naturopathic nutrition year 1

© CNM: Nutrition Year 1: Vitamins. GH/BQ.

Vitamins

Naturopathic Nutrition Year 1

1

In this lesson you will learn:

• Specific characteristics of vitamins

A, C, D, E, K and the B vitamins.

• Dietary sources, bioavailability

and interactions.

• Functions, deficiency states,

therapeutic uses and safety

considerations.

• Dosage levels and preferred

forms for micronutrients.

Learning Outcomes

© CNM: Nutrition Year 1: Vitamins. GH/BQ. 2

Introduction

• Biochemist Casimir Funk coined the term vitamines in 1911.He discovered ‘beriberi’, which causes mostlyneurological symptoms such as numbness andmostly affects those on a diet of white rice. Funk identified that the cause was a lack of thiamine (vitamin B1).

• Thiamine was named to reflect the belief that all vitamins contained nitrogen (amines). However, it was later discovered that not all vitamins contain nitrogen. ‘Vitamine’ was changed to ‘vitamin’ (no e).

• Different chemical forms of each vitamin exist, these are called ‘vitamers’. Vitamers are generally similar in structure.

• For example, a person who is vitamin B3 deficient could be relieved by either of the B3 vitamers: niacinamide or nicotinic acid.

vita - life

amine - contains nitrogen


Vitamins


• There are 13 vitamins – vitamins A, C, D, E, K, and the B vitamins (thiamine, riboflavin, niacin, pantothenic acid, biotin, B6, B12, and folate).

• Key functions of vitamins include:- Supporting the immune system - Regulating gene expression- Supporting neurological activity- Facilitating ATP production- Manufacturing of blood cells- Regulation of hormones

• Vitamins are absorbed in the small intestine.It is, therefore, vital to optimise GIT health.

4

Vitamins

• Vitamins are carbon-containing compounds that are essentialto the body in small amounts for normal growth and function.

• The body cannot produce vitamins (with the exception of vitamin D).

• Vitamins cannot be directly converted into energy or tissues, like macronutrients can. However:

- Some vitamins are essential in the process of energyproduction (B1, B2, B3, B5). If deficient, this can result in poor ATP production, e.g. vitamin B5 is needed for the synthesis of coenzyme A (review Biochemistry 2).

• Vitamins facilitate physiological functions in the body, e.g. Vitamin C facilitates collagen synthesis (but is not a physical ‘part’ of collagen).

© CNM: Nutrition Year 1: Vitamins. GH/BQ. 5(Liska et al. 2004)

Vitamins

• Vitamins do not occur in isolation in nature. Therefore, be mindful that supplements do not offer the same therapeutic advantages as consuming a spectrum of nutrients via food.

• Vitamins (as they occur in food) are relatively ‘inert’ until the body activates them.

Vitamin-Dependent Enzymes:

• Vitamins are required for the activation of vitamin-dependent enzymes (they hence function as ‘cofactors’).

• E.g. B-vitamins are vital cofactors for the action of the CYP450 enzyme system, needed for phase 1 liver detoxification. Therefore, B vitamins can be used as part of a liver support programme.


cofactor = an essential component for enzyme activity

6

Vitamins Classification

There are 2 types of vitamins – fat- and water-soluble.

1. Fat-soluble vitamins: A, D, E, K.

• Fat-soluble vitamins are soluble in fats.

• Absorbed with fat in the small intestine into the lymphatic

capillaries and then into the blood. They are readily stored.

• Tighter range between efficacy and toxicity than water soluble.

2. Water-soluble vitamins: B vitamins and vitamin C.

• Water-soluble vitamins are soluble in water.

• Absorbed in the small intestine directly into the blood. Storage is minimal (exception = B12), and easily excreted, if in excess.


Vitamin Insufficiency to Deficiency

• Progression of insufficiency to

deficiency of vitamins:

1. Preliminary reduction of stores.

2. Reduction in enzyme activity.

3. Physiological impairment

(early signs and symptoms).

4. Classical deficiency syndromes.

5. Terminal tissue pathology.

• True vitamin deficiencies are rare (except for vitamin B12

and vitamin D). Most cases in clinic are insufficiency states.

insufficiency = sub-clinical

deficiency (i.e. vague symptoms)

deficiency = clinical signs &

symptoms of deficiency


Vitamin A


• Vitamin A was the first vitamin to be discovered (hence ‘A’).

• The active forms (vitamers) which execute the functions

of vitamin A are: Retinol, Retinal and Retinoic Acid.

• Depending upon what the

body requires, retinol will

be oxidised to the different

forms (retinol → retinal →

retinoic acid). If the body

doesn’t need it, it will

remain as retinol and be

stored in the liver.

Fat-Soluble Vitamins:

9

Vitamin A


The 2 Forms of Vitamin A:• Pro-vitamin A → converted into the active (usable) form of

vitamin A (retinol) in the small intestinal epithelium and liver.

- Carotenes (or carotenoids) are examples of pro-vitamin A. The most active pro-vitamin carotenes are: α- (alpha), β- (beta) and γ- (gamma) carotenes and cryptoxanthin.

- Found in non-animal foods.

• Pre-formed vitamin A → this is active vitamin A the body can use as it is.- Only found in animal foods.

carotene – from the Greek karoton for ‘carrot’- orange pigments

Pro-vitamin = a substance that can be converted into a vitamin

Pre-formed vitamin = a vitamin that is already formed

10(Bender, 2002; Liska et al. 2004)

Vitamin A


Food Sources:

• Pro-vitamin A are produced by

plants, algae, fungi and bacteria.

Rich food sources: Dark green,

yellow / orange vegetables and

fruit, e.g. carrots, squash, mango,

spinach, sweet potatoes.

• Pre-formed vitamin A is only

found in animal foods e.g. liver, fish

liver oils, egg yolk, mackerel, salmon.

11(Osiecki, 2014)

Vitamin A

Pro-vitamin A Absorption:

• Dietary carotenes are converted to vitamin A

only as needed, so do not have toxicity concerns.

• The absorption of carotenoids in the small

intestine varies between 5% and 60%.

• Ensure that there are adequate healthy fats in

the diet as carotenoids are fat-soluble. Drizzle

with coconut oil or olive oil to optimise absorption.

• Another way to increase the bioavailability of carotenoids is to cook

(slightly steam) these foods, e.g. carrots. This cooking method is

thought to most effectively liberate carotenoids from cells.


Carotenoids & Conversion

• The enzyme which converts carotenoids to retinal (in the intestinal epithelium and liver) is encoded by the BCO1 gene. This enzyme activity is subject to much genetic variation.

• Carotene conversion is reduced by: hyperlipidaemia, liver disorders, diabetes and hypothyroidism (consider your clients).

• Excessive intake of carotenoids can lead to a non-dangerous yellowing on the skin. However, yellowing of the skin might also be associated with disorders of the liver, gallbladder, etc.

• A sallow yellow complexion (i.e. pale or pasty), especially in the face, can indicate a Spleen Qi deficiency. In TCM, this refers to ‘weakness’ in digestion function.


Vitamin A


Pre-formed Vitamin A Absorption:

• About 70-90% of dietary retinol is absorbed - this is a key reason that animal food sources of vitamin A can lead to vitamin A toxicity (liver particularly).

Dosage:

• Supplemental Range: Adults maximum 3000mcg preformed A. Higher doses are appropriate in some situations but should only be used short-term.

• It is recommended to avoid isolated beta-carotene supplementation, as it was shown to worsen the progression of lung cancer patients in a research study (recall that antioxidants do not work in isolation).

