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SportSNutritioNEditEd by Ronald J. Maughan
tHE ENCYCLopAEDiA oF SportS MEDiCiNEAN ioC MEDiCAL CoMMiSSioN puBLiCAtioN
SPORTS NUTRITION
SPORTS NUTRITION
VOLUME XIX OF THE ENCYCLOPAEDIA OF SPORTS MEDICINE
AN IOC MEDICAL COMMISSION PUBLICATION
EDITED BY
RONALD J. MAUGHAN, PhD
This edition fi rst published 2014 © 2014 International Olympic Committee
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Library of Congress Cataloging-in-Publication DataSports nutrition (John Wiley & Sons)
Sports nutrition/edited by Ronald J. Maughan.
p. ; cm. – (Encyclopaedia of sports medicine ; volume XIX)
“An IOC medical commission publication.”
Includes bibliographical references and index.
ISBN 978-1-118-27576-4 (cloth : alk. paper) – ISBN 978-1-118-69231-8 – ISBN 978-1-118-69232-5 (emobi) –
ISBN 978-1-118-69233-2 (epdf) – ISBN 978-1-118-69235-6
I. Maughan, Ron J., 1951- editor of compilation. II. IOC Medical Commission, issuing body.
III. Title. IV. Series: Encyclopaedia of sports medicine ; v. 19.
[DNLM: 1. Nutritional Physiological Phenomena. 2. Sports–physiology.
3. Athletic Performance. 4. Exercise–physiology. 5. Sports Medicine–methods. QT 13 E527
1988 v.19/QT 260]
RC1235
613.7’11–dc23
2013018143
A catalogue record for this book is available from the British Library.
Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not
be available in electronic books.
Cover image: © IOC/Juilliart
Cover design by Rob Sawkins for Opta Design Ltd
Set in 9/12pt Palatino by Aptara Inc., New Delhi, India
1 2014
v
Contents
List of Contributors, viii
Foreword, xii
Preface, xiii
Part 1 The Underpinning Science
1 Human Nutrition, 3
david a. bender
2 Exercise Physiology, 20
w. larry kenney, robert murray
3 Biochemistry of Exercise, 36
michael gleeson
Part 2 Energy and Macronutrients
4 How to Assess the Energy Costs of Exercise
and Sport, 61
barbara e. ainsworth
5 Energy Balance and Energy Availability, 72
anne b. loucks
6 Assessing Body Composition, 88
timothy r. ackland,
arthur d. stewart
7 Carbohydrate Needs of Athletes in
Training, 102
louise m. burke
8 The Regulation and Synthesis of Muscle
Glycogen by Means of Nutrient Intervention, 113
john l. ivy
9 Carbohydrate Ingestion During Exercise, 126
asker jeukendrup
10 Defi ning Optimum Protein Intakes
for Athletes, 136
stuart m. phillips
11 Dietary Protein as a Trigger for Metabolic
Adaptation, 147
luc j.c. van loon
12 Fat Metabolism During and After Exercise, 156
bente kiens, jacob jeppesen
13 Metabolic Adaptations to a High-Fat Diet, 166
john a. hawley, wee kian yeo
14 Water and Electrolyte Loss and Replacement
in Training and Competition, 174
ronald j. maughan
15 Performance Effects of Dehydration, 185
eric d.b. goulet
16 Rehydration and Recovery After Exercise, 199
susan m. shirreffs
17 Nutritional Effects on Central Fatigue, 206
bart roelands, romain meeusen
vi contents
30 The Aging Athlete, 369
christine a. rosenbloom
31 The Vegetarian Athlete, 382
jacqueline r. berning
32 The Special Needs Athlete, 392
elizabeth broad
33 Overreaching and Unexplained
Underperformance Syndrome:
Nutritional Interventions, 404
paula robson-ansley,
ricardo costa
34 The Traveling Athlete, 415
susie parker-simmons, kylie andrew
35 Environment and Exercise, 425
samuel n. cheuvront,
brett r. ely, randall l. wilber
36 Food and Nutrition Considerations at Major
Competitions, 439
fiona pelly
Part 5 Health-Related and Clinical Sports
Nutrition
37 Nutrition, Physical Activity, and Health, 455
barry braun, benjamin f. miller
38 Exercise, Nutrition, and Infl ammation, 466
michael j. kraakman, martin
whitham, mark a. febbraio
39 Exercise, Nutrition, and Immune Function, 478
david c. nieman
40 The Diabetic Athlete, 490
gurjit bhogal, nicholas peirce
41 The Overweight Athlete, 503
helen o’connor
42 Eating Disorders in Male and Female
Athletes, 513
monica k. torstveit,
jorunn sundgot-borgen
Part 3 Micronutrients and Dietary Supplements
18 Vitamins, Minerals, and Sport Performance, 217
stella l. volpe, ha nguyen
19 Iron Requirements and Iron Status of
Athletes, 229
giovanni lombardi, giuseppe lippi ,
giuseppe banfi
20 Calcium and Vitamin D, 242
enette larson-meyer
21 Exercise-Induced Oxidative Stress: Are
Supplemental Antioxidants Warranted?, 263
john c. quindry, andreas kavazis,
scott k. powers
22 Dietary Phytochemicals, 277
j. mark davis, benjamin gordon,
e. angela murphy, martin d.
carmichael
23 Risks and Rewards of Dietary Supplement Use
by Athletes, 291
ronald j. maughan
24 Creatine, 301
francis b. stephens, paul l.
greenhaff
25 Caffeine and Exercise Performance, 313
lawrence l. spriet
26 Buffering Agents, 324
craig sale, roger c. harris
27 Alcohol, Exercise, and Sport, 336
ronald j. maughan, susan m.
shirreffs
Part 4 Practical Issues
28 The Female Athlete, 347
susan i . barr
29 The Young Athlete, 359
flavia meyer, brian w. timmons
c o n t e n t s v i i
48 Cycling, 584
peter hespel
49 Gymnastics, 596
dan benardot
50 Swimming, 607
louise m. burke, gregory shaw
51 Winter Sports, 619
nanna l. meyer
52 Team Sports, 629
francis holway
53 Weight-Category Sports, 639
hattie h. wright, ina garthe
Index, 651
43 Importance of Gastrointestinal Function to
Athletic Performance and Health, 526
nancy j. rehrer, john mclaughlin,
lucy k. wasse
44 Hyponatremia of Exercise, 539
timothy d. noakes
Part 6 Sport-Specifi c Nutrition: Practical Issues
45 Strength and Power Events, 551
eric s . rawson, charles e.
