrition. A study of nutrition inter-vention in primary care (Moore and Adamson,2002) found that there were good levels of nutri-tional knowledge among members of the primarycare team. Diet was discussed with a proportionof patients, although practical aspects of foodwere not well covered. There is thus evidence ofprogress in widening the availability of nutri-tional information to patients. Multi-disciplinarynutrition teams have been established in manyhospitals to ensure adequate feeding of at-riskpatients in this setting.

Media/advertising

A major source of information for the lay personis the media and advertising. Because the mosteye-catching news items are the ones that aim tosurprise or shock, it is the sensational aspects ofnutrition that tend to reach prominence in themedia. An expert opinion, which apparently dis-agrees with the accepted viewpoint, becomesnewsworthy and is published in the press. Wherea number of experts have agreed, however, this isoften not considered important and so receivesno publicity. Thus, the overall impression given is that ‘experts’ always contradict one another,and there is no point in following any advice, as it is inevitably contradicted within the nextfew months. Regrettably, this is believed bymany and frequently cited as the reason for notfollowing any dietary advice. Information fromprofessionally accredited nutritionists and stateregistered dietitians is sound and based on scien-tific evidence. Unfortunately, a proportion of theinformation provided by the media is not.

The food chain

The food industry is in a very powerful positionto determine the nutritional quality of the dietconsumed. It is, therefore, essential that healthpromoters work with the industry. The potentialfor the development of modified products ornew products with a healthier nutritional profileis there, and whether they appear on the super-market shelves depends on the manufacturers.

In the UK in recent years, there has been ahuge growth in the consumption of ready-madeand convenience food products, and, therefore, agreat responsibility rests with the food industrywith respect to these. The provision of compre-hensive nutritional labelling can help the con-sumer decide whether products are healthy ornot. Eating a diet containing many pre-preparedmeals makes it difficult to achieve the holisticview of the diet, as many complete dishes spanvarious segments of the Balance of Good Health,and make it impossible to gauge exactly howmuch of each component has been eaten. It isprobably easier to achieve the balanced dietusing more basic foods than predominantly com-posite dishes. Unfortunately, many people havelittle time and/or perhaps ability to do this, and


392

may resort to eating a largely pre-prepared diet.There is evidence that cooking skills are grad-ually declining in parallel with the more hecticlifestyle and the use of ready meals. This high-lights the importance of the food industry inmaking sure that this type of diet is balanced andhealthy. A further challenge for the food industryis to respond to the drive for an increase in fruitand vegetable intake. Traditionally, there hasbeen very little profit margin for the sale of fruitand vegetables, as minimal processing is required.However, if public health is to be improved andthe food industry is to be involved, new andmore creative ways of promoting plant-basedfoods will need to be developed.

Catering outlets also have a great responsi-bility, as over one-third of the meals now con-sumed in the UK are eaten away from home.Guidelines on healthy catering practice for hos-pitals, restaurants, fast-food outlets and in theworkplace are available, with awards for goodpractice. Recommendations for the training ofcaterers have been drawn up. These initiativesshould make it easier for consumers to be able tochoose healthy eating in all outside venues,although, in practice, this is not always the case.

Constraints

Change is difficult for most people. Even if thehealth promotion is well designed and appropri-ately targeted, there may be some for whom it is not appropriate or for whom it is not possibleto change. Some groups that are more difficultto reach by health-promotion programmes are:■ those on a low income;■ the elderly;■ people in minority ethnic groups;■ single men;■ children – who need specifically focused

programmes.

A targeted policy

It is useful to consider a more targeted policy as an illustration of how the process describedabove can be applied within a more specifichealth promotion context. The Folic Acid

Campaign in the UK, initially commissioned bythe Department of Health in 1995, is an example of a policy that was specifically targeted (seeFigure 18.2).

The planning stage reviewed the evidence inthe literature that the estimated risk of neuraltube defects (NTDs) was progressively reducedwith an increasing dose of folic acid intake, andthat supplementation with folic acid would sig-nificantly impact on the risk of NTD in the popu-lation. A daily dose of 400 �g folic acid wasindicated as appropriate to achieve a reduction inNTD incidence of at least 50 per cent. The pri-mary target group for the campaign were womenintending to become pregnant and the aim wasto reduce the incidence of NTDs, such as spinabifida, in their offspring. However, since almosthalf of the conceptions in the UK are reported tobe unplanned, the target audience was initiallyexpanded to all women of child-bearing age, andlater to young people, as future parents. It wasthus intended that, as an outcome, all womenwould gain an awareness of the importance offolic acid supplementation.

The intervention stage of the campaign wasdesigned to increase the baseline intake of folatefrom foods, as well as promote the use of folic acidsupplements at the appropriate time before con-ception and during early pregnancy. This entaileddeveloping cooperative partnerships with foodproducers and the commercial sector to increasethe availability of fortified products, as well as anincreased range of appropriate supplements inorder to increase access to the vitamin in shops.The increased demand was to come as a result ofdissemination of the message about the import-ance of folate, by health professionals, teachersand journalists. Manufacturers of pregnancytesting kits were also involved at this stage.Many diverse strategies were used to disseminatethe message about folate. These included leafletsand posters, a new labelling symbol for foodsfortified with folic acid, promotion of fortifiedproducts by advertising, and development ofteaching packs for use in schools.

