Learn — Vitamins & deficiencies

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Vitamin deficiency and excess — table

Vitamins are organic micronutrients that the body cannot synthesise in adequate amounts and must take from the diet, where they work almost entirely as coenzymes, antioxidants or hormones rather than as fuel. They divide into the fat-soluble group A, D, E and K, which need bile and dietary fat for absorption and are stored in liver and adipose tissue so that deficiency follows fat malabsorption and excess accumulates to real toxicity, and the water-soluble B complex and C, which are not stored apart from B12, are lost in urine and in cooking water, and therefore produce deficiency within weeks but toxicity only rarely.

Vitamin A (retinol) deficiency is the leading preventable cause of childhood blindness and progresses in a fixed order — night blindness first, then conjunctival xerosis, Bitot's spots, corneal xerosis and finally keratomalacia, which destroys the eye; India's programme gives 100,000 IU at nine months with measles vaccine and 200,000 IU every six months to five years, while excess causes headache and raised intracranial pressure acutely, bone pain, hair loss and liver damage chronically, and retinoids are teratogenic in pregnancy.
Vitamin D is made in skin from 7-dehydrocholesterol under ultraviolet light, hydroxylated in the liver to 25-hydroxycholecalciferol (the storage form measured in blood) and in the kidney to 1,25-dihydroxycholecalciferol or calcitriol (the active hormone); deficiency causes rickets in the growing child (craniotabes, rachitic rosary, widened wrists, bow legs, delayed closure of the fontanelle) and osteomalacia in the adult, with a low or normal calcium, low phosphate and a characteristically raised alkaline phosphatase, while excess causes hypercalcaemia, vomiting, polyuria and nephrocalcinosis.
Vitamin E (tocopherol) is the main lipid-soluble antioxidant of cell membranes; deficiency causes haemolytic anaemia in the preterm newborn and, in prolonged fat malabsorption, a peripheral neuropathy with ataxia.
Vitamin K is the cofactor for gamma-carboxylation of clotting factors II, VII, IX and X and of proteins C and S, so deficiency prolongs the prothrombin time first (factor VII has the shortest half-life); a single intramuscular dose is given to every newborn to prevent vitamin K deficiency bleeding, and warfarin works by blocking the recycling of vitamin K and is reversed by giving it.
Thiamine (B1) is the coenzyme thiamine pyrophosphate for pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase and transketolase; deficiency gives dry beriberi (peripheral neuropathy), wet beriberi (high-output cardiac failure with oedema), infantile beriberi, and in the alcoholic the Wernicke triad of confusion, ataxia and ophthalmoplegia which, untreated, becomes Korsakoff's amnesic psychosis with confabulation.
Riboflavin (B2, as FAD and FMN) deficiency gives angular stomatitis, cheilosis, a magenta glossitis, seborrhoeic dermatitis and corneal vascularisation; niacin (B3) can be made from tryptophan at a ratio of about 60 mg of tryptophan to 1 mg of niacin, and its deficiency is pellagra with the three Ds of photosensitive dermatitis (Casal's necklace), diarrhoea and dementia, seen with a maize-based diet, in Hartnup disease, in carcinoid syndrome and with isoniazid.
Pyridoxine (B6) is the coenzyme of transamination, of delta-aminolaevulinate synthase in haem synthesis and of GABA formation; isoniazid inactivates it, so a peripheral neuropathy develops unless 10 mg of pyridoxine is given daily with antitubercular treatment, and deficiency also causes sideroblastic anaemia and convulsions in infants.
Folate (B9) is needed for thymidylate and therefore for DNA synthesis; deficiency causes megaloblastic anaemia, and 400 micrograms daily periconceptionally (5 mg in a woman with a previous affected pregnancy or on antiepileptics) prevents neural tube defects — which means it must be started before conception, since the neural tube closes by the fourth week.
Vitamin B12 (cobalamin) needs intrinsic factor from the gastric parietal cells and is absorbed in the terminal ileum, so deficiency follows pernicious anaemia, gastrectomy, ileal resection or Crohn's disease, a strict vegan diet, and long use of metformin or proton pump inhibitors; it causes megaloblastic anaemia and subacute combined degeneration of the spinal cord, and giving folate alone corrects the blood picture while the cord damage silently advances.
Vitamin C (ascorbic acid) hydroxylates proline and lysine in collagen synthesis and reduces dietary ferric iron to the absorbable ferrous form; scurvy therefore presents with perifollicular haemorrhages, corkscrew hairs, swollen bleeding gums, delayed wound healing and, in infants, painful subperiosteal haemorrhage with pseudoparalysis of the legs.

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