brightbill, michael j. stec
46 Sprinting: Optimizing Dietary Intake, 561
gary slater, helen o’connor,
bethanie allanson
47 Distance Running, 572
trent stellingwerff
viii
GURJIT BHOGAL, MBChB, MSc, MRCGP, Queen’s
Medical Centre, Nottingham, UK
BARRY BRAUN, PhD, Department of Kinesiology,
University of Massachusetts, Amherst, MA, USA
CHARLES E. BRIGHTBILL, BS, Department of
Exercise Science, Bloomsburg University, Bloomsburg, PA, USA
ELIZABETH BROAD, PhD, Sports Nutrition,
Australian Institute of Sport, Canberra, ACT, Australia
LOUISE M. BURKE, OAM, PhD, APD, Sports
Nutrition, Australian Institute of Sport, Canberra, ACT, Australia
MARTIN D. CARMICHAEL, PhD, Department of
Physical Education and Exercise Studies, College of Education,
Lander University, Greenwood, SC, USA
SAMUEL N. CHEUVRONT, PhD, RD, Thermal &
Mountain Medicine Division, US Army Research Institute of
Environmental Medicine, Natick, MA, USA
RICARDO COSTA, PhD, RD, RSEN, Department of
Nutrition and Dietetics, Faculty of Medicine Nursing and
Health Sciences, Monash University, Melbourne, VIC, Australia
J. MARK DAVIS, PhD, Psychoneuroimmunology of
Exercise and Nutrition Lab, Division of Applied Physiology,
Department of Exercise Science, University of South Carolina,
Columbia, SC, USA
BRETT R. ELY, MS, Thermal & Mountain Medicine
Division, US Army Research Institute of Environmental
Medicine, Natick, MA, USA
TIMOTHY R. ACKLAND, PhD, School of Sport
Science, Exercise and Health, University of Western Australia,
Crawley, WA, Australia
BARBARA E. AINSWORTH, PhD, MPH, Program
in Exercise and Wellness, School of Nutrition and Health
Promotion, Arizona State University, Phoenix, AZ, USA
BETHANIE ALLANSON, Hons Diet, Faculty of
Computing, Health and Science, Edith Cowan University,
Joondalup, WA, Australia
KYLIE ANDREW, M Diet & Nut, Victorian Institute of
Sport, Albert Park, VIC, Australia
GIUSEPPE BANFI, MD, Laboratory of Experimental
Biochemistry and Molecular Biology, IRCCS Galeazzi
Orthopaedic Institute, Milan, Italy; Department of Biomedical
Sciences for Health, University of Milan, Milan, Italy
SUSAN I. BARR, PhD, Faculty of Land and Food Systems,
University of British Columbia, Vancouver, BC, Canada
DAN BENARDOT, PhD, Department of Nutrition,
Division of Health Professions, Byrdine F. Lewis School of
Nursing and Health Professions, Georgia State University,
Atlanta, GA, USA
DAVID A. BENDER, PhD, Emeritus Professor of
Nutritional Biochemistry, University College London, London, UK
JACQUELINE R. BERNING, PhD, RD, CSSD,
Biology Department, University of Colorado, Colorado
Springs, CO, USA
List of Contributors
l i s t o f c o n t r i b u t o r s i x
MARK A. FEBBRAIO, PhD, Cellular and Molecular
Metabolism Laboratory, Baker IDI Heart and Diabetes
Institute, Melbourne, VIC, Australia; Department of
Biochemistry and Molecular Biology, Monash University,
Melbourne, VIC, Australia
INA GARTHE, PhD, Department of Sports Nutrition,
Olympic Sports Centre, Oslo, Norway
MICHAEL GLEESON, PhD, School of Sport, Exercise
and Health Sciences, Loughborough University, Loughborough,
UK
BENJAMIN GORDON, MS, Psychoneuroimmunology
of Exercise and Nutrition Lab, Division of Applied Physiology,
Department of Exercise Science, University of South Carolina,
Columbia, SC, USA
ERIC D.B. GOULET, PhD, Research Centre on Aging
and Faculty of Physical Education and Sports, University of
Sherbrooke, Sherbrooke, QC, Canada
PAUL L. GREENHAFF, PhD, MRC/Arthritis
Research UK Centre for Musculoskeletal Ageing
Research, School of Biomedical Sciences, University of
Nottingham Medical School, Queen’s Medical Centre,
Nottingham, UK
ROGER C. HARRIS, PhD, Junipa Ltd, Newmarket,
Suffolk, UK
JOHN A. HAWLEY, PhD, Exercise Metabolism Group,
School of Medical Sciences, RMIT University, Bundoora, VIC,
Australia
PETER HESPEL, PhD, Exercise Physiology
Research Group, Department of Kinesiology, Faculty of
Kinesiology and Rehabilitation Sciences, KU Leuven,
Leuven, Belgium
FRANCIS HOLWAY, MSc, Departamento de Medicina
Aplicada a los Deportes, Club Atlético River Plate, Buenos
Aires, Argentina
JOHN L. IVY, PhD, Exercise Physiology and Metabolism
Laboratory, Department of Kinesiology and Health Education,
University of Texas, Austin, TX, USA
JACOB JEPPESEN, PhD, Molecular Physiology Group,
Institute of Nutrition, Exercise and Sports, University of
Copenhagen, Copenhagen, Denmark
ASKER JEUKENDRUP, PhD, Gatorade Sports
Science Institute, Barrington, IL, USA; School of Sport and
Exercise Sciences, University of Birmingham, Edgbaston,
Birmingham, UK
ANDREAS N. KAVAZIS, PhD, Department of
Kinesiology, Mississippi State University, MS, USA
W. LARRY KENNEY, PhD, Noll Laboratory,
Pennsylvania State University, University Park, PA,
USA
BENTE KIENS, Dr Scient, Molecular Physiology Group,
Institute of Nutrition, Exercise and Sports, University of
Copenhagen, Copenhagen, Denmark
MICHAEL J. KRAAKMAN, BPhEd (Hons),
Cellular and Molecular Metabolism Laboratory, Baker IDI
Heart and Diabetes Institute, Melbourne, VIC, Australia;
Department of Biochemistry and Molecular Biology, Monash
University, Melbourne, VIC, Australia
ENETTE LARSON-MEYER, PhD, RD,
Nutrition and Exercise Laboratory, Department of Family
and Consumer Sciences, University of Wyoming, Laramie,
WY, USA
GIUSEPPE LIPPI, PhD, Laboratory of Clinical
Chemistry and Hematology, Department of Pathology and
Laboratory Medicine, University Hospital of Parma,
Parma, Italy
GIOVANNI LOMBARDI, PhD, Laboratory of
Experimental Biochemistry and Molecular Biology, IRCCS
Galeazzi Orthopaedic Institute, Milan, Italy
ANNE B. LOUCKS, PhD, Department of Biological
Sciences, Ohio University, Athens, OH, USA
RONALD J. MAUGHAN, PhD, School of Sport,
Exercise and Health Sciences, Loughborough University,
Loughborough, UK
x list of contributors
NICHOLAS PEIRCE, MD, Queen’s Medical Centre,
Nottingham, UK; National Cricket Performance Centre,
Loughborough University, Loughborough, UK
FIONA PELLY, PhD, APD, School of Health and Sport
Sciences, University of the Sunshine Coast, Maroochydore DC,
QLD, Australia
STUART M. PHILLIPS, PhD, Department of
Kinesiology, Exercise Metabolism Research Group, McMaster
University, Hamilton, ON, Canada
SCOTT K. POWERS, PhD, Department of Applied
Physiology and Kinesiology, University of Florida, Gainesville,
FL, USA
JOHN C. QUINDRY, PhD, Department of Kinesiology,
Auburn University, Auburn, AL, USA
ERIC S. RAWSON, PhD, Department of Exercise
Science, Bloomsburg University, Bloomsburg, PA, USA
NANCY J. REHRER, PhD, School of Physical
Education, University of Otago, Dunedin, New Zealand;
Department of Human Nutrition, University of Otago,
Dunedin, New Zealand
PAULA ROBSON-ANSLEY, PhD, Department of
Sports, Exercise and Rehabilitation, Faculty of Health and
Life Sciences, Northumbria University, Newcastle upon
Tyne, UK
BART ROELANDS, PhD, Department of Human
Physiology and Sports Medicine, Vrije Universiteit Brussel,
Brussels, Belgium; Fund for Scientifi c Research Flanders
(FWO), Brussels, Belgium
CHRISTINE A. ROSENBLOOM, PhD, RD, CSSD,
Division of Nutrition, Byrdine F. Lewis School of Health
Professions, Georgia State University, Atlanta, GA, USA
CRAIG SALE, PhD, Sport, Health and Performance
Enhancement (SHAPE) Research Group, Biomedical Life
and Health Sciences Research Centre, School of Science and
Technology, Nottingham Trent University, Nottingham, UK
GREGORY SHAW, BHSc, Sports Nutrition, Australian
Institute of Sport, Canberra, ACT, Australia
JOHN MCLAUGHLIN, MBChB, PhD,
Gastrointestinal Centre, Institute of Infl ammation and Repair,
Faculty of Medical and Human Sciences, University of
Manchester, Manchester, UK; Manchester Academic Health
Sciences Centre, University of Manchester, Salford Royal
Hospital, Salford, UK
ROMAIN MEEUSEN, PhD, Department of Human
Physiology and Sports Medicine, Vrije Universiteit Brussel,
Brussels, Belgium
FLAVIA MEYER, MD, PhD, Exercise Research
Laboratory (LAPEX), Federal University of Rio Grande do Sul
(UFRGS), Porto Alegre, Brazil
NANNA L. MEYER, PhD, RD, CSSD, University of
Colorado, Colorado Springs, CO, USA; United States Olympic
Committee, Colorado Springs, CO, USA
BENJAMIN F. MILLER, PhD, Department of Health
and Exercise Science, Colorado State University, Fort Collins,
CO, USA
E. ANGELA MURPHY, PhD, Department of