The campaign finished in 1998, althoughmany elements of the promotion of folic acidremain in place as part of health promotion.Initial evaluation results indicated an increase in

ECONOMICS OF HEALTH PROMOTION ❚

393

awareness about the issue among women, wideravailability of folic acid supplements and forti-fied products, and an increased usage of folicacid supplements. However, women whose preg-nancies are unplanned remain at risk as a resultof low uptake of folic acid at the critical timearound conception. The campaign can thus beviewed as only partly successful and demon-strates that the challenge of achieving change,with a simple supplement and at a highly vul-nerable time of life, is enormous.

Economics of healthpromotion

It is generally assumed that health promotion isinexpensive and will reduce health care costs.Thus, many see health promotion as a way ofsaving money. However, although it is possiblethat money may be saved through health pro-motion, this cannot be the primary objective.Health promotion involves various cost inputs,most obviously in the form of resources, such ashealth professionals, their time and materials.There generally needs to be an input in the form

of government action whether through legislationor financial ‘pump priming’. In addition, betterhealth is also achieved by efforts on the part ofindividuals, which are more difficult to evaluateeconomically.

To evaluate the cost–benefit of health pro-motion, it is necessary to identify what isgained as a result of the programme and whathas been forgone by diverting these resourcesfrom elsewhere (see Figure 18.3).

Because the outcomes of nutritional healthpromotion are often difficult to measure, deci-sions of this nature are rarely straightforward.Various measures of health gain may need to beused that show incremental advantages, ratherthan simply the ultimate goal of reducing chronicdisease incidence. Balanced against this are thecosts of treating these diseases and the loss ofearnings that chronic disease can cause. Each casemay need to be evaluated separately and on itsmerits. However, the more information is pro-vided about nutrition and health and the morethat people can be empowered to make their ownchoices in an informed way, the greater will bethe potential benefit for health.

Figure 18.2 The folic acidcampaign. NTDs, neural tubedefects.


394

A health economist might wish to compare the costs (C) of a programme to reduce obesity, againstthe potential saving in the treatment of diabetes (D)associated with obesity. If C is greater than D, thenclearly the programme would appear not to be costeffective as it stands. However, if one also could

show that reducing obesity would cause a potentialsaving in treatment for arthritis and hypertension (A � H), it is now possible that the combined savings(D � A � H) could be greater than the cost C. In thisway, a multiple benefit can make the programmecost effective.

1 Nutrition plays an important part in the causation of chronic disease. It is, therefore, essential thatdietary change is introduced to reverse the high prevalence of some diseases.

2 Guidelines have been established by various national and international bodies that propose change.3 The consensus on change recommends reductions in fat, increases in starchy carbohydrates, fruits and

vegetables.4 Health promotion can facilitate change.5 Health promotion involves partnerships between the various players in the food system and the citizen,

in a process of education and empowerment.

SUMMARY

1 Improving health involves more than just anawareness of dietary guidelines. What otheraspects of life must be considered and changedto make dietary improvements possible?

2 List the major participants in the food chain andindicate how you think each could be involvedin promoting healthier eating.

3 Discuss with colleagues:a Where they have obtained information about

healthy eating (if at all)?b Have they understood the information?c Have they acted on the information? If not,

why?4 Do you believe that nutrition information

available generally to the public is adequate

and/or an appropriate way of producingchanges in the diet?

5 Survey newspaper articles describingnutritional issues over a period of 3–4 weeks.Try to look at a ‘popular’ newspaper and onewhich is considered to be of higher ‘quality’.a Are issues handled differently and, if so, in

what way?b Do you find either of the article types more

credible?c As a result of reading the articles are you

encouraged to change your diet?d What can you conclude from this

investigation?

STUDY QUESTIONS

Figure 18.3 Economics of health promotion.


395


DoH (UK Department of Health) 1994: Eat well! An action plan from the Nutrition Task Force toachieve the Health of the Nation targets on diet and nutrition. Wetherby: Department of Health.

DoH (Department of Health) 1996: Eat well II. A progress report from the Nutrition Task Force onthe action plan to achieve the Health of the Nation targets on diet and nutrition. Wetherby:Department of Health.

DoH (Department of Health) 2000: Folic acid and the prevention of disease. Report on Health andSocial Subjects 50. London: The Stationery Office.

Eurodiet core report 2001: Nutrition and diet for healthy lifestyles in Europe: science and policyimplications. Public Health Nutrition 4(2A), 265–73.

Eurodiet Working Party 2. 2001: A framework for food-based dietary guidelines in the EuropeanUnion. Public Health Nutrition 4(2A), 293–305.

Food and Agriculture Organisation/World Health Organisation (FAO/WHO) 1998: Preparation anduse of food-based dietary guidelines. Geneva: WHO.

