08 - Vitamins

Naturopathic Nutrition Year 1: Vitamins

Introduction

• In 1911, biochemist Casimir Funk coined the term 'vitamines'.

• Funk identified that ‘beriberi’, which causes mostly neurological symptoms, such as numbness, and mostly affects those on a diet of white rice, was caused by 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, so ‘vitamine’ was changed to ‘vitamin’ (no e).

• Different chemical forms of each vitamin exist, and 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
  • 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, so it is vital to optimize GIT health.
• Vitamins are carbon-containing compounds that are essential to 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 energy production (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).
• 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 ‘co-factors’).
  • E.g., B-vitamins are vital co-factors 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 program.
    • co-factor = an essential component for enzyme activity

Vitamins Classification

• There are 2 types of vitamins: Fat- and water-soluble.

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.

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 the clinic are insufficiency states.

  • insufficiency = sub-clinical deficiency (i.e., vague symptoms)
  • deficiency = clinical signs and symptoms of deficiency

Fat-soluble Vitamins

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 oxidized 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.

• 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.

    • carotene = from the Greek karoton for 'carrot' — orange pigments

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

  • Pre-formed vitamin A → this is active vitamin A the body can use as it is.

    • Only found in animal foods.
    • Pre-formed vitamin = a vitamin that is already formed

• Food sources:

  • Pro-vitamin A is 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.

• 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 optimize 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 and 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 of 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.

• 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 3000 mcg 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).

• 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)
  • $1 IU \, retinol = 0.3 mcg \, RAE$
  • mcg = micrograms

• Functions:

  • Vision and 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.

    • rhodopsin = the ‘visual purple’

    • Also necessary for corneal health.

    • Therapeutic uses:

      • Photosensitivity
      • Visual loss
      • Night-blindness
      • Senile cataracts

  • Immunity:

    • Enhances T-cell proliferation and interleukin-2 secretion.
    • Supports first line of immune defense (skin and mucous membrane barrier).
    • Therapeutic uses:
      • Recurrent infections, e.g., respiratory tract infections.

  • 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.
    • Therapeutic uses:
      • Acne
      • Anemia
      • Cervical dysplasia
      • Hair loss in women
      • Fracture repair
      • Lichen planus
      • Osteoarthritis
      • GIT ulceration
      • Vaginitis
      • Periodontal disease

  • Reproduction:

    • Reproductive & embryonic health.
    • Required for spermatogenesis in men.
    • Required for egg (ovum) development and implantation.
    • Therapeutic uses:
      • Infertility (male and female)
      • Fibrocystic breast disease

  • Antioxidant 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
    • 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 oxidizing.

  • 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.

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

    • 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).

    • Add 1–2 portions of beta-carotene-rich foods a day to address these, before considering supplementation.

  • Factors affecting individual requirements:

    • Diabetes mellitus, thyroid and liver disease — ↓carotene conversion.
    • Alcoholism:
      • Accelerates the breakdown of liver-stored retinol; absorption and carotene conversion is reduced.
      • Increased vitamin A toxicity potential; not supplemented 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 utilization.
      • Without zinc, vitamin A is trapped. So optimize intake of zinc-rich foods.

  • 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).

      • hepatocyte = liver cell

      • 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).

Vitamin D

• Vitamin D is not strictly a vitamin since it can be synthesized in the skin in response to sunlight.

  • ergo = plant sourced D
  • chole = animal sourced D

• 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).

• 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).

• 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.
    • endogenous = from within the body
  • Note that vitamin D can be stored in the liver for 4 months.

• Dosage:

  • Our focus should be on first addressing the cause of the deficiency, to avoid a ‘symptom-based’ approach.
  • A supplemental dose of 4000 IU / day has been used without adverse effects. $1 μg$ of cholecalciferol = $40 IU$.
    • μg = microgram
  • 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 favored 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.

• 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.

  • nuclear = nucleus
  • transcription = copying a segment of DNA (a gene)

• Functions:

  • Bone health:

    • Supports bone density (along with vitamin K2), by increasing intestinal calcium absorption.
    • Therapeutic uses:
      • Osteoporosis
      • Osteomalacia and 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.

      • cytokines = immune messenger proteins

    • Therapeutic uses:

      • Allergies
      • Autoimmunity, e.g., multiple sclerosis
      • Infections (e.g., viral and bacterial)
      • Musculoskeletal pain reduction

  • GIT health:

    • The vitamin D receptor (VDR) helps to regulates mucosal inflammation.
    • Vitamin D has a role in commensal bacterial colonization.
    • • Intestinal VDR stabilizes tight junctions.
    • Therapeutic uses:
      • Intestinal inflammation, e.g., inflammatory bowel diseases (as well as intestinal permeability)

  • Anti-cancer:

    • Enhances the anti-tumor activity of innate immune cells.

    • Regulates multiple genes through the VDR, and inhibits angiogenesis.