Pathology, Microbiology & Immunology, School of Medicine,
University of South Carolina, Columbia, SC, USA
ROBERT MURRAY, PhD, Sports Science Insights,
LLC, Crystal Lake, IL, USA
HA NGUYEN, BS, Department of Nutrition Sciences,
Drexel University, Philadelphia, PA, USA
DAVID C. NIEMAN, DrPH, Human Performance
Laboratory, Appalachian State University, Kannapolis, NC, USA
TIMOTHY D. NOAKES, MBChB, MD, DSc,
UCT/MRC Research Unit for Exercise Science and Sports
Medicine, Department of Human Biology, University of Cape
Town, Sports Science Institute of South Africa, Newlands,
South Africa
HELEN O’CONNOR, PhD, Faculty of Health
Sciences, University of Sydney, Sydney, NSW, Australia
SUSIE PARKER-SIMMONS, MEd, M Diet & Nut,
United States Olympic Committee, Colorado Springs, CO, USA
l i s t o f c o n t r i b u t o r s x i
SUSAN M. SHIRREFFS, PhD, GlaxoSmithKline,
Brentford, Middlesex, UK; School of Sport, Exercise and Health
Sciences, Loughborough University, Loughborough, UK
GARY SLATER, PhD, Faculty of Science, Health and
Education, University of the Sunshine Coast, Maroochydore
DC, QLD, Australia
LAWRENCE L. SPRIET, PhD, Department of Human
Health & Nutritional Sciences, University of Guelph, Guelph,
ON, Canada
MICHAEL J. STEC, MS, Department of Cell,
Developmental, and Integrative Biology, University of
Alabama at Birmingham, Birmingham, AL, USA
TRENT STELLINGWERFF, PhD, Canadian Sports
Institute—Pacifi c, Pacifi c Institute for Sport Excellence,
Victoria, BC, Canada
FRANCIS B. STEPHENS, PhD, MRC/Arthritis
Research UK Centre for Musculoskeletal Ageing Research,
School of Biomedical Sciences, University of Nottingham
Medical School, Queen’s Medical Centre, Nottingham, UK
ARTHUR D. STEWART, BSc, BPE, MPhil, PhD,
Centre for Obesity Research and Epidemiology, Robert Gordon
University, Aberdeen, Scotland, UK
JORUNN SUNDGOT-BORGEN, PhD,
Department of Sport Medicine, Norwegian School of Sport
Sciences, Oslo, Norway
BRIAN W. TIMMONS, PhD, Child Health and
Exercise Medicine Program, McMaster University, Hamilton,
ON, Canada
MONICA K. TORSTVEIT, PhD, Faculty of Health
and Sport Sciences, University of Agder, Kristiansand, Norway
LUC J.C. VAN LOON, PhD, Department of Human
Movement Sciences, NUTRIM School for Nutrition,
Toxicology and Metabolism, Maastricht University Medical
Centre, Maastricht, The Netherlands
STELLA L. VOLPE, PhD, RD, LDN, Department of
Nutrition Sciences, Drexel University, Philadelphia, PA, USA
LUCY K. WASSE, PhD, Gastrointestinal Centre,
Institute of Infl ammation and Repair, Faculty of Medical and
Human Sciences, University of Manchester, Manchester, UK;
Manchester Academic Health Sciences Centre, University of
Manchester, Salford Royal Hospital, Salford, UK
MARTIN WHITHAM, PhD, Cellular and Molecular
Metabolism Laboratory, Baker IDI Heart and Diabetes
Institute, Melbourne, VIC, Australia
RANDALL L. WILBER, PhD, United States Olympic
Committee, Colorado Springs, CO, USA
HATTIE H. WRIGHT, PhD, Centre of Excellence for
Nutrition, Faculty of Health Sciences, North-West University,
Potchefstroom, South Africa
WEE KIAN YEO, PhD, Division of Research and
Innovation, National Sports Institute of Malaysia, Kuala
Lumpur, Malaysia
xii
volume appears in this rapidly expanding fi eld of
research and practice.
A highly qualifi ed team of international author-
ities present a comprehensive coverage of macro-
nutrients, micronutrients, and dietary supplements
for the athlete. Extensive coverage is given both to
general practical issues and to sports-specifi c issues.
Professor Ronald J. Maughan has been a fre-
quent contributor to both the Encyclopaedia of Sports Medicine series and the Handbook of Sports Medicine and Science series as published by the IOC Medical
Commission. We welcome with great appreciation
his latest publication project related to the science
and medicine of sport.
Dr Jacques Rogge
IOC President
The publication of the Encyclopaedia of Sports Medi-cine, Volume VII Nutrition in Sport, by the IOC Medi-
cal Commission in 2000 constituted a milestone in
the rapid growth of research on sports nutrition
during the last quarter century. Concomitant with
this growth has been the increasing body of evi-
dence concerning the important interactive roles of
proper nutrition and a balanced program of physi-
cal exercise for each person’s health and welfare.
Since the appearance of that volume, a large
amount of research has appeared in scientifi c jour-
nals concerning the role of nutrition in the training
programs of athletes and in their preparation for
competition. It is, therefore, timely that this new
Foreword
xiii
Preface
A comparison of the content of the two volumes
will reveal some constants and some changes. Per-
haps the most important change that has taken
place in recent years is the recognition that the pri-
mary role of nutrition in the athlete’s life is to sup-
port consistent training and to enhance the process
of adaptation that takes place in every tissue of the
body in response to each individual training ses-
sion. It is the sum of these vanishingly small incre-
mental changes that translates into an enhanced
performance. Nutrition support is more about
promoting those changes rather than simply allow-
ing the athlete to recover more effectively between
training sessions and, therefore, to train harder.
Training harder undoubtedly brings some benefi ts
in terms of performance improvement, but it also
brings increased risks of illness and injury. Training
more effectively, rather than just training harder, is
surely a better option.
Those who work at the molecular level have
given us an understanding of the signaling path-
ways within cells that modulate gene expression in
response to training and diet. This understanding
was almost completely absent until very recently,
and these new approaches have great promise for
identifying strategies that might allow even bet-
ter performances than those of today’s athletes. At
the same time, however, there has been a renewed
interest in the adaptations that take place at the
whole body level, including perhaps especially the
links between the brain and the peripheral tissues.
The two approaches, the molecular and the whole
body, have emphasized the individuality of the res-
ponse to both diet and exercise and of the need for
Most of us eat every day, indeed several times every
day. What we eat will affect how we feel and how
we perform, both in the short term and in the long
term. The immediate effects are often small and eas-
ily dismissed. However, after only a short period—
a few days at most—without food, performance in
most tests of physical and mental performance will
inevitably decline. Similar effects are seen if some
food is allowed but the intake of carbohydrate or
water is restricted. It is easy, therefore, to demon-
strate the impact of nutrition on athletic perfor-
mance. Nutrition, though, has many far more subtle
effects on the athlete’s well-being and performance.
A whole range of essential nutrients must be sup-
plied in the right amounts and at the right times if
health and performance are to be optimized. Food,
and the pleasures as well as the nutrients it gives to
the consumer, is a vital part of everyday life. Sports
nutrition must therefore be concerned not only with
the identifi cation of the athlete’s nutritional goals but
also with the translation of these goals into an eating
strategy that takes account of personal preferences,
social and cultural issues, and a whole range of other
factors.
The Medical Commission of the International
Olympic Committee (IOC) has consistently recog-
nized the importance of nutrition in every aspect
of the elite athlete’s life. In choosing to commission
a new encyclopedia volume on the relationships
between diet and performance, the IOC has recog-
nized the great changes that have taken place in our
understanding since the publication of the earlier
version that appeared three Olympic cycles previ-
ously.
xiv preface
view of the key issues. Those who seek to advise
athletes or whose aspiration is to make the next
great advance in our understanding must be pre-
pared to dig much deeper, but perhaps this volume
will provide a framework and a reference point for
further study.