Food Standards Agency 2001: The balance of good health. London: FSA.Food Standards Agency Wales 2002: Nutrition Strategy for Wales, Consultation Document.

London: FSA.Gillespie, A.H., Shafer, L. 1990: American Dietetic Association position paper on nutrition education

for the public. Journal of the American Dietetic Association 90, 107–10.Gregory, J., Foster, K., Tyler, H., Wiseman, M. 1990: The dietary and nutritional survey of British

adults. London: HMSO.HEA (Health Education Authortiy) 1994: Introducing the National Food Guide: The balance of good

health. Information for educators and communicators. London: HEA.Jackson, A.A. 2001: Human nutrition in medical practice: the training of doctors. Proceedings of the

Nutrition Society 60(2), 257–63.James, W.P.T. 1988: Healthy nutrition: preventing nutrition-related diseases in Europe. WHO

Regional Publications, European Series, No. 24. Copenhagen: WHO Regional Office for Europe.Margetts, B.M., Thompson, R.L., Speller, V. et al. 1998: Factors which influence ‘healthy’ eating pat-

terns: results from the 1993 HEA health and lifestyle survey in England. Public Health Nutrition1(3), 193–8.

Moore, H., Adamson, A.J. 2002: Nutrition interventions by primary care staff: a survey of involve-ment, knowledge and attitude. Public Health Nutrition 5(4), 531–6.

Posner, B.M., Franz, M., Quatromoni, P. and the INTERHEALTH Steering Committee 1994: Nutritionand the global risk for chronic diseases: the INTERHEALTH Nutrition Initiative. NutritionReviews 52(6), 201–7.

Prochaska, J.O., DiClemente, C.C., Norcross, J.C. 1992: In search of how people change. AmericanPsychologist 47, 1102–14.

Roe, L., Hunt, P., Bradshaw, H. et al. 1997: Health promotion interventions to promote healthy eatingin the general population – a review. London: Health Education Authority.

Royal College of Physicians 2002: Nutrition and patients: a doctor’s responsibility. London: RoyalCollege of Physicians.

World Health Organization 1986: The Ottawa Charter: principles for health promotion. Copenhagen:WHO Regional Office for Europe.

World Health Organization 1990: Diet nutrition and the prevention of chronic diseases. WHOTechnical Report No. 797. Geneva: WHO.

397

acceptability of foods 28, 30–4acetic acid 59, 76acetylcoenzyme A 175acrodermatitis enteropathica 209adipocytes 90, 91adipose tissue 90–1, 92, 93–4, 234adolescents 281

athletes 274dietary intake information 11dieting 275–6diet surveys 268–70growth 266, 267influences on nutritional intake

265–6nutritional needs 266–8pregnancy 240, 274–5smoking and alcohol use 276vegetarian 273–4

adverse reactions to food 338–45advertising and health promotion

391aflatoxin 331, 339Afro-Caribbean community 286–7,

288age

and BMR 134and coronary heart disease 310and obesity 151

ageing 294AIDS see HIV infectionalanine 59, 65, 255alcohol 52–3, 149, 222

abuse 357–9, 360and cancer 329and coronary heart disease 318,

320energy content 124, 125teratogenic effects 233–4use in childhood and adolescence

276allergens 340alpha-linolenic (n-3) acid 79–80,

84, 95, 96, 309alpha-tocopherol 171, 318amino acids 57–60

absorption 61–3in breast milk 255chemical (reference) score 69classification 60deamination 63essential/indispensable 58, 63, 255glucogenic 63ketogenic 63limiting 64, 68, 69metabolism 63–6pool 63–5and protein quality 68–70transamination 63

amylases 107–8, 254amylopectin 102–3, 104, 108amylose 102, 104, 108anaemia 206–7, 283, 288, 382

anaphylactic shock 341–2, 343anorexia nervosa 32, 34, 152, 158,

174, 209, 232, 275, 339anthocyanins 370anthropometric indicators of

nutritional status 11–13antioxidants 79, 213, 292, 294, 296

and athletics 356and cancer 332–3carotenoids 372and coronary heart disease

318–20phenolic compounds 370–1vitamin A 165vitamin C 189–90vitamin E 171–2

apolipoproteins 88, 89, 90appetite 20, 31, 360arginine 63, 255, 373–4arm muscle circumference 12ascorbic acid see vitamin CAsian community 169–70, 285–6,

287–8aspartame 367aspartate 65athletes 274, 351–7atopy 342ATP 128, 140, 202, 352–3availability of foods 28–9

Babyfriendly Hospital Initiative(BFHI) 257

Bacillus cereus 339bacteria, functional foods

containing 374–6, 377balanced diet 40, 51Balance of Good Health see National

Food Guide (Balance of GoodHealth)

basal metabolic rate (BMR) 131–2,133–5, 137, 139, 234

behaviour therapy 156beriberi 175, 176beta-carotene 163, 165, 318, 319,

332–3, 372beta-sitosterol 81Better Hospital Food project 72bicarbonate–urea method 130bifidus factor 259bile acids 86biochemical indicators of

nutritional status 13–14bioelectrical impedance 147biotechnology 367–8biotin 187birthweight 231–2, 236, 241–5, 311blindness 164, 166bliss points 24blood analysis 13blood clotting 67, 174, 198, 243blood pressure 201, 219, 220–1,

