Vitamin B 12 is essential for normal energy metabolism of carbohydrate, fat and protein. As a cofactor for methylmalonyl-CoA mutase enzymes, vitamin B 12 helps convert odd chain fatty acids and branched chain amino acids into succinyl-CoA, a common citric acid cycle intermediate. Vitamin B 12 is also required for nucleic acid (DNA) synthesis, methionine synthesis from cysteine, and normal myelin synthesis in the nervous system. Along with vitamin B 6 and folic acid, adequate levels of vitamin B 12 are required to maintain normal plasma homocysteine levels. Elevated plasma homocysteine may be an independent risk factor for developing cardiovascular disease. There are two distinct mechanisms for intestinal vitamin B 12 absorption; receptor-mediated absorption and passive diffusion. In the first, vitamin B 12 attaches to a salivary “R-binder” protein which transports it into the small intestine, where vitamin B 12 is released. The vitamin then binds to “Intrinsic Factor” (IF), a glycoprotein normally produced by the gastric parietal cells. This vitamin B 12 -IF complex is carried down to the ileum, where it binds to mucosal receptors. Finally, the complex is absorbed and bound to serum vitamin B 12 -binding proteins. The second absorption mechanism, passive diffusion, does not require any carriers, such as B-binder or IF. Only about 1% of free vitamin B 12 is passively absorbed, but this can be nutritionally significant with higher dietary vitamin B 12 intakes. Almost 40% of the population is suggested to have “low normal” plasma B 12 levels. Strict vegetarians, the elderly, and, HIV/AIDS patients are often at risk for vitamin B 12 deficiency, either due to low dietary intake or impaired absorption. In the elderly, hypo- or achlorhydria maintains the binding of the vitamin with dietary proteins, leading to malabsorption. Vitamin B 12 deficiency can lead to CNS impairment, including cognition.