Ronald J. Maughan
Loughborough, UK
individualization and periodization of nutrition
strategies to allow athletes to reach their genetic
potential.
The contributors to this book are, without excep-
tion, world leaders in their fi elds. Each has given
unstintingly of their knowledge and experience in
preparing their chapters. The result is a substan-
tial volume, but such is the scope of the science and
practice of sports nutrition that even this can be no
more than an introduction to the fi eld and an over-
PART 1
THE UNDERPINNING
SCIENCE
Sports Nutrition, 1st Edition. Edited by Ronald J. Maughan.
© 2014 International Olympic Committee. Published 2014 by
John Wiley & Sons, Ltd.
3
Chapter 1
Human Nutrition
DAVID A. BENDER
University College London, London, UK
tissue with increasing age (even when body weight
remains constant). The gender difference is because
women have a greater percentage of body weight as
essential and storage adipose tissue than do men.
Table 1.1 shows equations for calculating BMR from
age, gender, body weight, and height.
The energy cost of different activities is most
commonly expressed as a multiple of BMR—the
physical activity ratio (PAR) for any given activity.
As shown in Table 1.2, PAR ranges from about 1.2×
BMR for sedentary activities up to 6× or more times
BMR for vigorous exercise, and signifi cantly higher
for some sports. Table 1.3 shows the classifi cation of
occupational work by PAR over the 8-hour working
day, excluding leisure activities.
Summing the PAR for different activities through-
out the day, multiplied by the time spent in each
activity as a fraction of 24 hours, allows the calcu-
lation of a person’s physical activity level (PAL),
again as a multiple of BMR. A person’s total energy
expenditure is then (PAL × BMR) + an allowance for
diet-induced thermogenesis (DIT)—the energy cost
of digestion and absorption, plus the cost of synthe-
sizing glycogen, fat, and protein after a meal. DIT is
about 10–15% of the energy yield of a meal. For peo-
ple with a markedly sedentary lifestyle BMR may
represent 80–90% of total energy expenditure.
Measurement of BMR and Energy Expenditure
in Activity
The gold standard method of measuring BMR and
energy expenditure in an activity is by measurement
of heat output from the body. This is done using
a calorimeter—an insulated chamber in which a
The fi rst requirement in human nutrition is for an
energy source; the metabolic fuels that provide this
are carbohydrates, fats, protein, and alcohol. There
is also a need for protein, not only in growth when
the total amount of protein in the body is increasing
but also throughout life to permit turnover of tissue
proteins. In addition, there is a need for some essen-
tial fatty acids and for relatively small amounts
(milligrams or micrograms per day) of vitamins and
minerals.
Energy Nutrition
Even when completely at rest there is a requirement
for energy to maintain nerve and muscle tone, cir-
culation and breathing, and metabolic homeosta-
sis. When measured under controlled conditions
of thermal neutrality (so that energy is not being
expended in keeping warm or cooling down) and
completely at rest (but not asleep, since some people
increase their metabolic rate when asleep, while
others reduce it), this is the basal metabolic rate
(BMR). When the measurement is made under less
strictly controlled conditions, the result is termed
the resting metabolic rate (RMR). BMR depends on
body weight, age, and gender and refl ects mainly
the metabolically more active lean tissues of the
body, although adipose tissue makes a modest
contribution to BMR. The effect of age on BMR
refl ects the replacement of muscle tissue by adipose
4 chapter 1
Table 1.1 Equations for estimating basal metabolic rate from weight or weight and height, at different ages
Age (years)
Males Females
MJ/day kcal/day MJ/day kcal/day
0–3 0.2548w − 0.226 60.9w − 54 0.255w − 0.213 61.0w − 51
0.007w + 6.349h − 2.584 1.673w + 1517h − 617 0.068w + 4.281h − 1.730 16.252w + 1023h − 413
3–10 0.0949w + 2.07 22.7w + 495 0.0941w + 2.09 22.5w + 499
0.082w + 0.545h + 1.736 19.59w + 130h + 415 0.071w + 0.677h + 1.5453 16.97w + 161h + 531
10–17 0.0732w + 2.72 17.5w + 651 0.0510w + 3.12 12.2w + 746
0.068w + 0.574h + 2.157 16.25w + 137h + 516 0.035w + 1.948h + 0.837 8.365w + 465h + 200
18–29 0.0640w + 2.84 15.3w + 679 0.0615w + 2.08 14.7w + 496
0.063w − 0.042h + 2.953 15.06w + 10.04h + 705 0.057w + 1.184h + 0.411 13.62w + 283h + 98
30–59 0.0485w + 3.67 11.6w + 879 0.0364w + 3.47 8.7w + 829
0.048w − 0.011h + 3.670 11.47w + 2.629h + 877 0.034w + 0.006h + 3.530 8.126w + 4.434h + 843
>60 0.0565w + 2.04 13.5w + 487 0.0439w + 2.49 10.5w + 596
Source: Data reported by Schofi eld (1985a, 1985b); recalculated for estimation of BMR in kcal. w, body weight (kg); h, height (m).
Table 1.2 Energy cost of activity, by Physical Activity Ratio (PAR) or multiple of BMR
PAR
1.0–1.4 Lying, standing, or sitting at rest, e.g., watching TV, reading, writing, eating, playing cards, and
board games
1.5–1.8 Sitting: sewing, knitting, playing piano, drivingStanding: preparing vegetables, washing dishes, ironing, general offi ce and laboratory work
1.9–2.4 Standing: mixed household chores, cooking, playing snooker or bowls
2.5–3.3 Standing: dressing, undressing, showering, making beds, vacuum cleaningWalking: 3–4 km/h, playing cricketOccupational: tailoring, shoemaking, electrical and machine tool industry, painting and
decorating
3.4–4.4 Standing: mopping fl oors, gardening, cleaning windows, table tennis, sailingWalking: 4–6 km/h, playing golfOccupational: motor vehicle repairs, carpentry and joinery, chemical industry, bricklaying
4.5–5.9 Standing: polishing furniture, chopping wood, heavy gardening, volley ballWalking: 6–7 km/hExercise: dancing, moderate swimming, gentle cycling, slow joggingOccupational: laboring, hoeing, road construction, digging and shoveling, felling trees
6.0–7.9 Walking: uphill with load or cross-country, climbing stairsExercise: jogging, cycling, energetic swimming, skiing, tennis, football
Source: Department of Health (1991) and WHO (1985).
h u m a n n u t r i t i o n 5
confi ned to the laboratory. If the production of car-
bon dioxide is also measured then it is possible to
calculate the relative amounts of fat, carbohydrate,
and protein being metabolized from the respiratory
quotient (RQ)—the ratio of carbon dioxide pro-
duced to oxygen consumed. When carbohydrate is
being oxidized the RQ = 1, while for fat oxidation
RQ = 0.707. The amount of protein being metabo-
lized can be calculated separately from the excretion
of urea, the end product of amino acid metabolism.
