Page 3 of 8

BI8.1-6 | Vitamins and Nutrition — Part 2

Vitamins E and K — Antioxidant and Coagulation

Vitamin E (alpha-tocopherol):
- Most potent lipid-soluble antioxidant in the body
- Protects polyunsaturated fatty acids (PUFAs) in cell membranes from free radical attack
- Deficiency (rare in adults; seen in premature neonates and fat malabsorption): haemolytic anaemia in neonates, peripheral neuropathy, spinocerebellar ataxia in adults
- Sources: vegetable oils, nuts, seeds, green leafy vegetables

Figure: Vitamins E and K — Antioxidant and Coagulation

Vitamin K:
- Required for activation of clotting factors II (prothrombin), VII, IX, X and anticoagulant proteins C and S, and osteocalcin
- Mechanism: vitamin K-dependent carboxylase converts glutamate residues in these proteins → gamma-carboxyglutamate (Gla) residues → can bind Ca²⁺ → form is activated
- Vitamin K1 (phylloquinone): from green vegetables
- Vitamin K2 (menaquinone): synthesised by gut bacteria (important contribution)
- Deficiency: prolonged PT and PTT, haemorrhage
- Haemorrhagic disease of the newborn (HDN): neonates have low Vitamin K stores (poor placental transfer), sterile gut (no bacteria), low breast milk content → all newborns in India receive prophylactic Vitamin K at birth (1 mg IM)
- Fat malabsorption (celiac, cholestasis)
- Warfarin (vitamin K antagonist) → anticoagulation therapy

Water-Soluble Vitamins — The B-Complex

The B-complex vitamins are 8 vitamins that function predominantly as coenzymes in metabolic pathways. Most are not stored — daily dietary intake is essential.

Figure: Water-Soluble Vitamins — The B-Complex

Overview:

Vitamin	Active Form	Key Role	Deficiency Disease
B1 (Thiamine)	Thiamine pyrophosphate (TPP)	Pyruvate/α-KG dehydrogenase, pentose shunt	Beriberi, Wernicke's
B2 (Riboflavin)	FAD, FMN	ETC, fatty acid β-oxidation	Cheilosis, angular stomatitis
B3 (Niacin)	NAD⁺/NADH, NADP⁺/NADPH	Redox reactions (>400 enzymes)	Pellagra (3 Ds)
B5 (Pantothenic acid)	Coenzyme A (CoA)	Acyl transfers, TCA cycle, fatty acid synthesis	Rare — burning feet
B6 (Pyridoxine)	Pyridoxal phosphate (PLP)	Amino acid transamination, decarboxylation, δ-ALA synthase	Peripheral neuropathy, sideroblastic anaemia
B7 (Biotin)	Carboxylase cofactor	Pyruvate carboxylase, ACC, propionyl-CoA carboxylase	Alopecia, dermatitis (raw egg white consumption)
B9 (Folate)	THF (tetrahydrofolate)	1-carbon transfer; nucleotide synthesis	Megaloblastic anaemia, NTDs
B12 (Cobalamin)	Methylcobalamin, adenosylcobalamin	Methionine synthase, methylmalonyl-CoA mutase	Megaloblastic anaemia + subacute combined degeneration

All coenzymes in the Krebs cycle directly or indirectly depend on B vitamins — this is why vitamin deficiency impairs energy metabolism systemically.

Key B Vitamin Deficiencies in India

Thiamine (B1) deficiency → Beriberi:
- TPP is the cofactor for pyruvate dehydrogenase, α-ketoglutarate dehydrogenase, and transketolase (pentose phosphate pathway)
- Without TPP: pyruvate cannot enter TCA cycle → accumulates → lactic acidosis
- Wet beriberi: high-output cardiac failure, oedema (heart cannot use glucose efficiently)
- Dry beriberi: peripheral neuropathy — polyneuritis; foot drop
- Wernicke's encephalopathy: ataxia, ophthalmoplegia, confusion (in chronic alcoholics — alcohol interferes with B1 absorption and increases demand; also in patients on prolonged IV glucose without thiamine supplementation)
- Cause in India: polished (milled) rice diet (removes bran where thiamine is stored)

Figure: Key B Vitamin Deficiencies in India

Niacin (B3) deficiency → Pellagra:
- NAD⁺/NADP⁺ are coenzymes in ~400 oxidation-reduction reactions
- Pellagra = the 4 Ds: Diarrhoea, Dermatitis, Dementia, Death
- Dermatitis is photosensitive — affects sun-exposed areas (necklace distribution = Casal's necklace)
- Endemic in sorghum (jowar)-eating populations of Maharashtra, Karnataka — jowar has niacin in bound (unavailable) form + high leucine (excess leucine inhibits conversion of tryptophan to niacin)
- Tryptophan → niacin: 60 mg tryptophan = 1 mg niacin. Maize is niacin-deficient.

Folate and B12 deficiency → Megaloblastic Anaemia:
- Folate (THF) and B12 are both needed for thymidylate synthesis → DNA synthesis
- Deficiency: DNA synthesis impaired while cytoplasmic growth continues → large immature red cells (megaloblasts) → macrocytic anaemia
- Folate deficiency in pregnancy → Neural Tube Defects (spina bifida, anencephaly) → all women of childbearing age should take 400 mcg folic acid daily
- B12 deficiency (common in vegetarians — B12 only in animal foods): besides megaloblastic anaemia, causes subacute combined degeneration of the spinal cord (SACD) — demyelination of posterior and lateral columns → loss of vibration sense, proprioception, then spastic weakness