14(Bender, 2002; Bender, 2005)

Dosage (further information):

• Carotenes (provitamin A) don’t have the same vitamin A activity as preformed vitamin A. The amounts of vitamin A are expressed as mcg of Retinol Activity Equivalents (RAE).

• 1 RAE = 1 mcg of retinol = 12 mcg of beta-carotene = 24 mcg of alpha-carotene or beta-cryptoxanthin from dietary sources.

• Supplements conversion is: 2mcg beta-carotene = 1mcg retinol.

• Vitamin A content using international units (IU) is being phased out of supplements by January 2021. 1 IU retinol = 0.3 mcg RAE.


Vitamin A mcg = micrograms


Vitamin A

Functions: Therapeutic Uses:

Vision & Eye

Health:

• Required for rhodopsin – the light-

sensitive protein involved in

converting light into an electrical

signal that goes into the brain’s visual

cortex, giving the message of sight.

• Also necessary for corneal health.

• Photosensitivity

• Visual loss

• Night-blindness

• Senile cataracts

Immunity: • Enhances T-cell proliferation and

Interleukin-2 secretion.

• Supports first line of immune defence

(skin and mucous membrane barrier)

• Recurrent

infections, e.g.

respiratory tract

infections


rhodopsin = the

‘visual purple’

16(Rodrigo Mora et al. 2008)

Vitamin A


Gene

Expression

and cell

differentiation

• Control of cell differentiation and

turnover. Regulating the

expression of over 500 genes,

affecting the synthesis of proteins

that regulate cell functioning.

• Key as a preventive measure to

support healthy gene expression.

• Synthesis of glycoproteins which

support normal development of

bones, teeth and skin.

• Acne

• Anaemia

• Cervical dysplasia

• Hair loss in women

• Fracture repair

• Lichen planus

• Osteoarthritis

• GIT ulceration

• Vaginitis

• Periodontal disease

© CNM: Nutrition Year 1: Vitamins. GH/BQ. 17(Higdon et al. 2015)

Vitamin A


Reproduction: • Reproductive & embryonic health.

• Required for spermatogenesis in

men.

• Required for egg (ovum)

development and implantation.

• Infertility (male &

female)

• Fibrocystic breast

disease

Anti-oxidant

properties:

• Preformed and provitamin A have

antioxidant properties.

• The foods rich in carotenoids are

also rich in other antioxidants,

again highlighting that they don’t

work in isolation.

• Used in various

therapies, including

carrot juicing for

cancer (Gerson

therapy).

• Disease prevention

© CNM: Nutrition Year 1: Vitamins. GH/BQ. 18(Bender, 2005; Liska et al. 2004; Chatterjee et al.

2012; Higdon et al. 2015)

Therapeutics: Carrot & Apple Juice


• Try this juice used in the Gerson therapy. It is rich in carotenoids (antioxidants) and supports liver detoxification.

• Approx. 3 large carrots: 1 large green apple (8-12 oz each).

• Use only organic produce and a cold-press juicer.

• Use sour apples such as Granny Smith (these are higher in malic acid and pectin which support heavy metal chelation, and also extract more nutrients from the carrots / apple).

• Wash and brush the carrots; cut off the ends. Do not peel.

• Wash the apples, cut them and remove the stem / seeds.

• Consume as soon as possible to stop the juice oxidising.19

Deficiency Signs and Symptoms:

• Vision impairment at night is an early sign: Loss of sensitivity to green light, unable to adapt to dim light and night blindness. Prolonged deficiency can lead to blindness.

• Hyperkeratosis of skin of upper arms.

• Reduced skin integrity – rough dry skin, acne, eczema, poor wound healing. Dry hair.

• Poor bone growth / development.

• Poor sense of taste and smell.

• Lowered immunity (recurrent infections).

hyperkeratosis = thickening of the stratum corneum (‘goose flesh’)


Vitamin A

Add 1-2 portions

of beta-carotene-

rich foods a day to

address these,

before considering

supplementation.


Factors Affecting Individual Requirements:

• Diabetes mellitus, thyroid & liver disease – ↓carotene conversion.

• Alcoholism: accelerates the breakdown of liver-stored retinol; absorption and carotene conversion is reduced. Increased vitamin A toxicity potential; not supplement with preformed A.

• Poor gut health (lack of absorption in small intestine) and conditions that affect fat absorption, e.g. cystic fibrosis, statins, etc.

• Zinc deficiency and/or protein malnutrition: zinc and protein are required to make Retinol Binding Protein (RBP). RBP moves vitamin A from liver storage to tissues for utilisation. Without zinc, vitamin A is trapped. So optimise intake of zinc-rich foods.


Vitamin A

21(Bender, 2002; Liska et al. 2004; Bender, 2005)

Vitamin A Toxicity: long-term and regular intake (roughly 5-10 times the recommended nutrient intake over many months):

• Can negatively affect gene regulation during embryological development leading to birth defects (e.g. cleft lip).

• May increase osteoclast activity and lead to bone fractures.

• Can damage hepatocyte cell membranes (causing liver disease).

• Can lead to hyperlipidaemia, amenorrhoea and anorexia.

• Can cause dry, red and scaling skin.

Vitamin A Drug Interactions:

• Be wary of vitamin A supplementation with those taking warfarin, as it decreases vitamin K absorption (increasing bleeding risk).


hepatocyte

= liver cellVitamin A

22

Exercise: Case Study

Review the following case study and create ONE recipe

suitable for this client. The recipe should also contain high

levels of zinc. What is your thinking behind this recipe?

• Female, aged 19, vegan.

• Presents with acne - suffering from since puberty.

• She describes her day-to-day life as “very

stressful”, and often suffers with mouth ulcers and viral infections.

• Her current diet diary includes lots of white potatoes, bread,

tofu, curries (e.g. lentil, chickpea) and alliums (onions, leeks etc.).

• She is quite ‘weight conscious’ and always checks fat content.


Vitamin D


‘ergo’ = plant sourced D

‘chole’ = animal sourced D

• Vitamin D is not strictly a vitamin since it can be

synthesised in the skin in response to sunlight.

• Dietary sources are only required in the absence of

adequate sunlight (UVB), and include 2 types of vitamin D:

- Plant source: vitamin D2 (ergocalciferol D2) – found in

mushrooms (fungi), but these require good sun exposure.

- Animal source: vitamin D3 is 7-dehydroxycholesterol

(cholecalciferol D3) – found in cod liver oil, oily fish (herring,

mackerel, sardines, wild-caught salmon) and organic egg yolks.

• Vitamin D2 and D3 do not have any direct functions;

they both first need to be converted (hydroxylated).24(Bender, 2002)

SkinProvitamin D

Sunlight

Cholecalciferol (D3) D3 or D2

25(OH)D (Calcidiol)

1,25-Calcitriol (active form of vitamin D)

Cholecalciferol

D3

Ergocalciferol

D2• D2 and D3 have the same activation

pathway via the liver and then kidney.

• Conventional medicine often considers serum ranges (of calcidiol) over 50 nmol/L to be sufficient.

• Below 25 nmol/L is almost universally agreed to be deficient.

• However, the optimal range is generally considered to be 75-125 nmol/L (some variance). So are your clients levels ‘sufficient’ or ‘optimal’?


Vitamin D

25

Vitamin D Synthesis

• If outside and your shadow is the same height or shorter than you are, you’re getting enough sunlight to make vitamin D.

• Serum levels are usually highest at the end of the summer and lowest at the end of winter.

• Summer: even on cloudy days, UV light can penetrate thin clothes and create vitamin D. Sunscreens and window glass block the conversion to vitamin D by blocking UVB radiation.