If respirometry includes the measurement of car-
bon dioxide and oxygen, as well as urinary nitrogen,
then it is possible to estimate both energy expendi-
ture and the proportions of different fuels being uti-
lized, from the following formulae (Weir, 1949):
• Energy expenditure (kJ) = 16.849 × ml oxygen con-
sumed + 4.628 × ml carbon dioxide produced −
9.079 × g N excreted
• Energy expenditure (kcal) = 4.025 × ml oxygen
consumed + 1.106 × ml carbon dioxide pro-
duced − 2.168 × g N excreted
If urinary nitrogen is not determined, and it is
assumed that protein provides 15% of energy, then
• Energy expenditure (kJ) = 16.318 × ml oxygen
consumed + 4.602 × ml carbon dioxide produced
• Energy expenditure (kcal) = 3.898 × ml oxygen
consumed + 1.099 × ml carbon dioxide produced
The amount of each fuel being utilized can be cal-
culated from
• Grams carbohydrate oxidized = 4.706 × ml carbon
dioxide produced − 3.340 × ml oxygen con-
sumed − 2.714 × g N excreted
constant temperature is maintained by running cold
water through pipes and measuring the increase in
the temperature of the water. Obviously, the range
of activities that can be achieved in a small chamber
is limited, and rather than direct calorimetry, most
studies use indirect calorimetry, i.e., the measure-
ment of the rate of oxygen consumption (Levine,
2005). As shown in Table 1.4, to fi rst approximation,
1 liter of oxygen consumed is equivalent to 20 kJ of
energy expenditure. This means that measurement
of oxygen consumption can be used to estimate
energy expenditure in a wide range of activities, not
Table 1.3 Classifi cation of types of occupational work
by PAR (average PAR through 8-hour working day,
excluding leisure activities)
PAR
Men Women
Light 1.7 1.7 Professional, clerical,
and technical workers,
administrative and
managerial staff, sales
representatives, housewives
Moderate 2.7 2.2 Sales staff, domestic service,
students, transport workers,
joiners, roofi ng workers
Moderately
heavy
3.0 2.3 Machine operators,
laborers, agricultural
workers, forestry, hunting
and fi shing, bricklaying,
masonry
Heavy 3.8 2.8 Laborers, agricultural
workers, bricklaying,
masonry where there is
little or no mechanization
Source: Department of Health (1991).
Table 1.4 Oxygen consumption and carbon dioxide production in the oxidation of metabolic fuels
Energy
yield (kJ/g)
Oxygen
consumed (l/g)
Carbon dioxide
produced (l/g)
Respiratory
quotient (CO2/O2)
Energy/oxygen
consumption (kJ/l oxygen)
Carbohydrate 16 0.829 0.829 1.0 19.3
Protein 17 0.966 0.782 0.809 17.5
Fat 37 2.016 1.427 0.707 18.35
6 chapter 1
From records of food eaten, the average RQ over the
period can be estimated and hence, allowing for any
changes in body weight, the total oxygen consump-
tion and energy expenditure can be calculated.
Recommendations and Reference Levels for
Energy Intake
Unlike reference intakes for protein and micronu-
trients which allow a margin of 2× standard devia-
tion above the observed average requirement, so as
to allow for individual variation and cover almost
all of the population, reference levels for energy
intake (see Table 1.5) are based on average require-
ments, since adding 2× standard deviation would
result in half the population being over-provided
with energy, and hence contribute to the devel-
opment of obesity. At its simplest, energy intake
should match energy expenditure and hence,
assuming that body weight is within the desirable
range (a body mass index of 20–25 kg/m2), should
be such that a constant body weight is achieved.
• Grams fat oxidized = 1.768 × ml oxygen con-
sumed − 1.778 × ml carbon dioxide produced −
2.021 × g N excreted
• Grams protein oxidized = 6.25 × g N excreted
Although classical respirometer studies have
allowed the measurement of energy expenditure in
many activities (and indeed provided the data for
PAR shown in Table 1.2), such studies are, of neces-
sity, short term. A more recent development has
been the use of double stable isotopically labeled
water (2H218O), which provides a noninvasive
method of measuring energy expenditure over a
period of 1–3 weeks. As shown in Figure 1.1, the
label from 18O is lost from the body faster than that
from 2H. This is because the labeled hydrogen is lost
from the body only as water, while the oxygen is
lost in both water and carbon dioxide, because of
the rapid equilibrium between carbon dioxide and
bicarbonate (Heymsfi eld et al., 2006; Ritz & Cow-
ard, 1995; Speakman, 1997).
Following an oral dose of 2H218O, the iso-
topic enrichment of water in plasma, saliva, or
urine is determined at intervals over a period of
10–21 days. The rate of carbon dioxide production
is then calculated from the greater rate of loss of 18O than 2H, as
• Carbon dioxide production rate = (0.5 × total
body water) × (rate constant for 18O disappear-
ance − rate constant for 2H disappearance)
0
Rela
tive isoto
pe e
nrichm
ent
0
20
40
60
80
100
5 10 15 20 25
Time (days)
2H
18O
Figure 1.1 Loss of label from 2H218O—the basis of the
dual isotopically labeled water method for estimating
total energy expenditure.
Table 1.5 Estimated average requirements for energy
Males Females
Age MJ/day kcal/day MJ/day kcal/day
0–3 months 2.28 545 2.06 515
4–6 months 2.89 690 2.69 645
7–9 months 3.44 825 3.20 765
10–12 months 3.85 920 3.61 865
1–3 years 5.15 1230 4.86 1165
4–6 years 7.16 1715 6.46 1545
7–10 years 8.24 1970 7.28 1740
11–14 years 9.27 2220 7.92 1845
15–18 years 11.51 2755 8.83 2110
19–50 years 10.6 2550 8.10 1940
51–59 years 10.6 2550 8.00 1900
60–64 years 9.93 2380 7.99 1900
65–74 years 9.71 2330 7.96 1900
>75 years 8.77 2100 7.61 1810
Source: Department of Health (1991).
h u m a n n u t r i t i o n 7
a contributory factor in atherosclerosis and cor-
onary artery disease. The current consensus is
that fat should provide 30% of energy intake for
the general population (Prentice, 2005), though
the fraction may be higher or lower for athletes,
depending on the training load and therefore
on the energy demand. At very low fat intakes,
it is diffi cult to absorb the fat-soluble vitamins
A, D, E, and K, which are absorbed in lipid
micelles together with the products of dietary fat
digestion.
The type of dietary fat is also important.
Figure 1.2 shows the families of fatty acids and
Table 1.6, the main dietary fatty acids. There is
a convenient shorthand notation for fatty acids
showing the number of carbon atoms, and the
number of double bonds and the position of the
fi rst double bond from the methyl group as either
n–3, 6, or 9 or ω3, 6, or 9.
Carbohydrate, Fat, and Protein as Metabolic Fuels
There is no absolute requirement for a dietary
source of carbohydrate or fat (apart from essential
fatty acids, see below), but there is a need to main-
tain an adequate supply of glucose for the brain
(which is largely dependent on glucose) and red
blood cells (which are completely dependent on
glucose).
The current consensus (Prentice, 2005) is that
carbohydrates should provide about 55% of
energy intake for the general population, largely
as starches and other complex carbohydrates,
with sugars providing no more than about 10% of
energy intake. For athletes, it is more common to
express daily carbohydrate requirements in abso-
lute terms, as grams of carbohydrate per kilogram
of body mass, as this is independent of energy
intake which may vary widely. Sugars are divided
into intrinsic sugars, contained within the cells of
plant foods, and extrinsic sugars in free solution;
it is these extrinsic sugars that should be limited,
mainly to reduce the risk of dental caries and also
because it is easy to overconsume sugars in bever-
ages, etc., leading to obesity. In the United King-
dom, lactose in milk is considered separately from
other extrinsic sugars, since it does not contribute
to the development of dental caries and milk is
an important source of calcium and ribofl avin in
most diets.
Glucose needs for the brain and red blood cells
can be met by gluconeogenesis from amino acids
and glycerol in fasting (or when the diet is low in
carbohydrate and high in protein), albeit at a rela-
tively high energy cost. The increase in metabolic
rate associated with gluconeogenesis explains much
of the weight loss associated with very low carbohy-
drate diets that permit more or less unlimited con-
sumption of protein-rich foods.
When the diet provides less than about 15% of
energy from fat, it is diffi cult to eat a suffi cient
volume of food to meet energy requirements.
Conversely, when the diet provides more than
about 35% of energy from fat it is easy to overcon-
sume food, leading to obesity. More importantly,
a high fat intake leads to persistence of athero-
genic chylomicron remnants in the bloodstream,
OH
OH
O
OH
O
Saturated fatty acid (stearic acid, C18:0)
Monounsaturated fatty acid (oleic acid, C18: ω19)
Polyunsaturated fatty acid (linoleic acid, C18:2 ω6)
Polyunsaturated fatty acid (α-linolenic acid, C18:3 ω3)OH
O
cis-
trans-
Figure 1.2 The families of fatty acids and cis–trans isom-
erism in unsaturated fatty acids.