242, 269, 312

body composition 144–6average values 147–8measurement 146–7

body density 147body fat 12, 145–6, 148body mass index (BMI) 12, 144–5,

149, 152–3, 232body weight 144–6

and basal metabolic rate 131–2and bone mass 199–201control 143–4and coronary heart disease 313in HIV infection 347–9stability 137, 142–3

bomb calorimeter 124–5bone

analysis 13densitometry 13role of calcium 197–8, 199–201role of phosphorus 202

bone marrow biopsy 13bottle-feeding 252, 256–60breastfeeding 245–9, 254, 257–60,

292, 342brown adipose tissue (BAT) 90, 93,

140bulimia nervosa 32, 152, 158, 275

caeruloplasmin 210, 211caffeine 222, 223, 331, 344calcitonin 198calcitriol see vitamin Dcalcium 194, 195–201

absorption 196–7and athletics 356and cancer 331, 334and coronary heart disease 317excretion 198functions 197–8and health 199–201in infancy 256in pregnancy 237–8, 240sources 195–6and vitamin D 167, 168, 169,

196, 198calories 123Campylobacter 339cancer

colon 201, 329, 332, 334and diet 324–37environmental causes 327–34oesophageal 329prevention 334–6prostate 329protective factors 331–4stomach 329–30, 332, 333studies 325–7

cannibalism 30carbohydrates 99–122

absorption 110in childhood and adolescence

268, 269

INDEX

❚ INDEX

398

carbohydrates cont.conversion to fat 21dietary reference values 43, 44,

113digestion 106–10energy content 124–6and exercise 353–4, 354–5function in diet 112–13and health 113–21in infancy 255–6metabolism 111–12, 149–50in milk 258

carboxypeptidase 61carcinogenesis 325, 326cardiovascular disease see coronary

heart diseasecarotenoids 162, 163, 164, 165,

332–3, 372–3catalase 319catechins 370cellular differentiation, role of

vitamin A 164–5cellulose 103, 105, 106challenges to nutritional status

338–63chest circumference 12chewing 252children

anthropometric measurementsand development 12

dietary intake information 11diet surveys 268–70influences on nutritional intake

265–6nutritional needs 266–8pre-school 263–5school-age 265–8smoking and alcohol use 276vegetarian 273–4see also infants

Chinese community 287Chlamydia 312chloride 194, 217–20, 299, 329–30cholecystokinin (CCK) 20, 143, 144,

254cholesterol 81, 86, 88, 89, 94, 117,

243, 373and coronary heart disease

307–8, 314–15chromium 194, 216chronic disease and diet 380–7chylomicrons 86, 87–9, 92, 168,

173, 312–13chymotrypsin 61clinical indicators of nutritional

status 14Clostridium botulinum 339cobalt 194coeliac disease 170, 343coffee 222, 225cognitive function of older people

296collagenase 61colostrum 62, 254conception and nutrition 232–4

conjugated linoleic acid (CLA) 80,317

copper 194, 210–12, 256core foods 6–7, 30, 31, 261coronary heart disease 15, 40, 241,

288, 304–23changes in rates 305risk factors 309–21studies 307–9

corrinoids see vitamin B12creatine phosphate 352, 356–7cretinism, endemic 215Crohn’s disease 117culture and food acceptability 30–1cysteine 63

DAFNE (Data Food Networking)initiative 8

Data into Nutrients forEpidemiological Research 9

dehydration 222, 224, 295dehydroascorbic acid see vitamin Cdementia 296demispan 12–13dental health 115–17, 288depression 297DEXA 147, 200diabetes mellitus 117, 118, 120,

242–3, 288, 311–12diarrhoea 222dietary fibre see non-starch

polysaccharidesdietary guidelines 40, 279–80

adult men 280–1adult women 281–2national/international 385–7

dietary informationcollection 7–11individual 8–11population and household 8

Dietary and Nutritional Survey ofBritish Adults 14, 126

dietary patterns 6–7, 269dietary planning 46–51dietary reference values (DRVs)

42–6, 279calcium 201carbohydrates 43, 44, 113in childhood and adolescence

267–8folate 185in infancy 254–6iron 207in lactation 247nicotinic acid 180potassium 221in pregnancy 238proteins 70–1riboflavin 178sodium 219thiamin 176vitamin A 166–7vitamin B6 181vitamin B12 187vitamin C 191

vitamin D 170vitamin E 173vitamin K 174zinc 209

dietingin adolescence 275–6yo-yo 143

diet interview 10digestive tract

bacterial flora 374–5development 254and drug therapy 350effects of alcohol abuse 358older people 295, 297, 298and probiotic/prebiotic foods

374–6, 377DINER 9direct calorimetry 128, 129disability and nutrition 359–62disaccharides 100, 101–2, 107diuretics 222, 223doubly labelled water technique