• Winter: temperate regions may not have adequate UV for synthesis.

• 10 minutes of summer sun exposure results in endogenous production of about 400IU in fairer skin types. In darker skin tones it can take 3-6 times longer to produce the same amount of D3.

• Note that vitamin D can be stored in the liver for 4 months.© CNM: Nutrition Year 1: Vitamins. GH/BQ.

endogenous =

from within the body



μg = microgramVitamin D

Dosage:• Our focus should be on first addressing the cause of the

deficiency, to avoid a ‘symptom-based’ approach.

• A supplemental dose of 4000IU/day has been used without adverse effects. 1 μg of cholecalciferol = 40 IU.

• It is advisable to test vitamin D levels every four months to adjust dosing where appropriate.

• Ergocalciferol is less than one-third as potent as cholecalciferol, so D3 is favoured for supplementation. D3 supplements also stay in circulation longer.

• Pronounced deficiency: (<10 ng/mL) 50,000 IU of vitamin D3 orally once weekly for 2-3 months, or 3 times weekly for 1 month.

27(Kennel et al. 2010)

• A key function of vitamin D is to maintain serum calcium and

phosphorus homeostasis. This balance impacts many body

processes, including heart and nervous system functioning.

• Vitamin D also performs a variety of other functions in the body.

• The actions of vitamin D are mediated

through a nuclear transcription factor

known as the Vitamin D Receptor (VDR)

within the nucleus of each cell. VDR

activation is thought to directly and/or

indirectly regulate 100 to 1,250 genes.


Vitamin D nuclear = nucleustranscription = copying a segment of DNA (a gene)

28(Higdon et al. 2015)


Bone Health:

• Supports bone density (along with vitamin K2), by increasing intestinal calcium absorption.

• Osteoporosis • Osteomalacia

& Rickets

Immune function & Regulation:

• Supports immune function by:

- Enhancing innate immune system

- Regulation of T-helper cells

- Producing antibacterial peptides.

- Inhibiting eosinophils

- Reducing inflammatory cytokines (e.g. IL-6 and TNF-α) and prostaglandin production.

• Allergies• Autoimmunity,

e.g. multiple sclerosis

• Infections (e.g. viral and bacterial)

• Musculoskeletal pain reduction


Vitamin D cytokines = immune

messenger proteins

29(Zamora et al. 1999; Munger et al. 2004; Munger et

al. 2006; Christodoulou et al. 2013)


GIT health: • The vitamin D receptor (VDR) helps

to regulates mucosal inflammation.

• Vitamin D has a role in commensal

bacterial colonisation.

• Intestinal VDR stabilises tight

junctions.

• Intestinal

inflammation,

e.g. inflammatory

bowel diseases

(as well as

intestinal

permeability)

Anti-cancer: • Enhances the anti-tumour activity of

innate immune cells.

• Regulates multiple genes through the

VDR, and inhibits angiogenesis.

• Cancer

prevention and

support

angiogenesis = blood vessel formation


Vitamin D

30(Cantorna et al. 2006; Sun, 2010; Li et al. 2015;

Tagliabue et al. 2015)


Insulin: • Vitamin D:

- Activates transcription of the insulin

gene (increasing insulin secretion).

- Increases cellular sensitivity to

insulin.

• Diabetes Mellitus

(Type 2, but also

type 1)


Vitamin D

Exercise: A client is vitamin D deficient and suffering from

recurrent infections, such as bronchitis, in winter months.

1. What guidance could you give your client to

help them increase their vitamin D status?

2. How would low vitamin D impact the client’s immune system?

31(Hanafy & Elkatawy, 2018)

Vitamin A & D Interaction

• The balance of vitamin A

and D is essential for proper

gene transcription.

• The Retinoid X Receptor (RXR)

is a type of nuclear receptor

that is activated by vitamin A.

• Together the VDR/RXR form

a complex with DNA for transcription.

• So, from a disease-prevention approach, maintaining healthy

levels of vitamins A and D is crucial for correct gene expression.


Deficiency Signs & Symptoms:

• Rickets & osteomalacia – demineralised bones. Rickets occurs in children, whilst osteomalacia affects adults. Presents with bone pain and bowing of lower limb bones.

• Osteoporosis (brittle bones) – fractures.

• Severe asthma in children.

• Poor immunity or immune dysfunction (autoimmunity, allergies), insomnia, nervousness, depression.

• Menstrual irregularities (increases FSH / LH production).

• Non-specific musculo-skeletal pain and fatigue


Vitamin D osteo = bone malacia = softening (from Greek)

33(Bender, 2002; Bender, 2005; Annweiler et al. 2010)

Causes of vitamin D deficiency:

• Inadequate UVB sun exposure and overuse of conventional sunscreens.

• Dietary factors such as excessive animal protein or calcium intake can lead to lower blood levels of vitamin D by affecting its rate of formation and clearance.

• Lack of dietary fats (it is a fat-soluble vitamin), and a lack of magnesium (it is a co-factor for vitamin D synthesis.

• Breastfeeding without adequate sunlight / supplementation.


Vitamin D UVB = Ultraviolet B rays

34(Bender, 2002; Liska et al. 2004; Bender, 2005)

Causes of vitamin D deficiency (cont.):

• Impaired liver functionality (compromised vitamin D conversion) due to excess alcohol, drug and caffeine use, as well as a large toxic burden from the diet (e.g. pesticides), environmental and household chemicals. Therefore, it is crucial to support liver functionality by removing the toxic burden, etc.

• Elderly patients and those with a history of kidney disease.

• Poor intestinal absorption of dietary vitamin D (e.g. due to cystic fibrosis, coeliac disease, dysbiosis) and a lack of bile. Therefore, it is crucial to support digestive health (i.e. good digestive secretions, a healthy microflora).


Vitamin D

35

Toxicity:

• Vitamin D synthesis due to sunlight does not produce toxicity.

• Main toxicity symptoms due to vitamin D-related hypercalcaemia: nausea, diarrhoea, vomiting, weakness, hypertension, constipation.

• Toxicity can occur taking supplemental vitamin D at more than 50,000 IU per day for one to several months.

• Individuals with vitamin D toxicity usually have blood levels above 375 nmol/L.

• EFSA Tolerable Upper Intake Level for Adults: 4000 IU/day.

Drug Interactions:

• Osteomalacia risk due to low vitamin D is increased with use of barbiturates and anticonvulsants.


Vitamin D EFSA = European

Food Safety Authority

36(FSA, 2007)



• Female, aged 49, mostly indoors due

to her job as an office manager.

• She is one year into the menopause, and

is experiencing hot sweats and irritability.

• Recently diagnosed with early stages of

osteoporosis following a DXA scan.

• She is also experiencing dry skin and some hair loss.

• You decide to test her Vitamin D levels, which come

back as 23 nmol/L.

• Tongue: Red with brown coating at the back of the tongue.

Review the following case study:

DXA = Dual X-Ray Absorptiometry

37


Questions:

1. Draft a handout for your client on how to increase vitamin D levels. This should include clear lifestyle and dietary recommendations.

2. Find a good quality supplement and write clear guidelines on how your client should use this.

3. Why would you also want to optimise this client’s vitamin A status?

4. What do you make of the tongue observations, and how might this support / guide your approach for this client? Consider the energetics in your answer.


38

Vitamin E

• Vitamin E is a generic term for two families of fat-soluble

compounds with vitamin E activity: Tocopherols &

Tocotrienols. Both families contain at least four forms: alpha,

beta, gamma & delta. All forms exist within natural foods.