8 chapter 1
fatty acids are poor substrates for esterifi cation of
cholesterol, while monounsaturated are better, and
polyunsaturated are the best substrates. Stearic acid
(C18:0), although saturated, has less adverse effect
on LDL cholesterol than other saturated fatty acids
because it is readily unsaturated to oleic acid (C18:1
ω9). It is recommended that no more than one-third
of fat intake (10% of energy intake) should be from
saturated fatty acids, with 6% from polyunsaturated
fatty acids.
Trans-isomers of unsaturated fatty acids arise
during the catalytic hydrogenation of vegetable
oils to yield spreadable fats, and also occur in mod-
est amounts in fats from ruminants. They do not
have the same benefi cial effect on LDL cholesterol
as do the cis-isomers, but are atherogenic, and may
adversely affect the fl uidity of cell membranes. It
is therefore recommended that trans-fatty acids
should provide less than 2% of energy intake (Brit-
ish Nutrition Foundation, 1995).
As shown in Figure 1.2, there are three families
of unsaturated fatty acids, with the fi rst double
bond at the ω3, ω6, or ω9 position. Human beings
have an enzyme that can introduce a double bond
into a saturated fatty acid at the ω9 position and
enzymes that can introduce double bonds between
ω3 or ω6 and the carboxyl group, but not between
ω9 and the methyl group. This means that there is
a requirement for a dietary source of both ω3 and
ω6 polyunsaturated fatty acids, which are precur-
sors of prostaglandins and other eicosanoids that
acts as signaling molecules. These are the essential
fatty acids—linoleic and linolenic acids, which can
undergo chain elongation and further desaturation
in the body. The same enzymes are involved in the
chain elongation, desaturation, and onward metab-
olism to eicosanoids for both ω3 and ω6 polyunsatu-
rated fatty acids, and the balance between the two
families of fatty acids in the diet, is important.
In addition to the requirement for protein per se,
protein must also be considered as a metabolic fuel.
For an adult in nitrogen balance, whose total body
protein content is constant, an amount of amino
acids equivalent to the dietary intake of protein
will be metabolized each day, as an energy source.
The metabolism of amino acids is less effi cient than
that of carbohydrates, since there are a number of
High intakes of saturated fatty acids lead to an
increase in low-density lipoprotein (LDL) chol-
esterol and are therefore a major factor in atherogen-
esis. Compared with monounsaturated fatty acids,
saturated fatty acids lead to an increase in LDL
cholesterol proportional to twice the intake. Polyun-
saturated fatty acids lead to a decrease in LDL chol-
esterol proportional to their intake (Anderson et al.,
1957; Armstrong et al., 1957; Hegsted et al., 1965,
1993; Keys et al., 1957). This is because saturated
Table 1.6 Fatty acid nomenclature
C atoms
Double bonds
ShorthandNumber First
Saturated
Butyric 4 0 – C4:0
Caproic 6 0 – C6:0
Caprylic 8 0 – C8:0
Capric 10 0 – C10:0
Lauric 12 0 – C12:0
Myristic 14 0 – C14:0
Palmitic 16 0 – C16:0
Stearic 18 0 – C18:0
Arachidic 20 0 – C20:0
Behenic 22 0 – C22:0
Lignoceric 24 0 – C24:0
Monounsaturated
Palmitoleic 16 1 7 C16:1 ω7
Oleic 18 1 9 C18:1 ω9
Nervonic 24 1 9 C24:1 ω9
Polyunsaturated
Linoleic 18 2 6 C18:2 ω6
α-Linolenic 18 3 3 C18:3 ω3
γ-Linolenic 18 3 6 C18:3 ω6
Arachidonic 20 4 6 C20:4 ω6
Eicosapentaenoic 20 5 3 C20:5 ω3
Docosatetraenoic 22 4 6 C22:4 ω6
Docosapentaenoic 22 5 3 C22:5 ω3
Docosapentaenoic 22 5 6 C22:5 ω6
Docosahexaenoic 22 6 3 C22:6 ω3
h u m a n n u t r i t i o n 9
a safe level of protein intake is set at 0.8 g/kg body
weight or 56 g/day for a 70 kg adult. Safe here
means safe and (more than) adequate to prevent
defi ciency and does not imply that higher levels
of intake are unsafe, although there is some evi-
dence that exceptionally high levels of habitual
protein intake are associated with bone and kid-
ney disease.
The safe level of protein intake is equivalent
to 8–9% of energy from protein, so that people in
western countries consuming the recommended
14–15% of energy from protein are more than ade-
quately supplied. However, the 10% increase in the
estimated average requirement of the 2007 report
greatly increases the number of people in develop-
ing countries whose protein intake is deemed mar-
ginal or inadequate.
Protein Quality and Amino Acid Requirements
The need for protein is not just for total protein, but
for an intake of amino acids in the amounts required
for body protein synthesis and turnover. Classical
studies of the amounts of individual amino acids
required to maintain N balance in the 1950s and
1960s established that 8 of the 20 amino acids found
in body proteins are dietary essentials and cannot
be synthesized in the body. These essential or indis-
pensable amino acids are isoleucine, leucine, lysine,
methionine, phenylalanine, threonine, tryptophan,
and valine. It was not until 1975 that histidine was
also recognized to be an essential amino acid; for
reasons that are unclear, it is possible to maintain N
balance on a histidine-free diet for at least a week.
These early studies permitted determination of the
amounts of each essential amino acid needed to
maintain N balance, as shown in Table 1.7.
More recent studies have attempted to deter-
mine the requirements for essential amino acids
using amino acids labeled with the stable iso-
topes 15N or 13C. One approach is to measure the
incorporation of the labeled amino acid of interest
into body proteins, and its subsequent catabolism
and the excretion of 13CO2 or 15N urea. The prob-
lem with this direct approach is that the amount
of stable isotopically labeled amino acid that has
to be administered in order to achieve adequate
thermogenic steps in which ATP is synthesized and
then consumed (Bender, 2012) but, nevertheless,
protein can be a factor in the development of obesity
if total energy intake is greater than expenditure. If
carbohydrate is to provide 55% of energy and fat
30%, the recommendation is that protein should
provide 14–15% of energy (with alcohol, if con-
sumed, providing about 1%). This is almost twice
the requirement for protein turnover. Athletes with
a high energy intake can achieve an adequate pro-
tein intake even if protein accounts for even a much
lower fraction of total energy intake.
Protein Requirements
For an adult whose total body protein content is
constant, the intake of nitrogenous compounds
(mainly protein) in the diet will be equal to the uri-
nary and fecal losses of nitrogenous compounds.
This is nitrogen (N) balance or equilibrium. If the
dietary protein intake is inadequate then the losses
of N will be greater than the intake—negative N bal-
ance and a net loss of body protein. This also occurs
in response to a variety of pathological conditions.
In growth, pregnancy, and recovery from losses
there will be positive N balance—excretion is less
than intake and there is an increase in total body
protein.
The determination of protein requirements
remains controversial. Apart from times of growth
and recovery from losses, N balance can be main-
tained at any level of protein intake above the
requirement. In principle, it is easy to measure N
balance in people maintained at different levels of
protein intake and so determine their requirement.
The problem is that the rates of protein turnover
and catabolism of amino acids change with protein
intake, so that apparent protein requirements are
infl uenced by prior protein intake. This means that
studies of N balance require a long period of adap-
tation at each level of intake.
Reexamination of the results of N balance stud-
ies led to the 2007 WHO/FAO/UNU report (WHO,
2007) that increased the average requirement for
protein by 10%, from the previously accepted fi g-
ure of 0.6 g of protein/kg body weight/day to 0.66.
Allowing for individual variation in requirements,
10 chapter 1
Table 1.7 Reference patterns of essential amino acids
From N balance studies From stable isotope studies
mg/kg bw/day mg/g protein mg/kg bw/day mg/g protein
Histidine – – 10 15
Isoleucine 10 15 20 30
Leucine 14 21 39 59
Lysine 12 18 30 45
Methionine + cysteine 13 20 15 22
Methionine – – 10 16
Cysteine – – 4 6
Phenylalanine + tyrosine 14 21 25 38
Threonine 7 11 15 23
Tryptophan 3.5 5 4 6
Valine 10 15 26 39
Total essential amino acids 93.5 141 184 277
Source: WHO (2007).
sensitivity is so large that it distorts the body
pool of the amino acid and so overestimates the
apparent requirement.