130drug therapy and nutrition 349–51dry eye 164, 166

eating, reasons for 19–25eating disorders see anorexia

nervosa; bulimia nervosaeating habits, influences on 18–35economic factors in food

availability 29education and health promotion

390eggs, omega-enriched 373eicosanoids 95Eight guidelines for a healthy diet

(MAFF) 40, 334elastase 61elderly people see older adultselectrolytes 195embryo 232–4energy

balance 5, 124, 127, 137–60,358–9

content of foods 124–6cost of lactation 246–8cost of pregnancy 234–5diet surveys 126–7estimated average requirements

(EAR) 135, 254–5, 299and fat metabolism 91intake 124–7, 137, 138–9, 269,

299and cancer 328and coronary artery disease

317metabolizable 125needs 123–36

of athletes 352–5in childhood and adolescence

267in infancy 254–5in old age 298

output 127–35, 137, 139–42

INDEX ❚

399

ratio of intake to expenditure 11and sugars 114units of measurement 123–4

energy-controlled diets 154–5enterogastrones 86enzymes 66EPIC study 9Escherichia coli 339ethnic minorities 169–70, 283–8,

289EURODIET project 381, 383, 384European Union 381evening primrose oil 79exercise see physical activityexpenditure on food 289–91Expenditure and Food Survey

(EFS) 8

faeces, fluid loss in 222failure to thrive 263familial hypercholesterolaemia 89FAO 8fasting 93fat replacers 366–7fats 75–97

amount in the diet 96, 149and cancer 328–9in childhood and adolescence

268, 269content of foods 82and coronary heart disease

307–9, 314–17in the diet 81–5dietary reference values 43, 44digestion and absorption 85–7energy content 124–6energy provision 91, 353and food palatability 85functions in the body 90–6and the immune system 346–7in infancy 255intake of preschool children 265metabolic roles 91–6metabolism 21, 150, 348in milk 259in pregnancy 234, 235sources in British diet 84storage 90–1, 91–2transport in the body 87–90trends in intake 82–3utilization 92–3visible/invisible 81–2

fatty acidsabsorption 85–7and cancer 329cis 77, 78, 316classification 77–9and coronary heart disease

307–8, 315–17eggs enriched with 373essential 79–80, 84, 95–6, 240,

255implications of unsaturation 77–9long-chain 76–7, 96, 239, 240,

255

medium-chain 76–7, 88monounsaturated 77–9, 83, 96,

234, 315non-esterified (NEFA) 92, 93polyunsaturated 77–9, 83, 96,

173, 234, 240, 315–16,346–7

saturated 77, 83, 96, 307–8, 315short-chain 76–7, 86, 88sources in British diet 84structure 59, 76–7trans 77, 78, 316–17

female athlete triad 356ferritin 206, 207fetal alcohol syndrome 234fetus, consequences of intrauterine

events 240–5fidgeting 141–2fish oils 79, 239flavanones 370flavonoids 370–1fluid balance 221–5

athletes 357in infancy 256

fluoride 200, 216–17foam cells 306folate 181–5, 186

absorption and metabolism 182before and during pregnancy

232, 233, 237, 239and cancer 331deficiency 183–4, 288Folic Acid Campaign 392–3in food 181–2and homocysteine 320supplements 184–5, 233, 239

food additives 344food allergy 62, 254, 340–3

see also food intolerancefood aversion 338, 339food balance sheets 8food choices 27–34, 36–7, 38food diaries 9–10food frequency questionnaires 10food groups 30, 46

and energy intake 127food intake record based on 10

food guides 6, 7, 46–51food habits 25–34, 264, 283–4food handling 29food industry and health promotion

391–2food intake

adjustment 138–9and alcohol abuse 358in disability 360–1and drug therapy 350glucostatic theory 20habitual 9in HIV infection 348lipostatic theory 20and obesity 148–50older people 296–7physiological factors 19–21in pregnancy 236–9

preschool children 264–5recording and estimating 8–11

food intolerance 62, 338, 339–45food labelling 29, 46, 124food poisoning 338–9food policies, national 15food refusal 264food rejection 23foods for specific health use

(FOSHU) 365Food Standards Agency (FSA) 14,

15, 386Food Standards Agency for Wales

386–7food tests 344–5fortified foods 368–9Framingham study 308free radicals 78–9, 171–2, 189–90,

319, 372fructans 376fructose 100–1, 111fruit intake and cancer 332fruit juice 225functional foods 368–76, 377

galactose 100, 101, 111gamma-linolenic acid (GLA) 79gastric distension 20gender and obesity 151genetically modified organisms

367–8genetic component of weight

150–1genetic predisposition to coronary

heart disease 310geographical factors in coronary

heart disease 311gla-proteins 174gluconeogenesis 65, 112, 353glucose 100

blood levels 110function 112metabolism 92, 93, 111–12

glucosinolates 333, 371–2glutamine 63, 65, 255, 373glutathione peroxidase 319gluten sensitivity 170, 343glycaemic index 110, 118, 354, 355glycerol 76, 88glycine 59, 65, 255glycogen 111–12, 353, 354goitre 214–16growth

in adolescence 266, 267and cancer 328charts 253in childhood 264, 266in infancy 252role of vitamin A 165

gut hormones 20

habit and eating behaviour 21–2haemoglobin 67, 203haemorrhagic disease of the

newborn 174

❚ INDEX

400

hair, trace elements 13head circumference 12health alliances 15health claims 365–6health education 387health gain rhomboid 388Health of the Nation (white paper)