• The only form recognised for human nutrition

is α-tocopherol. The role and use of other

forms is still being investigated.

• Up to 80% of vitamin E is destroyed by freezing, whilst heating destroys around 30% of vitamin E.

• Fresh, raw food sources are best: Sunflower seeds,

almonds, pine nuts, olive oil, avocado, sweet potato, spinach.© CNM: Nutrition Year 1: Vitamins. GH/BQ.

Tocopherols / Tocotrienols = from Greek for ‘to bear a pregnancy’, after being first identified as a dietary fertility factor in rats

39(Bender, 2002)

• The liver takes up all forms of vitamin E and preferentially secretes α-tocopherol into circulation within lipoproteins. Circulated everywhere, stored to greatest extent in adipose tissue.

• Polyunsaturated Fatty Acid (PUFA) intake increases the requirement for vitamin E, due to its antioxidant properties which protect the fatty acid double bonds from oxidation.

• Naturally sourced vitamin E = d-alpha-tocopherol.Synthetically produced form = dl-alpha-tocopherol.L isomers are less active. Synthetic forms of vitamin E are derived from petroleum oil and should be avoided.

• Vitamin E is measured in mg of α-tocopherol equivalents: 1 mg of natural α-tocopherol = 1 α-tocopherol equivalent (αTE).


Vitamin E

40



Anti-oxidant • Protects the following from oxidation:

- Polyunsaturated Fatty Acids

(PUFA) cell membranes

- Nerve sheaths

- Cholesterol (↓ LDL oxidation)

• A vital ‘chain-breaking antioxidant’.

• Vitamin C and selenium support the

activity of vitamin E by rejuvenating

oxidised vitamin E. So, ensure an

adequate intake of all antioxidants to

optimise the effects of vitamin E.

• Atherosclerosis & cardiovascular disease

• Male fertility• Healthy ageing• Cataracts• Alzheimer’s &

cognitive decline• Anti-cancer (also

stimulates the p53 tumour suppressor gene)

chain-breaking antioxidant = stops the formation of more unstable radicalsVitamin E

41(Bender, 2002; Bender, 2005; Farina et al. 2017)



Immunity • Increases phagocyte activity• Differentiation of immature T cells

in the thymus• Antioxidant and mild anti-

inflammatory properties

• HIV/AIDS

• Healthy immune functioning

• Infections

Anti-coagulant

• Inhibits platelet aggregation and vitamin K activity (↓clotting factors)

• Cardiovascular disease

Endocrine • Improves insulin action (& possibly improves insulin resistance)

• Modulates oestrogen receptors and activity

• Diabetes Mellitus• Dysmenorrhoea • Menopause (e.g.

vaginal dryness)

Skin Repair

• Traditional topical use, although mechanism not understood.

• Scarring• Acne

Vitamin E

42(Ziaei et al. 2001; Ziaei et al. 2005; Ziaei et al. 2007)

Vitamin E


Vitamin E Deficiency: • A marginal subclinical deficiency is common. Serious deficiencies

are rare unless significantly impaired absorption (i.e. cystic fibrosis).

• Typically presents as:- Red blood cell destruction (due to erythrocyte oxidation → haemolytic anaemia) – exhaustion after light exercise.

- Easy bruising and slow healing (fewer antioxidants).

- Nerve damage (e.g. neuropathy) due to oxidation.

Toxicity (rare):

• High doses with vitamin K deficiency and/or warfarin, can

increase bleeding risk. Caution supplements with chemotherapy.

High supplement doses create potential for pro-oxidant effect.43

Vitamin K


quinone = refers to

chemical structure

• Named after K for koagulation (German spelling) - discovered

during investigation of bleeding disorders in animals. Three

types of compound have vitamin K activity: K1, K2, K3.

• K1 (Phylloquinone): the dietary source found in green leafy

vegetables – natural form, making up about 80-90% of daily

intake. K1 must be converted to K2 in the body to be utilised.

• K2 (Menaquinones): synthesised by bacteria, found in

fermented foods, making up around 10%. Probiotics can support

intestinal K2 production. K2 synthesis by bacteria occurs in the

human jejunum and ileum, and is absorbed to a limited extent.

• K3 (Menadione): a potentially toxic, synthetic form used in livestock.

44(Schurgers et al. 2007)

Richest food sources:

• Natto and dark green leafy vegetables. Best absorbed with some dietary fat, e.g. steamed broccoli and kale with extra virgin olive oil.

Dosage & Absorption:

• Optimal intake is 300-500mcg/day. Few countries set a daily req. K2 is better absorbed and tends to stay within the body for longer.

• Only small amounts are stored (mainly in the liver) and a regular dietary supply is required. Approximately 30-40% of ingested vitamin K is retained – the rest is excreted.

• Reduced absorption: High vitamin A intake, aspirin.Low bile secretion and poor fat absorption disease states.


Vitamin K

Natto

45(Bender, 2002; Liska et al. 2004; Schurgers et al.

.2007; Lord & Bralley, 2008)


Vitamin K


Blood Clotting • Vitamin K is required for the formation of 4 out of the 13 clotting factors (II, VII, IX, X)

• Prevents bleeding (it is an antidote to warfarin).Vitamin K is recycled via the Vitamin K Cycle –warfarin inhibits this.

Bone Mineralisation

• Osteocalcin (a calcium binding protein in bones) requires vitamin K for synthesis.

• Osteocalcin synthesis by osteoblasts is regulated by active vitamin D (calcitriol).

• Osteoporosis (45mg/day, and by supporting microflora)

• Prevents calcium accumulation in arteries and kidneys

46(Iwamoto et al. 2000; Cockanye et al. 2006;

Purwosunu et al. 2006)

Causes of Deficiency:

• Liver diseases, warfarin, antibiotic-use, fat malabsorption issues.

• Maternal considerations: vitamin K transfer to the foetus via the placenta is not significant (although it is generally adequate). Maternal medications such as antibiotics, anticonvulsants and warfarin can dramatically reduce stores.

• A vitamin K injection is offered at birth to newborns to prevent potential haemorrhagic disease (next slide).

Deficiency signs and symptoms:

• Excessive bleeding (haemorrhages), bruising, bone fractures, soft tissue calcification.

Toxicity: K1 & K2 are not known to be toxic (K3 can be).© CNM: Nutrition Year 1: Vitamins. GH/BQ.

Vitamin K

47


‘Vitamin K Injection for Newborns’

Considerations of the ‘Vitamin K Injection’:• Undesirable preservatives (e.g. polysorbate 80; aluminium in the US).• Has not been tested for adverse effects such as mutagenicity.• It is a synthetic chemical (despite the name ‘vitamin’).• The risk in full-term babies is 1:100,000.• A larger dose is given than a newborn requires.

What’s the Alternative? • Delayed cord clamping until the placenta has fully pulsed out.• Increase intake of vitamin K-rich foods (e.g. leafy greens)

before due date, and support mother’s microflora (K2). • Nettle leaf infusions are a great source of vitamin K2, too.• Vitamin K amounts in the newborn’s blood increase daily.

https://www.youtube.com/watch?v=Cw53X98EvLQ

48

https://www.youtube.com/watch?v=Cw53X98EvLQ

Vitamin B1 - Thiamine• Vitamin B1 (thiamine) functions in the body as the active form

‘thiamine pyrophosphate’ (TPP); conversion to this enzyme is

dependent on magnesium, and impaired by alcohol.

• Bodily stores of B1 would last for approximately 1 month.

• B1 content is very easily reduced by processing including milling,

chopping, canning, adding sulphites (e.g. dried fruit), baking soda.

