Vitaminab12

Nutrition & Dietetics 2007; 64 (Suppl. 4): S120–S125

DOI: 10.1111/j.1747-0080.2007.00198.x

Vitamin B12
A Stewart TRUSWELL
University of Sydney, Sydney, New South Wales, Australia

KEY POINTS
• Subclinical vitamin B12 deficiency (low serum vitamin B12, and/or raised methylmalonate) occurs in 10% or more of older people, in Australia and other developed countries. Causes includeinadequate liberation of vitamin B12 from its natural binding to the protein in foods because of poor gastric acid production. There is evidence that in some cases, the diet has been inadequate in animal foods. At present, it is not clear whether these low biochemical values lead to any serious consequences. • The recent recommended dietary allowance reports for vitamin B12 in the USA and Canada recommendthat older people should obtain most of their vitamin B12 from fortified foods or from supplements of free (crystalline) vitamin B12. In Australia and New Zealand, advice in the Nutrient Reference Values report is that older people with low stomach acid secretion ‘May require higher intakes of vitamin B12 rich foods “(e.g. meat)” vitamin B12 fortified foods “(not generally available here)” orsupplements’. • Dietary deficiency of vitamin B12 occurs in strict vegans. It is usually subclinical. But very severe clinical deficiency has been reported in infants breastfed by a vegan mother. • Now that folate intakes have been increased by fortification of foods—mandatory in North America, at present voluntary in Australia and New Zealand—some experts and some evidence warn that it may be advisablefor people to increase B12 intake. • Meat and meat products are the major source of vitamin B12 in Britain. Presumably this would be similar in Australia. Liver and kidney are the foods richest in this vitamin.

sheep, which require traces of cobalt in the pasture. Humans eat this vitamin preformed in animal foods: meat, milk, eggs and fish. No plant food has ever been shown to contain vitamin B12consistently unless it is contaminated, for example by manure. In McCance and Widdowson’s food tables,4 all the vitamin B12 columns for vegetables and fruits and cereals have an ‘0’ unless the line is for a mixed dish or a fortified (British) breakfast cereal. This review discusses the biochemical functions of vitamin B12, clinical deficiency diseases associated with vitamin B12, causes ofdeficiency, vegan infants and the elderly, nutritional intakes in Australia and New Zealand and meeting dietary requirements.

BIOCHEMICAL FUNCTIONS
Methionine synthase (in the cytosol) requires methylcobalamin as cofactor, and methylmalonyl CoA mutase (in mitochondria) requires 5′ deoxyadenosylcobalamin as coenzyme. In bacteria, vitamin B12 participates in several other enzyme reactions. Methioninesynthase is also called N-5 methyltetrahydrofolate: homocysteine methyltransferase. It sits at the junction between two important metabolic processes: synthesis of DNA and the methylation reactions via S-adenosylmethionine. If vitamin B12 is lacking, folate is trapped as methyl tetrahydrofolate. The metabolite 5, 10 methylene tetrahydrofolate is not formed, and this is specifically required forconversion of deoxyuridylate to thymidylate, one of the four essential bases in DNA synthesis. In this situation, cell nuclei cannot divide, and there is megaloblastic change which affects rapidly dividing cells of the bone marrow (making blood cells), the gastrointestinal epithelium and germinal epithelium. Effects include anaemia and increased plasma homocysteine. Methylmalonyl CoA mutase (MMCoA mutase)is the second and less central enzyme that requires vitamin B12. It deals with products of oxidation of odd-chain fatty acids and of the carbon skeletons of four amino acids as well as propionate itself. Propionyl CoA is converted to L-methylmalonyl CoA and the mutase (with vitamin B12 as coenzyme) converts this to succinyl CoA, which is part of the tricarboxylic acid (Krebs) cycle of...