15, 266, 293–4, 386, 388‘health-promoting’ foods 39health promotion 380–95health service, health promotion 391Health Survey for England 14, 286healthy diet 36–54heart attack see coronary artery

diseaseheartburn in pregnancy 235–6Helicobacter pylori 312, 324, 330,

333high-density lipoproteins (HDLs)

88, 89–90, 117, 313, 351Hindu religion 285–6hip fracture 295–6histidine 63, 255HIV infection 259, 347–9homelessness 289homocysteine 184, 186, 320–1hormone replacement therapy 200hormones 66hospitals, undernutrition in 72Household Budget Surveys 8Household Food Consumption and

Expenditure Survey 8hunger 20, 22hydrochloric acid 61hypothalamus 21

illness and weight loss 158–9immigrants 30, 169–70, 283–8, 289immune system 213, 259, 296,

345–7, 375–6immunity 67immunoglobulins 62

IgA 340IgE 340, 341

immunological acceptance 340income

and nutrition 288–93and pregnancy 240

indirect calorimetry 128, 129–30infants 251–63

digestive tract development 254growth 252nutritional needs 254–7nutrition and development 252weaning 260–3

infectionconcurrent with HIV infection 348effect on nutritional status 345–6

infertility 232insulin 65–6, 111, 117, 143–4, 216

in pregnancy 235resistance 93, 94, 242–3, 311–12

iodine/iodide 194, 214–16, 232deficiency 382

IQ and nutrition 276

iron 190, 194, 203–7and athletics 356and cancer 331in childhood and adolescence 270deficiency 206–7, 283, 288, 347dietary reference values 207in infancy 256, 261, 263intake of preschool children 265in milk 259in pregnancy 238, 239

Islam 286isoflavones 371isoleucine 63, 65, 255

Kashin–Beck disease 213keratomalacia 164, 166Keshan disease 213ketone bodies 93, 112ketosis 93, 112, 113kidney function in older people 295kilocalories (Calories) 123, 124kilojoules 123–4Korsakoff’s syndrome 176, 359kwashiorkor 71–2

lactase 107, 109deficiency 344

lactation 245–9lactic acid 353Lactobacillus rhamnosus 181–2lactoferrin 259lactose 101, 107, 196, 255–6, 258lactulose 376lecithin 80legislation and food availability 29leptin 20, 21, 93, 143–4, 234, 252leucine 63, 65, 255lifestyle and diet 39–40lignans 371linoleic (n-6) acid 79–80, 84, 95, 96lipaemia 93, 312lipases 85, 86, 254lipids 76

see also fatslipodystrophy 348lipoprotein(a) 312lipoprotein lipase 20, 88, 89, 91–2,

216lipoproteins 88–90, 312–13

see also specific typesListeria monocytogenes 32, 238–9,

262low-calorie/low-fat foods 369–70low-density lipoproteins (LDLs) 88,

89–90, 260, 306, 312, 373Low Income Project Team 293lungs, fluid loss through 223lutein 163, 164, 372lycopene 165, 372lysine 63lysozyme 259

McGovern Report 118magnesium 194, 202–3, 232, 256,

270

malabsorption 139, 170, 176,348–9

malnutrition 145, 346maltose 101, 102manganese 194marasmus 71–2meals 22

and food habits 26–7patterns 5planning tools 46–51

meat analogues 367meat intake and cancer 330media 6

and food habits 27role in health promotion 391

megajoules 123–4membrane structure 90Menkes’ disease 211menu records 9–10metabolic equivalents (METs)

133metabolism

and disability 361and food intake 21in HIV infection 348see also basal metabolic rate

methionine 63micelles 86microminerals see trace elementsmicronutrients

dietary reference values 43–4and income 292intake by older adults 299see also specific nutrients

milk 225breast 245, 252, 254, 255, 256,

258–60, 262, 340carbohydrates in 258cows’ 262ejection/let-down 245, 246fats 259follow-on 262formula 252, 256–60, 262low-fat 262minerals 259proteins 258soya-based 260vitamins 259

minerals 194–5in childhood and adolescence

270contaminants 195dietary reference values 43–4in infancy 256intake in older adults 299major 195–203in milk 259supplements 356

mobility of older people 295–6MONICA Project 15, 318monosaccharides 100–1, 107, 110monosodium glutamate 344morning sickness 236–7mucopolysaccharides 112–13Muslims 286