Boiling or freezing reduces B1 content by 50%. Toasting bread

reduces B1 by 30%. Fresh, raw sources are best.

Food sources:

• Yeast extract, peas, oranges, nuts (e.g. macadamia),

pulses, sunflower seeds, wholegrains, meat / fish.


Water-Soluble Vitamins:

49(Bender, 2002)



Energy (ATP) production

• Crucial for carbohydrate, as well as fat and protein metabolism.

• Needed for the formation of Acetyl-CoA (key for ATP production).

• Fatigue• Supporting energy

production in increased need (e.g. pregnancy, heart failure)

• Fertility

Nervous System Functioning

• Acetyl-CoA is an important precursor of acetylcholine →

• The amino acids that are metabolised by thiamine can be used to create neurotransmitters e.g. GABA.

• Cognitive decline and memory loss

• Alzheimer’s • Low mood• Parkinson’s• Nerve repair

Vitamin B1 - Thiamine

50

Dietary requirements:

• The more carbohydrate you eat, the more B1 you need (i.e. to create ATP from it). An average of 0.4-0.5 mg/1000kcal is recommended.

Absorption is impaired by:

• Alcohol, tea (tannins), coffee, the OCP, stress and antacids.

Deficiency (Beriberi):

• Beriberi is the primary deficiency disease. Most forms are rare in the West. A white rice diet is thiamine depleted (these are at risk).

• Alcoholics are particularly prone to deficiency – ‘cerebral beriberi’ (Wernicke-Korsakoff syndrome) is most common Western cause.


Vitamin B1 - ThiamineOCP = oral

contraceptive pill

51

• Like the antioxidants, B vitamins generally work synergistically and are often found together in nature.

Symptoms of subclinical deficiency:

• Depression, irritability, fatigue, memory loss, muscle weakness and cramps, GIT disturbance.

• Be aware that elderly people are frequently more depleted of thiamine and can benefit from it.

Toxicity:

• Only seen in supplementation (i.e. 5g daily), but is rare.


Vitamin B1 - Thiamine

Exercise: recap

the process of ATP

production, and list

the nutrient

cofactors needed

52

Vitamin B2 - Riboflavin

• Vitamin B2 (Riboflavin) is vital for energy production

and the metabolism of carbohydrates, fats and protein.

• B2 is a fluorescent green/yellow compound –

supplements over 27mg (maximum absorbed

amount) will colour urine bright yellow.

• Riboflavin is very sensitive to light, and content

is also reduced by heating/boiling, freezing and

leeching into cooking water (yellows the water).

• Food sources: Yeast extract, spinach, wild salmon, mushrooms,

almonds, quinoa, lentils, kidney beans, organic eggs, meat.

© CNM: Nutrition Year 1: Vitamins. GH/BQ. 53(Bender, 2002)



Energy (ATP) Production

• Metabolism of carbohydrates, fats and proteins.

• For Krebs cycle & beta-oxidation

• B2 is a constituent of 2 key energy carriers: FAD (flavin adenine dinucleotide) & FMN (flavin mononucleotide)

• Fatigue

• Migraines (400mg/day)

• Stress (multiple B vitamins are depleted during times of stress)

Liver Detoxification • Detoxification via CYP450 enzymes (phase I liver detoxification system).

• Regeneration of glutathione

• Liver detox programmes

Iron metabolism

• B2 is required for iron metabolism • Anaemia


54(Boehnke et al. 2004; Liska et al. 2004)

Absorption:

• Maximum absorption from a single dose is 27mg. Bile salts help intestinal absorption. Antacids and alcohol impair absorption.

Bioavailability is impaired by:

• Copper, zinc, caffeine, theophylline (in chocolate), saccharin.

Dosage:

• Doses between 90-400mg per day (split through the day).

• Smoking can reduce levels in the body. B2 demands are increased with heavy exercise, pregnancy and ageing. Do not exceed daily recommendations in pregnancy and lactation.

Toxicity: Generally considered non-toxic. © CNM: Nutrition Year 1: Vitamins. GH/BQ.


55(Pinto & Zempleni, 2016)

Deficiency:

• Depletion is common but deficiency is rare. More likely to occur in combination with other water-soluble vitamin deficiencies. There is extremely efficient reutilisation of riboflavin in deficiency.

Signs & Symptoms of poor intake include:

• Sores at the margins of the lips / mouth corners.

• Red, dry, atrophic tongue.

• Scaly dermatitis (especially around the mouth,

nose, eyes and ears) and red, tired and gritty eyes.

• Fatigue, weakness, poor concentration, depression.

• Deficiency (although rare) can also cause alopecia.© CNM: Nutrition Year 1: Vitamins. GH/BQ.



Vitamin B3 - Niacin

• Vitamin B3 (niacin) is not strictly a vitamin as it can be synthesised by the body from the amino acid tryptophan: 60mg of tryptophan produces 1mg niacin.

• Vitamin B3 is only essential when tryptophan metabolism is altered.

• The two compounds with niacin activity are: nicotinic acid & nicotinamide. The active forms of niacin are: NAD (nicotinamide adenine dinucleotide) and NADP (nicotinamide adenine dinucleotide phosphate), which are energy carrying molecules.

• Food sources: Mushrooms, green leafy vegetables, yeast extracts, sunflower seeds, salmon, sardines, peanuts, avocado, meat and poultry. Cooking reduces B3 in foods. Tryptophan-rich foods, e.g. bananas, turkey.

© CNM: Nutrition Year 1: Vitamins. GH/BQ. 57(Garrow et al. 2000; Bender, 2002)

Dosage:

• Recommendations are stated as niacin equivalents (NE). Equal to the total niacin compounds in food plus 1/60th of the tryptophan content of the food (i.e. 60mg tryptophan → body produces 1mg B3).

• Synthesis of B3 from tryptophan requires B2, B6 & iron (cofactors).

• Niacin flush: Skin flush & itch due to supplementation. Avoid flush by using initial dose of 25mg (gradually increased) alongside 1g vitamin C.

Absorption & Storage:

• Absorption of vitamin B3 is in the small intestine.

• Stored niacin (NAD) is mostly in the liver, heart, muscles and kidney.© CNM: Nutrition Year 1: Vitamins. GH/BQ.

Vitamin B3 - Niacin

58(Osiecki, 2004)


Vitamin B3 - Niacin


Energy (ATP) Production

• The two coenzymes (NAD, NADP) participate in:

- Glycolysis

- Acetyl CoA formation

- Krebs Cycle

- Fatty acid oxidation

• Fatigue

• Supporting energy production in increased need

• Alzheimer’s

Cardiovascular • Lowers secretion of LDL

• Vasodilatory effects (lowers BP)

• Hyperlipidaemia • Cardiovascular

disease

Insulin • Glucose-tolerance factor (GTF), which plays an important role in the insulin response, employs niacin.

• Insulin resistance (i.e. type 2 diabetes, PCOS)

59(Liska et al. 2004; Morris et al. 2004)

Deficiency Signs & Symptoms:

• Severe deficiency (‘Pellagra’): four Ds – diarrhoea, dermatitis (characteristic collar rash), dementia, death (within 4-5 years). Pellagra can occur in diets deficient in both protein and niacin. It is common in Africa, Indonesia and China. In the West, pellagra is associated with homelessness, alcoholism, or anorexia nervosa. Crohn’s or intestinal disease may also lead to deficiency. Pellagra is treated with up to 500mg B3 daily by a doctor.

• Mild deficiency / insufficiency symptoms:Unrelenting fatigue, vomiting, depression, indigestion, canker sores, sensitivity to strong light, red tongue and inflamed gums.