    • angiogenesis = blood vessel formation

    • Therapeutic uses:

      • Cancer prevention and support

  • Insulin:

    • Vitamin D:
      • Activates transcription of the insulin gene (increasing insulin secretion).
      • Increases cellular sensitivity to insulin.
    • Therapeutic uses:
      • Diabetes mellitus (Type 2, but also Type 1)

• Vitamin A and 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 and symptoms:

  • Rickets and osteomalacia:

    • Demineralized 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

  • osteo = bone

  • malacia = softening (from Greek)

• Causes of vitamin D deficiency:

  • Inadequate UVB sun exposure and overuse of conventional sunscreens.
  • 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.
  • UVB = ultraviolet B rays

• 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).

• Toxicity:

  • Vitamin D synthesis due to sunlight does not produce toxicity.
  • Main toxicity symptoms due to vitamin D-related hypercalcaemia: nausea, diarrhea, 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.
    • EFSA = European Food Safety Authority
  • Drug interactions:
    • Osteomalacia risk due to low vitamin D is increased with use of barbiturates and anticonvulsants.

Vitamin E

• Vitamin E is a generic term for two families of fat-soluble compounds with vitamin E activity: Tocopherols and tocotrienols. Both families contain at least four forms: Alpha, beta, gamma, and delta. All forms exist within natural foods.

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

• The only form recognized 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.

• 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:

  • $1 mg \, of \, natural \, α-tocopherol = 1 \, α-tocopherol equivalent \, (αTE)$

• Functions:

  • Antioxidant

    • Protects the following from oxidation:

      • Polyunsaturated fatty acids (PUFA) cell membranes
      • Nerve sheaths
      • Cholesterol (↓ LDL oxidation)

    • A vital ‘chain-breaking antioxidant’.

    • chain-breaking antioxidant = stops the formation of more unstable radicals

    • Vitamin C and selenium support the activity of vitamin E by rejuvenating oxidized vitamin E. So, ensure an adequate intake of all antioxidants to optimize the effects of vitamin E.

    • Therapeutic uses:

      • Atherosclerosis and cardiovascular disease
      • Male fertility
      • Healthy aging
      • Cataracts
      • Alzheimer’s and cognitive decline
      • Anti-cancer (also stimulates the p53 tumour suppressor gene)

  • Immunity

    • Increases phagocyte activity
    • Differentiation of immature T cells in the thymus
    • Antioxidant and mild anti-inflammatory properties
    • Therapeutic uses:
      • HIV / AIDS
      • Healthy immune functioning
      • Infections

  • Anti-coagulant

    • Inhibits platelet aggregation and vitamin K activity (↓clotting factors)
    • Therapeutic uses:
      • Cardiovascular disease

  • Endocrine

    • Improves insulin action (possibly improves insulin resistance)
    • Modulates estrogen receptors and activity
    • Therapeutic uses:
      • Diabetes mellitus
      • Dysmenorrhea
      • Menopause (e.g., vaginal dryness)

  • Skin repair

    • Traditional topical use, although mechanism not understood.
    • Therapeutic uses:
      • Scarring
      • Acne

• 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 anemia) — 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.

Vitamin K

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

  • quinone = refers to chemical structure
  • Named after K for koagulation (German spelling); discovered during investigation of bleeding disorders in animals.

• 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 utilized.

• K2 (menaquinones):

  • Synthesized 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.

• 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 and absorption:

  • Optimal intake is 300–500 mcg / 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.

• Functions:

  • 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 mineralization
    • Osteocalcin (a calcium binding protein in bones) requires vitamin K for synthesis.
    • Osteocalcin synthesis by osteoblasts is regulated by active vitamin D (calcitriol).
    • Therapeutic uses:
      • Osteoporosis (45 mg / day, and by supporting microflora).
      • Prevents calcium accumulation in arteries and kidneys.

• Causes of deficiency:

  • Liver diseases, warfarin, antibiotic use, fat malabsorption issues.
  • Maternal considerations:
    • Vitamin K transfer to the fetus 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 and K2 are not known to be toxic (K3 can be).

• Vitamin K Injection for Newborns

  • Considerations of the vitamin K injection:
    • Undesirable preservatives e.g., polysorbate 80; aluminum 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.

Water-Soluble Vitamins

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, whole grains, meat / fish.

• Functions:

  • Energy (ATP) production
    • Crucial for carbohydrate, as well as fat and protein metabolism.
    • Needed for the formation of Acetyl-CoA (key for ATP production).
    • Therapeutic uses:
      • 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.
    • Therapeutic uses:
      • Cognitive decline and memory loss
      • Alzheimer’s
      • Low mood
      • Parkinson’s
      • Nerve repair

• 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 / 1000 kcal is recommended.

• Absorption is impaired by:

  • Alcohol, tea (tannins), coffee, the OCP, stress and antacids.
    • OCP = oral contraceptive pill

• 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 the most common Western cause.

• 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 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 27 mg (maximum absorbed amount) will color 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.

• Functions:

  • Energy (ATP) production
    • Metabolism of carbohydrates, fats and proteins.
    • For Krebs cycle and beta-oxidation
    • B2 is a constituent of 2 key energy carriers: FAD (flavin adenine dinucleotide) and FMN (flavin mononucleotide)
    • Therapeutic uses:
      • Fatigue
      • Migraines (400 mg / 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
    • Therapeutic uses:
      • Liver detox programs
  • Iron metabolism
    • B2 is required for iron metabolism
    • Therapeutic uses:
      • Anemia

• 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 90–400