INDEX ❚

401

myocardial infarction see coronaryheart disease

myoglobin 203

National Diet and Nutrition Survey(NDNS) 14, 264–5, 268

National Food Alliance 293National Food Guide (Balance of

Good Health) 10, 15, 48–51,268, 334, 386, 390

National Food Survey 8, 14, 27, 29,83, 84, 106, 113, 127, 182, 188

National Health and NutritionalExamination Survey (NHANES)15

nausea and vomiting of pregnancy236–7

neural tube defects 233, 392neuropeptide Y 20, 21, 143niacin 178–80nicotinamide 178nicotinic acid 178–80night-blindness 162, 164, 166nitrates 330nitrogen balance 67–8non-starch polysaccharides (NSPs)

103, 104–6, 195, 196and cancer 331–2in childhood and adolescence

269and coronary heart disease 318digestion 108–10health aspects 119–21in infancy 262in pregnancy 238

North Karelia project 308nutrients

choice of 38–9deficiencies 41density of diet 11estimated average requirement

(EAR) 42–3, 45, 46guideline daily amounts (GDA)

46intake 11lower reference nutrient intake

(LRNI) 42, 43, 45, 46, 292,299

recommended daily amount/dietary allowance (RDA)43, 44, 46

requirements 41–2nutrition

at conception 232–4before pregnancy 232definitions 3–4importance of 4–6and income 288–93in infancy 252and IQ 276levels of study 4, 5in pregnancy 234–6sources of advice and information

51–2nutritional status 11–14

nutritional supplements 39, 270,356–7, 390

nutritional surveillance programmes14–15

nutrition education 387nutrition policies, national 15Nutrition Strategy Framework 14, 15Nutrition Task Force (NTF) 15, 386

obesity 12, 34, 114–15, 138and cancer 328central/peripheral 145factors in 148–52health risks 152–4in immigrant communities 288older adults 301and pregnancy 232, 240treatment 154–7

oils 75–6see also fats

older adults 293–301factors affecting nutritional

status 296–8nutritional requirements 300–1nutritional state 298–300risk factors 294–6

Olestra 367oligosaccharides 100, 102, 108Optimal Nutritional Status Research

programme 365optimizing nutrition 364–79optimum nutrition 4oral tolerance 340organic food 5, 39, 51, 376–8Orlistat 155osteomalacia 169–70, 288osteoporosis 174, 198, 199–201,

295–6Ottawa Charter for Health

Promotion 387overweight see obesityoxalates 196

pantothenic acid 187parathyroid hormone 168, 169,

196, 198, 202peanut allergy 254, 342–3pellagra 178, 179–80pepsin 61pepsinogen 61peptidases 61periodontal disease 312peripheral foods 7, 30, 31pernicious anaemia 186–7PETRA Scales system 9phenolic compounds 333, 370–1phenylalanine 63phospholipids 80, 86, 88phosphorus 194, 195–6, 201–2

in infancy 256and vitamin D 167, 168

physical activity 382–3and bone health 199, 200childhood and adolescence 266,

269

and coronary heart disease 313and energy balance 133, 140–2,

150and weight loss 156see also athletes

physical activity ratios (PARs) 133,134

physiological factorsin food acceptability 31–2in food intake 19–21

phytate 195, 196, 202, 204, 208phytochemicals 370–3, 377phyto-oestrogens 333, 371phytosterols 81, 373plant-based foods 36polypeptides 59–60polysaccharides 100, 102–6, 118–21

digestion 107–10Portable Electronic Tape Recording

Automated Scales system 9portion size 9, 37–8potassium 194, 217, 220–1, 270, 317poverty and nutrition 288–93, 383prebiotics 376, 377pregnancy 231–45

consequences of intrauterineevents 240–5

diet 236–9groups at risk 240, 241iodine deficiency 215iron requirements 207nutrition before 232nutrition during 234–6supplements in 239–40teenage 240, 274–5

pre-menstrual syndrome 181probiotics 375–6, 377programming 241, 242, 243prolactin 245propionic acid 59prostacyclins 95prostaglandins 95proteins 57–74

biological value 69–70in childhood and adolescence

267, 269deficiency 65, 71–2, 346denaturation 60, 61dietary reference values 70–1digestion and absorption 61–3energy content 124–6in food 60–1in human milk 248in infancy 255metabolism 63–6in milk 258needs of athletes 355–6needs in old age 298origins 58in pregnancy 234, 235quality 68–70requirements 70–1transport function 67turnover 64uses 66–7

❚ INDEX

402

proximate principles 125prunes 344psychological factors

in eating habits 23in food acceptability 32–4in obesity 151–2

public health nutrition 5, 380–95pyridoxine see vitamin B6

quercetin 370

Rastafarians 287reference man/woman 147–8reference nutrient intake (RNI) 42,

43, 45, 46folate 185in infancy 254–6iron 207nicotinic acid 180potassium 221proteins 70riboflavin 178sodium 219thiamin 176vitamin A 166–7vitamin B6 181vitamin B12 187vitamin C 191vitamin D 170zinc 209

replica foods 38residential care 301respiratory gas analysis 129–30respiratory quotient 128–9, 130,

150resting metabolic rate 131retinoids see vitamin Aretinol 162, 233

see also vitamin Arhodopsin 164riboflavin 176–8, 234, 237–8, 270rickets 169–70, 287–8ritual use of food 33RQ 128–9, 130, 150