Vitamin B3 - Niacin

60(Rolfes et al. 2006)

Toxicity / Adverse Events:

• Adverse events can occur at high levels: hypotension, hyperuricaemia, flush, hypothyroidism, hepatotoxicity.

• Do not megadose.

• Niacin competes with urate for excretion so supplementation can worsen gout (200mg+/day).


Vitamin B3 - Niacin

Energy Supportive Lunch (B1/B2/B3)Brown Rice Bowl Recipe for One.

• 1 medium avocado chopped (B2 & B3)

• 2 handfuls of spinach leaves (B2)

• ½ -1 cup cooked brown rice (B3)

• Nori sheets or sprinkles (B1, B2 & iodine)

• Sprinkling of mixed black and white

sesame seeds (B1)

• 2 cups sautéed mixed

mushrooms (B2 & B3)

• Splash of Tamari sauce

• Dash of cold pressed sesame oil

61

Pantothenic = from Greek for ‘found everywhere’ (i.e. found in many foods)

Vitamin B5 – Pantothenic Acid

• Vitamin B5 (pantothenic acid) is required to make

coenzyme A (CoA) - the same CoA that forms acetyl-CoA

(needed for ATP production). In this active form

it is involved in hundreds of different reactions.

Food Sources:

• Richest food sources include shiitake mushrooms,

avocados, nuts, seeds, fish and meat. However, it is

found widely distributed in almost all foods – hence the name.

• Synthesised by intestinal bacteria, but to as yet unknown level of

absorption. Theoretically, antibiotics may reduce synthesis.

• Sensitive to processing, cooking and freezing with up to 80% loss.© CNM: Nutrition Year 1: Vitamins. GH/BQ. 62

(Liska et al. 2004; Rolfes et al. 2006; Bender 2010;

Hechtman, 2012)




ATP Production • Metabolism of carbohydrates and proteins.

• Required for Acetyl CoA formation (review Biochem 2)

• Fatigue• Supporting energy

production in increased need

Fat Metabolism

• The synthesis and degradation of fatty acids.

• Acne vulgaris (sebum)

Stress Hormones • Acetyl-CoA → neurotransmitters(i.e. increased GABA)

• A cofactor for stress hormones (used up quickly when stressed)

• Adrenal fatigue

Anti-Histamine

• Antihistamine properties. • Allergies• Hay fever

63

Deficiency:

• Deficiency is rare. However, depletion

may occur with high alcohol use,

prolonged stress and recent surgery.

• Deficiency Symptoms: burning

sensation in feet and tender heels,

fatigue and abdominal distress.

Toxicity:

• No known toxicity.



Exercise: create

a B5-rich recipe,

which also

encompasses the

most appropriate

cooking methods

64

Vitamin B6 - Pyridoxine• Vitamin B6 (pyridoxine) is made up of a group of six related

vitamers. Active B6 is involved in over 100 enzymatic reactions.

The active forms are pyridoxal 5’-phosphate

(PLP) and pyridoxamine 5’-phosphate (P5P).

Food Sources:

• Widely distributed: wholegrains, green vegetables, sunflower

seeds, pistachios, walnuts, bananas, lentils, avocados, meat & fish.

• Vitamin B6 in a varied diet is approximately 75% bioavailable.

Intestinal flora synthesises large amounts but absorption is unknown.

• Processing, preserving, heating and light exposure reduce B6.

Alcohol excess, the OCP and GIT issues increase requirements.© CNM: Nutrition Year 1: Vitamins. GH/BQ. 65(Liska et al. 2004; NIH, 2020)


Vitamin B6 - Pyridoxine


Neurotransmitter Production

• Synthesis of:

- GABA

- Dopamine

- Noradrenaline

- Serotonin

• GIT motility (digestion)

• Carpal Tunnel Syndrome

• Morning sickness• Lactation & PMS

Red Blood Cell Formation

• Used for haem production • Anaemia

Methylation • Lowers homocysteine • Cardiovascular disease

Energy production

• Amino acid metabolism, releases stored glucose

• Fatigue

66

Increased need for vitamin B6 occurs in:

• Alcohol dependence, long periods of high

stress, pregnancy – particularly in third trimester,

hormonal imbalances, hyperhomocysteinemia

(with folate/folic acid and vitamin B12).

Deficiency:

• Deficiency is rare, and occurs alongside other deficiencies.

• Symptoms: Low B6 affects the metabolism of fatty acids leading

to skin lesions and dermatitis. Tongue inflammation, recurrent

mouth ulcers and sores on the corners of the mouth, hormonal

imbalance (e.g. PMS), anaemia (fatigue, pallor etc.), depression.© CNM: Nutrition Year 1: Vitamins. GH/BQ.


67(Liska et al. 2004; Osiecki, 2004)

Drug Interactions:

• Many drugs deplete B6 levels and so intake should be increased.

This includes anticonvulsants, antibiotics, alcohol, chemotherapy

drug ‘docetaxel’ and the oral contraceptive pill (OCP).

• Levodopa (Parkinson’s medication) - the combination of

carbidopa and levodopa do not have the B6 depletion

problem. However levodopa (on its own) is broken down

by B6 so it should not be supplemented (beyond 5-10mg/day).

Toxicity:

• 100-200mg/day supplements long term can lead to toxicity

symptoms including neuropathy, acne, headache, nausea.© CNM: Nutrition Year 1: Vitamins. GH/BQ.


68

Vitamin B7/B8/H – Biotin

• Biotin as a vitamin was discovered due to its deficiency state

brought about by raw egg consumption (at about 30% of the

diet for many weeks to years). It is considered part of the

B-vitamin complex and has no known toxicities.

• Raw egg whites contain a protein called avidin which joins with

biotin making it unabsorbable. Avidin is denatured by cooking.

• Biotin is an otherwise relatively stable B vitamin. Widespread in

foods but only in small amounts (micrograms) and also made by

intestinal bacteria which is also absorbed into circulation.

• Food sources include: Egg yolk, yeast, wholegrains,

cauliflower, sweet potato, nuts, meat, oily fish.

© CNM: Nutrition Year 1: Vitamins. GH/BQ. 69(Mahan & Escott-Stump, 2008)

70© CNM: Nutrition Year 1: Vitamins. GH/BQ.


Gene Regulation

• Regulates gene expressions(e.g. modifies the activity of transcription factors) which are crucial for metabolism.

• Particularly supportive of rapidly regenerating tissues, e.g. skin, hair and nails.

• Dandruff• Brittle nails• Dry/brittle hair• Cradle cap

Blood Sugar Regulation

• In combination with the mineral chromium, biotin has been shown to improve blood glucose control (reducing HbA1c); i.e. 2mg of biotin with 600mcg of chromium

• Diabetes mellitus

• PCOS


(Liska et al. 2004)

Deficiency:

• Symptoms: Dermatitis, dry scaly flaky skin (i.e. mouth and nose), smooth pale tongue, hair thinning and loss, depigmentation.

• Deficiency can occur in rare metabolic disorders (tested at birth), due to biotin deficient formula or tubal feeding.

• Intestinal production can be reduced due to prolonged use of antibiotics. A vegetarian diet may enhance biotin synthesis and absorption.

• Anticonvulsant drugs and alcohol may inhibit absorption. Steroid hormones and anticonvulsants may hasten breakdown of biotin in tissues. Biotin supplementation interferes with laboratory tests.



71

Vitamin B9 - Folate

• Vitamin B9 (folate) is named to reflect its main source, ‘foliage’.