The alternative approach is the indicator amino
acid method, in which varying amounts of the
amino acid of interest are fed and the catabolism
of a different essential amino acid (the indicator
amino acid) is measured. The principle here is that
when the amino acid of interest has been depleted
then all of the remaining indicator amino acid will
be catabolized, since it cannot be used for further
protein synthesis. Estimates of essential amino acid
requirements by isotope tracer methods are shown
in Table 1.7.
The essential amino acid that is present in diet-
ary protein in the least amount compared with the
requirement for body protein synthesis is termed
the limiting amino acid. Once supplies of this amino
acid have been exhausted, protein synthesis comes
to a halt and the remaining amino acids are catabo-
lized as metabolic fuel.
Two of the amino acids can only be synthesized
in the body from essential precursors: tyrosine
from phenylalanine and cysteine from methionine.
Providing these in the diet thus spares the require-
ment for the parent amino acid. This is especially
important in the case of cysteine and methionine
since, in many diets, it is the sum of these two amino
acids that is limiting.
The remaining amino acids are generally con-
sidered to be nonessential or dispensable, since
they can be synthesized in the body from more or
less common metabolic intermediates. However,
only three amino acids can be considered to be
completely dispensable since they are synthesized
from ubiquitous intermediates of carbohydrate
metabolism: alanine from pyruvate, glutamate from
2-oxoglutarate, and aspartate from oxaloacetate.
The remaining amino acids (arginine, asparagine,
glutamine, glycine, proline, and serine) must all
be considered to be semi-essential, in that under
conditions of metabolic stress or rapid growth the
capacity for their synthesis may be inadequate to
meet requirements.
The nutritional value or quality of individual
proteins depends on whether or not they contain
the essential amino acids in the amounts that are
required. A number of different ways of determin-
ing protein quality have been developed:
• Biological value (BV) is the proportion of
absorbed protein that is retained in the body. A
h u m a n n u t r i t i o n 1 1
quality between the “best” diets in devel-
oped countries and the “worst” in developing
countries.
2. The quality of the dietary protein is only impor-
tant when the total protein intake is marginal. If
the total amount of protein consumed is signifi -
cantly greater than requirements then the quality
of that protein is irrelevant.
Micronutrients: Vitamins and Minerals
Minerals
Any chemical element that has a metabolic or
other function in the body is obviously a dietary
essential, since elements cannot be interconverted.
Table 1.8 shows the minerals that are known to
be dietary essentials, classifi ed by their functions.
Some minerals appear under more than one head-
ing, since they have multiple functions in the body.
There is a small group of minerals (silicon, vana-
dium, nickel, and tin) that are known to be dietary
protein that is completely useable (e.g., egg and
human milk) has a BV of 0.9–1; meat and fi sh
have a BV of 0.75–0.8; wheat protein has a BV of
0.5; gelatin (which completely lacks tryptophan)
has a BV of 0.
• Net protein utilization (NPU) is the proportion of
dietary protein that is retained in the body (i.e., it
takes account of the digestibility of the protein).
By convention, it is measured at 10% dietary pro-
tein, at which level the experimental animal can
utilize all of the protein as long as the balance of
essential amino acids is correct.
• Protein effi ciency ratio (PER) is the gain in weight
of growing animals per gram of protein eaten.
• Relative protein value (RPV) is the ability of a test
protein, fed at various levels of intake, to sup-
port nitrogen balance, compared with a standard
protein.
• Chemical score is based on chemical analysis of
the amino acids present in the protein; it is the
amount of the limiting amino acid compared with
the amount of the same amino acid in egg protein
(which is completely useable for tissue protein
synthesis).
• Protein score (or amino acid score) is again based
on chemical analysis, but uses a reference pattern
of amino acid requirements as the standard. This
provides the basis of the legally required way of
expressing protein quality in the United States—
the protein digestibility-corrected amino acid
score (PDCAAS).
All of these measures of protein quality suffer from
two problems in practical nutrition:
1. No one eats a single food as their only protein
source. While individual vegetable proteins
may have a low BV, cereals are generally limited
by lysine (and hence have a relative excess of
the sulfur amino acids methionine + cysteine),
while legume proteins are limited by the sulfur
amino acids and hence have a relative excess
of lysine. There is complementation between
the amino acids in different proteins in a meal,
and a judicious mixture of cereals and legumes
can have a BV as high as that of meat. World-
wide there is very little difference in protein
Table 1.8 Essential minerals classifi ed by their function
Structural function Calcium, magnesium,
phosphate
Involved in membrane
function
Sodium, potassium
Function as prosthetic
groups in enzymes
Cobalt, copper, iron,
molybdenum, selenium,
zinc
Regulatory role or role in
hormone action
Calcium, chromium,
iodine, magnesium,
manganese, sodium,
potassium
Known to be essential, but
function unknown
Silicon, vanadium, nickel,
tin
Have effects in the body,
but essentiality is not
established
Fluoride, lithium
May occur in foods and
known to be toxic in excess
Aluminum, arsenic,
antimony, boron, bromine,
cadmium, cesium,
germanium, lead, mercury,
silver, strontium
12 chapter 1
the thyroid gland), is widespread in inland upland
areas over limestone soil. This is because the soil
over limestone is thin, and minerals, including
iodine, readily leach out, so that locally grown
plants are defi cient in iodine. Near the coast, sea
spray contains enough iodine to replace these
losses. Worldwide, many millions of people are at
risk of defi ciency, and in parts of central Brazil, the
Himalayas, and central Africa, goiter may affect
more than 90% of the population. A contributory
problem, in addition to low dietary iodine, may
be the presence of goitrogens (compounds that
interfere with iodine metabolism) in some foods.
Thyroid hormones regulate metabolic activity, and
people with thyroid defi ciency have a low meta-
bolic rate, and hence gain weight readily. They
tend to be lethargic and have a dull mental apa-
thy. Children born to iodine-defi cient mothers
are especially at risk, and more so if they are then
weaned onto an iodine-defi cient diet. They may
suffer from very severe mental retardation (goi-
trous cretinism) and congenital deafness (Institute
of Medicine, 2001).
Apart from iron and iodine, mineral defi ciencies
are likely to be a problem only for people whose
food comes entirely or largely from a limited
region where the soil may be defi cient. For peo-
ple whose food comes from a number of different
regions of the world, mineral defi ciencies are rela-
tively uncommon. Selenium intake in the United
Kingdom has fallen over the last three decades as a
result of increasing use of wheat grown in Europe,
where soils are relatively poor in selenium, com-
pared with earlier use of wheat from Australia
and North America, where soils contain more sele-
nium. Indeed, in some parts of the United States
soils contain so much selenium that grazing live-
stock suffer from selenium poisoning (Rayman,
1997, 2000).
The availability of minerals from foods also
presents a problem. Requirements are estimated from
balance and other studies, using crystalline mineral
salts. However, while chemical analysis reveals the
content of a mineral in a food, much of this may not
be available for absorption. Interactions between
different foods can also affect the availability of
minerals for absorption. Tannins in tea chelate iron
essentials for experimental animals maintained on
highly purifi ed diets, but whose metabolic function
is unknown. These ultra-trace minerals are not of
practical importance in human nutrition. Lithium
salts are known to have a pharmacological effect in
the treatment of bipolar psychiatric disease, and fl u-
oride is known to improve bone health and reduce
dental caries, but neither can be considered to be a
dietary essential.
Most minerals are required in milligram or micro-
gram amounts daily to match losses from the body.
In principle, it is easy to determine mineral require-
ments by balance studies—how much is required to
replace urinary and fecal losses? In practice, it is less
simple. Negative calcium balance may be the result
of bone loss (osteoporosis) in old age, and increas-
ing calcium intake may not restore balance, but sim-
ply lead to higher intake and output, but still with
negative balance.