Salmonella 32, 239, 262, 339salt 217–20, 317, 329–30satiety 20, 22, 115Saving Lives – Our Healthier Nation

305school meals 270–3, 285School Nutrition Action Group 270schools, role in health promotion

390–1Scientific Advisory Committee on

Nutrition (SACN) 15Scottish Heart Study 14–15scurvy 188, 189, 190–1secondary foods 7, 30, 31selenium 172, 194, 212–14, 215,

347SENECA study 15sensory appeal of food 23–5sensory signals and food intake 20serotonin 21

serving sizes 9, 37–8sibutramine 155Sikhism 286skin, fluid loss through 223skinfold thickness measurement 12,

146–7small round structured viruses 339smart foods 366–76smell, sense of 23smoking

and cancer 329in childhood and adolescence

276and coronary heart disease 312

snacks 22social factors

in eating habits 25in food acceptability 32–4

socio-economic statusand breastfeeding 257and coronary heart disease

310–11and obesity 151

SOD 319sodium 194, 217–20, 299, 317,

329–30sodium nitrite 344soft drinks 225special diets 32sports nutrition, functional foods

374SRSVs 339Staphylococcus aureus 339staple foods see core foodsstarch 102–4

digestion 107–8, 109and health 118resistant 104, 108, 109, 118

steatorrhoea 86, 155, 196steroid metabolism 94–5sterols 80–1stroke 15, 304, 307sucrose 101, 256sugar alcohols 100, 101sugars 99–102

absorption 110and dental health 115–17digestion 107, 109and health 114–18intrinsic/extrinsic 107, 114

sulphite 344sulphur 194, 203supermarkets, checkout data 8superoxide dismutase 319surgical weight loss procedures 156sweeteners 367

taboos 30–1tannins 370taste, sense of 23–4taurine 63, 65, 255tea 222, 225ten pound diet 293teratogenesis 233–4thermogenesis 133, 139–40

thiamin 175–6, 359thirst 223, 224threonine 63thrombosis 307thromboxanes 95thyroid hormones 214tocopherols/tocotrienols

see vitamin Etoxoplasmosis 239trace elements 194, 195, 203–21

hair 13in infancy 256

triglycerides 76–7, 86, 88, 91–2,117, 312

trypsin 61tryptophan 21, 63, 65, 66, 178–9tyrosine 63, 65

ultrasound 147undernutrition 12, 72underwater weighing 147underweight 157–8, 232, 240United Nations, Food and

Agriculture Organization 8urine

analysis 13volume and concentration 222

valine 63, 65veganism 185–6, 282vegetable intake and cancer 332vegetarianism 5, 32, 282–3, 284

and athletics 356calcium sources 195in childhood and adolescence

273–4and osteoporosis 200protein sources 61sterols 81and vitamin B12 187and vitamin D deficiency 170

very low density lipoproteins (VLDLs)88, 89, 92, 260, 312–13

vision, role of vitamin A 164, 165vitamin A 162–7

absorption 163–4and cancer 332–3in childhood and adolescence 270deficiency 162, 164, 165, 166, 347in food 162–3functions 164–6in HIV infection 349in infancy 263and lactation 248in pregnancy 237reference nutrient intake (RNI)

166–7toxicity/poisoning 166

vitamin B2 (riboflavin) 176–8, 234,237–8, 270

vitamin B6 178, 180–1, 181vitamin B12 185–7, 232, 283, 288vitamin C 172, 186, 187–91

absorption and metabolism 189as antioxidant 318, 319

INDEX ❚

403

and bone mass 200and cancer 333deficiency 190–1in food 188–9functions 189–90in infancy 261, 263in pregnancy 234, 237

vitamin D 167–70absorption 168and bone mass 200in breast milk 256and calcium 167, 168, 169, 196,

198and cancer 331, 334in childhood 268deficiency 169–70, 232, 287–8,

382in food 167functions 168–9in infancy 261, 263and lactation 248in pregnancy 237–8

reference nutrient intake (RNI)170

toxicity 170and vegetarian diet 283

vitamin E 171–3, 213as antioxidant 319and cancer 333deficiency 172in pregnancy 234

vitamin F see fatty acids, essentialvitamin K 173–4, 200, 256vitamins 161–93

dietary reference values 43–4fat-soluble 85, 86, 88, 162–74in infancy 256, 261, 263intake in older adults 299in milk 259supplements 356water-soluble 174–91

waist:height ratio 12waist:hip ratio 12, 145

waist measurement 12, 146, 313water

consumption 225gain 223–4loss 222–3

weaning 260–3, 342weighed inventory 9weight gain in pregnancy 231,

236weight loss 157–9

strategies 154–7Wernicke–Korsakoff syndrome 176,

359Wilson’s disease 211World Health Organization 380–1

xerophthalmia 164, 166

zinc 194, 207–9, 232deficiency 294and immune function 347in infancy 256, 259, 263

human nutrition - a health perspective, 2nd edition

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