• The active form of folate in the body is THF (tetrahydrofolate),and its methylated derivatives. As part of an enzyme complex, folate is active in numerous metabolic reactions.

• Folic acid is a synthetic supplement or fortification form and is not found in nature. Folinic acid and levomefolic acid are also synthetic forms of this vitamin. These synthetic forms can be dangerous (discussed shortly), so should be avoided.

Folate Food Sources:

• Leafy greens, asparagus, avocado, Brussel sproutslegumes, citrus fruit (especially oranges) and liver.

foliage = folium

‘leaf ‘(Latin)


Absorption & Bioavailability:

• Absorption requires adequate pancreatic enzymes.

After absorption, a methyl group (–CH3) is added to

folate and in this form, it is delivered to body cells.

• Without the vitamin B12 enzyme which removes the methyl group,

folate becomes trapped inside cells in its methyl form (5-methyl

THF), unavailable to perform its main functions (DNA synthesis

and cell growth) – a metabolic situation called the ‘folate trap’.

• Losses occur from processing & cooking foods. Main storage site is

the liver (50%). Some folate is recycled in the liver and reabsorbed.

The microbiota produce some B9, but absorption/use is not known.


Vitamin B9 - Folate

73(Hass 2006; Hechtman 2012)

B9 Forms & Adverse Effects:

• Dietary Folate Equivalents (DFE) have been developed

because bioavailability of folate varies in food compared

to supplements. 1mcg of natural folate = 1 DFE.

• Folic acid is considered 1.7 x more available than

dietary folate, which is problematic in that it is less regulated

and so absorption is uncontrolled in the body.

An adverse effect of high folic acid supplementation is nausea.

• Where supplementation of B9 is indicated, it is

advisable to recommend the methylated form of folate.


Vitamin B9 - Folate

74



Cardiovascular

Health

• Methylation of homocysteine to

methionine. Watch this video for

an explanation:

https://www.youtube.com/watch?

v=x1DzCeo7QK8

• Atherosclerosis• Alzheimer’s- Consume at least

300mcg per day of dietary folate

Formation

of Red

Blood Cells

• Required for erythrocyte

synthesis. Without this, they are

large & immature

• Anaemia (B9 deficiency induced)

Embryo

Health

• Required for the healthy

development of the neural tube

• Prevents spina bifida (600mcg/day

The functions of folate relate to its methyl donor action, including:

Vitamin B9 - Folate

75

https://www.youtube.com/watch?v=x1DzCeo7QK8

Deficiency signs and symptoms:

• Affecting rapidly dividing cell types; skin, GIT and blood cells – skin and digestive issues, megaloblastic anaemia (severe deficiency).

Factors related to deficiency:

• Alcoholism, OCP, diuretic and aspirin use. GIT disorders, diets low in green leafy vegetables and old age. Those on methotrexate and anticonvulsants should consult their GP regarding vitamin B9 use.

Dosage for conception:

• Preconception and conception care: 600mcg/day beginning prior to conception helps avoid neural tube defects.


Vitamin B9 - Folate

76(Bender, 2002; Rolfes et al. 2006)

Safety Considerations:

• Naturally occurring folate is considered safe to use.

• Folic acid supplements mask the megaloblastic anaemia of

vitamin B12 deficiency and may hasten the development of

irreversible nerve damage. B12 testing can combat this.

• People with an MTHFR polymorphism may be more

susceptible to issues arising from supplementation

with folic acid (or that in fortified foods). Active forms of

the vitamin ONLY should be recommended to clients.

• Folic acid supplements have the most drug

interactions of all vitamins; check rigorously.


Vitamin B9 - Folate

77

Vitamin B12 - Cobalamin

• Vitamin B12 refers to a family of cobalamin compounds containing the essential mineral cobalt in the centre.

• The most active B12 analogs include: methylcobalamin, hydroxycobalamin, adenosyl cobalamin and cyanocobalamin.These are the only analogs recognised by the body. There are others found in nature but they are not bioavailable to humans.

• Vitamin B12 is synthesised by bacteria. Vitamin B12 found in animal based foods originates from their ingestion of bacterial-contaminated feed, or from B12 that has been given to the animal. The human microbiota produces B12, but it is not absorbed.

78

cobalamin = from

cobalt + vitamin

© CNM: Nutrition Year 1: Vitamins. GH/BQ. (Mahan & Escott-Stump, 2008)

• B12 storage in the liver lasts between 3-5 years.

Vegan B12 Food Sources:

• Chlorella pyrenoidosa (e.g. 9g per day)

• A substantial amount (133.8 μg/100 g) of vitamin B12 has also been found in dried Korean purple laver (Porphyra sp.).

• Nutritional yeast, nori and kombu sea vegetables (nori, kombu,

kelp and dulse), shiitake & Lions mane mushrooms.

Animal B12 Food Sources:

• Meat, liver, milk, cottage and feta cheese, organic eggs, fish (esp. sardines, mackerel and wild salmon).



79(Mahan & Escott-Stump, 2008; Wantanabe et al. 2014;

Merchant et al. 2015)



Nervous System • Myelin production

• Neurotransmitter production (dopamine, serotonin)

• Choline – key for brain function

• MS

• Tingling / Pins and Needles

• Sciatica

Erythropoiesis • B12 is required for erythropoiesis.

• Megaloblastic anaemia

Methylation • Homocysteine cycle (conversion of the amino acid homocysteine to methionine)


• Alzheimer’s

Energy Production

• Energy production from fats and proteins

• Fatigue


80



Causes of B12 deficiency:

• Poor nutrition (malnutrition):

- Lack of dietary B12 intake, and a diet rich

in highly processed, nutrient-depleted foods.

• GIT causes (malabsorption):

- Stomach problems (e.g. lack of intrinsic

factor, low hydrochloric acid production)

- Low pancreatic enzymes, small intestine issues

(e.g. Crohn’s disease, coeliac), high alcohol.

• Note: if a client has a good dietary intake of B12, yet is deficient, it

highlights a possible absorption issue or problem with methylation.81

Deficiency States:

• The most common cause of deficiency is

malabsorption due to inadequate intrinsic factor

(IF) production. It is called pernicious anaemia.

Helicobacter pylori infection is also implicated.

• Pernicious anaemia is associated

with an autoimmune attack on parietal

cells in the stomach (the cells that

synthesise intrinsic factor).

• Increased vitamin B12 requirements are associated with:

pregnancy, thyrotoxicosis, malignancy, liver & kidney disease.



82(Mahan & Escott-Stump, 2008)


• Megaloblastic anaemia: presenting as fatigue, breathlessness,

pallor, etc. Supplementation with B9 will alleviate the anaemia,

however other symptoms of vitamin B12 deficiency progress.

• Neurological abnormalities: tingling, numbness, loss of balance, burning sensations, weakness, confusion and decreased reflexes.

• Anaemia typically develops first, but not always if the person is consuming lots of folate.

• Changes occur slowly, and once the patient experiences neurological symptoms, they may be irreversible.



(Mahan & Escott-Stump, 2008)

B12 Testing:

• Serum B12 Testing reference ranges are

typically anything between from 110ng/L

up to 900ng/L. This is the most common

means of assessing B12 conventionally.

• However, many people experience signs

of B12 deficiency with normal B12 serum.

• A more accurate reflection of B12 levels would

involve testing MethylMalonic Acid (available in serum

or urine testing) – gives an indication of how B12 is

used in cell metabolism and is the gold standard test.84© CNM: Nutrition Year 1: Vitamins. GH/BQ.