Iron defi ciency anemia is a major problem of
public health worldwide and, together with iodine
and vitamin A, is one of the WHO’s three micro-
nutrient priorities. The absorption of dietary iron is
strictly controlled by the state of body iron reserves,
because there is no mechanism for iron excretion.
However, excessive blood losses (as in menstrua-
tion or as a result of intestinal parasites) lead to
requirements for replacement that cannot readily
be met from the diet. As a result of menstrual blood
losses, most women between menarche and meno-
pause have negligible body iron reserves, while
men have relatively large reserves. Postmenopaus-
ally, women’s iron reserves increase, approaching
those of men. A further problem of iron nutrition
is that perhaps 10% of the population (and more
in some ethnic groups) are at risk of iron overload
because of genetic polymorphisms in the various
enzymes and proteins involved in iron homeosta-
sis. Iron overload (hemochromatosis) leads to liver
cirrhosis, cardiomyopathy, and pancreatic damage
(bronze diabetes) and can also lead to depletion
of vitamin C as a result of nonenzymic reactions,
and hence the development of scurvy (Institute of
Medicine, 2001).
Iodine is required for the synthesis of the thyroid
hormones, thyroxine and tri-iodothyronine. Defi -
ciency, leading to goiter (a visible enlargement of
h u m a n n u t r i t i o n 1 3
of normal metabolic integrity and homeostasis. In
order to be considered a vitamin, a compound must
be shown to be a dietary essential and have a meta-
bolic function; deprivation must lead to more or less
specifi c defi ciency signs that are reversed by restor-
ing the vitamin to the diet. Table 1.9 shows the vita-
mins and their principal metabolic functions and
defi ciency signs.
For a vitamin or any other nutrient, there is a
range of intakes between that which is clearly
and phytates in unleavened breads chelate calcium
and zinc, reducing their absorption.
Vitamins
Vitamins are organic compounds (and hence dis-
tinct from minerals) that are required in the diet in
small amounts (milligrams or micrograms daily, as
opposed to essential amino and fatty acids, which
are required in gram amounts) for the maintenance
Table 1.9 The vitamins
Vitamin Functions Defi ciency disease
A Retinol,
β-carotene
Visual pigments in the retina, regulation of
gene expression, and cell differentiation
Night blindness, xerophthalmia,
keratinization of skin
D Calciferol Maintenance of calcium balance, enhances
intestinal absorption of Ca2+, and mobilizes
bone mineral
Rickets = poor mineralization of bone,
osteomalacia = bone demineralization
E Tocopherols,
tocotrienols
Antioxidant, especially in cell membranes Extremely rare—serious neurological
dysfunction
K Phylloquinone,
menaquinonesCoenzyme in the formation of γ-carboxy-
glutamate in proteins of blood clotting and
bone matrix
Impaired blood clotting, hemorrhagic
disease
B1 Thiamin Coenzyme in pyruvate and 2-oxoglutarate
dehydrogenases and transketolase, role in
nerve conduction
Peripheral nerve damage (beriberi) or
central nervous system lesions (Wernicke–
Korsakoff syndrome)
B2 Ribofl avin Coenzyme in oxidation and reduction
reactions, prosthetic group of fl avoproteins
Lesions of corner of mouth, lips, and
tongue, seborrheic dermatitis
Niacin Nicotinic acid,
nicotinamide
Coenzyme in oxidation and reduction
reactions, functional part of NAD and NADP
Pellagra—photosensitive dermatitis,
depressive psychosis
B6 Pyridoxine,
pyridoxal,
pyridoxamine
Coenzyme in transamination and
decarboxylation of amino acids and
glycogen phosphorylase, role in steroid
hormone action
Disorders of amino acid metabolism,
convulsions
Folic acid Coenzyme in transfer of one-carbon
fragments
Megaloblastic anemia
B12 Cobalamin Coenzyme in transfer of one-carbon
fragments and metabolism of folatePernicious anemia = megaloblastic anemia
with degeneration of the spinal cord
Pantothenic
acid
Functional moiety of CoA and acyl carrier
protein in fatty acid metabolism and
synthesis
Peripheral nerve damage (burning foot
syndrome)
H Biotin Coenzyme in carboxylation reactions in
gluconeogenesis and fatty acid synthesis
Impaired fat and carbohydrate
metabolism, dermatitis
C Ascorbic acid Coenzyme in hydroxylation of proline and
lysine in collagen synthesis, antioxidant,
enhances absorption of iron
Scurvy—impaired wound healing, loss of
dental cement, subcutaneous hemorrhage
14 chapter 1
protein rather than defi ciency of the nutrient
itself.
• Low urinary excretion of the nutrient, refl ecting
low intake and changes in metabolic turnover.
• Incomplete saturation of body reserves.
• Adequate body reserves and normal metabolic
integrity.
• Possibly benefi cial effects of intakes that are more
than adequate to meet requirements—the promo-
tion of optimum health and life expectancy.
Having decided on an appropriate criterion of
adequacy, requirements are determined by feeding
volunteers an otherwise adequate diet, but lack-
ing the nutrient under investigation, until there is
a detectable metabolic or other abnormality. They
are then repleted with graded intakes of the nutri-
ent until the abnormality is just corrected. Prob-
lems arise in interpreting the results, and therefore
defi ning requirements, when different markers
of adequacy respond to different levels of intake.
This explains the difference in the tables of refer-
ence intakes published by different national and
international authorities (see Tables 1.10, 1.11, 1.12,
and 1.13).
Dietary Reference Values
Individuals do not all have the same requirement
for nutrients, even when calculated on the basis of
body size or energy expenditure. There is a range
of individual requirements of up to 25% around the
mean. Therefore, in order to set population goals
and assess the adequacy of diets, it is necessary to
set a reference level of intake that is high enough to
ensure that no one will either suffer from defi ciency
or be at risk of toxicity.
As shown in the upper graph in Figure 1.3, if it is
assumed that individual requirements are normally
distributed around the observed average require-
ment, then a range of ±2 × the standard deviation
(SD) around the mean will include the requirements
of 95% of the population. This 95% range is conven-
tionally used as the “normal” or reference range
(e.g., in clinical chemistry to assess the normality or
otherwise of a test result) and is used to defi ne three
levels of nutrient intake:
inadequate, leading to clinical defi ciency disease,
and that which is so much in excess of the body’s
metabolic capacity that there may be signs of tox-
icity. Any excess of the water-soluble vitamins is
generally excreted in the urine, but the fat-soluble
vitamins may accumulate in tissues with harmful
consequences. Between these two extremes is a level
of intake that is adequate for normal health and the
maintenance of metabolic integrity, and a series of
more precisely defi nable levels of intake that are
adequate to meet specifi c criteria, and may be used
to determine requirements and appropriate levels of
intake. In order of decreasing severity, or increasing
sensitivity as markers of adequacy, these are
• Clinical defi ciency disease, with clear anatomical
and functional lesions, and severe metabolic dis-
turbances, possibly proving fatal. Prevention of
defi ciency disease is a minimal goal in determin-
ing requirements.
• Covert defi ciency, where there are no signs of
defi ciency under normal conditions, but any
trauma or stress reveals the precarious state of the
body reserves and may precipitate clinical signs.
For example, an intake of 10 mg of vitamin C per
day is adequate to prevent clinical defi ciency, but
at least 20 mg per day is required for healing of
wounds.
• Metabolic abnormalities under normal condi-
tions, such as impaired carbohydrate metabolism
in thiamin defi ciency or excretion of methyl-
malonic acid in vitamin B12 defi ciency.
• Abnormal response to a metabolic load, such as
the inability to metabolize a test dose of histidine
in folate defi ciency or tryptophan in vitamin B6
defi ciency, although at normal levels of intake
there may be no metabolic impairment.
• Inadequate saturation of enzymes with (vitamin-
derived) coenzymes—this can be tested for three
vitamins, using red blood cell enzymes: thiamin,
ribofl avin, and vitamin B6.
• Low plasma concentration of the nutrient, indi-
cating that there is an inadequate amount in tissue
reserves to permit normal transport between
tissues. For some nutrients, such as vitamin A,
this may refl ect failure to synthesize a transport