Toxicity:

• Vitamin B12 is one of the safest vitamins. No adverse effects have been associated with large intakes (2mg) of vitamin B12 from food or supplements in healthy people.

Drug Interactions:

• The OCP, metformin, excessive alcohol, proton pump inhibitors and H2-receptor antagonists lower B12 levels.

• Calcium may enhance B12 absorption, including with metformin use.

• People with autoimmune disease are considered more at risk of pernicious anaemia.



85(Bender, 2002; Mahan & Escott-Stump, 2008;

Higdon et al. 2014)

Vitamin C – Ascorbic Acid

• Vitamin C functions as a key antioxidant, and as an enzyme cofactor. In both of these functions vitamin C is a potent reducing agent, meaning that it readily donates electrons to recipient molecules.

• Most animals can synthesise vitamin C: ascorbic acid / ascorbate. Some scientists postulate this has made humans more susceptible to viral illnesses, raised cholesterol, cardiovascular disease and cancer, and less resistant to stress.

• Vitamin C does not need to be modified by the body to function.

• Until the ‘cure’ for the vitamin C deficiency disease ‘Scurvy’ was found, more sailors died of scurvy than of any other cause (estimated 2 million sailors or 50% of any major voyage crew).


Food sources:

• All fresh raw fruit and vegetables, particularly

peppers, kiwi fruit, papaya, currants, berries,

citrus, crucifers, mangoes and tomatoes.

• Very significant losses occur as vegetables

wilt, or when they are cut as a result of the

release of ascorbate oxidase from the plant tissue.

• Ascorbate oxidase is why lemon or lime juice can

prevent the browning (oxidising) of other foods

(e.g. sliced apple) – the vitamin C creates an

antioxidant barrier from oxygen until it is all used up.87© CNM: Nutrition Year 1: Vitamins. GH/BQ.


(Bender, 2002; Osiecki, 2004)

Absorption:

• Absorbed in the mouth and in the small intestine (by active and passive means). Up to 100% absorption per 200mg serving.

• Transported into cells by glucose transporters; so high blood glucose levels can inhibit vitamin C uptake significantly. Think about diabetics and clients with sugar laden diets. High doses of vitamin C can also skew blood glucose test results.

• Vitamin C concentrates in the adrenal glands, white blood cells, thymus and pituitary – although there is no specific storage site.

• Factors that increase breakdown or excretion of vitamin C include: Stress – psychological, chemical, emotional or physiological, fever and viral illnesses. Alcohol, smoking, heavy metals, aspirin, OCP.





Anti-Oxidant (& immune-boosting

• Primary water soluble antioxidant in blood and tissues – protecting proteins, lipids, carbohydrates, RNA & DNA from damage from free radicals.

• Recycles other antioxidants such as vitamin E and glutathione - making them usable again as antioxidants.

• Up-regulates interferons, natural killer cells and T cells

• Cancer• Cardiovascular

disease • Alzheimer’s• Asthma/COPD• Cataracts• Immune support

e.g. cold sores -2g per day can halve healing time

Cholesterol-Lowering

• Conversion of cholesterol to bile acids (lowering blood LDL levels)



89



Iron

Absorption

• Enhances iron absorption by protecting

iron from oxidation. It keeps it in Fe2+

form, not allowing it to become Fe3+,

which is not a bioavailable form.

• A dose of 25mg of vitamin C taken

together with a meal increases iron

absorption by 65%. Optimum iron

absorption may require more than

100mg/day.

• Anaemia

Endocrine

Functions

• Synthesis of thyroxine and adrenal

steroid hormones.

• Adrenal fatigue• Hypothyroidism


90(Bender, 2002; Rolfes et al. 2006)



Collagen Synthesis

• Vitamin C is a co-factor required for collagen synthesis.

• Important for forming strong tendons, ligaments and bones, repairing wounds, improving gum health.

• Osteoarthritis• Cartilage injuries• Ligament injuries• Gum diseases• Bruising• Fracture repair• Blood vessels

Neurotransmitter synthesis

• A co-factor for the production of serotonin.

• Weak digestion

Energy Production

• Transport of long-chain fatty acids into the mitochondria for ATP production

• Fatigue• Chronic fatigue


91




• The two most notable signs of vitamin C deficiency

reflect its role maintaining blood vessel integrity:

- The gums bleed easily around the teeth.

- Capillaries under the skin break spontaneously

producing pinpoint haemorrhages.

• When intake falls to about 1/5 of its optimal store size (approx.

1 month on a vitamin C depleted diet), Scurvy symptoms appear:

- Further haemorrhaging from inadequate collagen synthesis.

- Muscle degeneration and rough, brown scaly skin.

- Wounds do not heal. Bone rebuilding falters - fractures develop.92(Rolfes et al. 2006)

Deficiency States:

• During stress, the adrenals release vitamin C with other hormones into the blood. The exact role of vitamin C in stress is unknown, but it is known that stress raises vitamin C needs – likely due to additional free radical damage.

• Burns, infections, toxic metal intakes, chronic use of medications and cigarette smoking are among the stresses that increase vitamin C demand.

• Smokers have lower levels of serum vitamin C –25mg of vitamin C is lost with every cigarette smoked.

• Subclinical deficiency is common: susceptibility to infections, poor wound healing, fatigue, skin and gum degeneration, petechiae.



(Rolfes et al. 2006)

Dosage & Tolerance:

• 500mg/day+ vitamin C is a sound general dose.

• A high dietary intake of vitamin C is cancer-protective, and can be mega-dosed (e.g. 25-75g intravenously) for cancer support.

• 250mg-1g of vitamin C prophylactically can reduce the incidence of colds by 50% in those who undertake strenuous exercise – potential support in sports nutrition.

• Unabsorbed ascorbate from very high doses (3g/day plus) is a substrate for intestinal bacterial metabolism causing gastrointestinal discomfort and diarrhoea (bowel tolerance).

• No high doses in third trimester of pregnancy. The baby becomes accustomed to high doses that are unsustainable when born.



94(Hemilä & Chalker, 2013)

Toxicity:

• Vitamin C is non-toxic, even at extremely high doses. No reliable scientific evidence of toxicity in adult doses up to 10g per day. No credible scientific evidence that supplemental vitamin C promotes oxidative damage in humans.

• People with kidney disease and those with a tendency toward gout are prone to forming kidney stones if they take large doses of Ascorbic Acid beyond a few months

• Be mindful of high dose vitamin C with haemochromatosis.

Drug interactions:

• May reduce effectiveness of warfarin, statins, some cancer drugs. Increases oestrogen therapy effects. Skews diabetes test results.


haemochromatosis

= iron overload


95

Male, Aged 53, salesman (high pressure/stress), sedentary.

Presenting with 3 issues he wants to address:

1. Fatigue (despite good sleep).

2. Worsening knee osteoarthritis (pain and stiffness), following a cartilage injury when running aged 29.

3. Wanting to reduce his risk of cardiovascular disease.

• Strong family history of cardiovascular disease and Alzheimer’s.

• Smoker (5 a day) and drinks 2 glasses of white wine most nights.

• High sugar intake, skips main meals, snacks frequently.

• Eats mostly ready meals (microwaved) and pre-cut frozen veg.



Review the following case study:

96


Questions:

1. Provide an overview of your understanding of this case.

2. Identify the key vitamins that are most suitable for this client, giving your reasons why. Ensurethat you address the presenting complaints.

3. List SIX foods for this client to increase in their diet, with an overview of their vitamin profile.

4. What are the implications of his food storage and preparation, with regards to his dietary vitamin intake? Make suitable recommendations to address this.



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naturopathic nutrition year 1

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