Niacin (nicotinic acid, nicotinamide) derivatives include nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP), which are coenzymes in oxidation-reduction reactions. They are vital in cell metabolism. Because dietary tryptophan can be metabolized to niacin, foods rich in tryptophan (eg, dairy products) can compensate for inadequate dietary niacin.
Dietary niacin deficiency (causing pellagra) is uncommon in developed countries. Clinical manifestations include the “three Ds”: localized pigmented rash (dermatitis); gastroenteritis (diarrhea); and widespread neurologic deficits, including cognitive decline (dementia). Diagnosis is usually clinical, and dietary supplementation (oral or, if needed, IM) is usually successful.
Primary deficiency results from extremely inadequate intake of both niacin and tryptophan, which usually occurs in areas where maize (Indian corn) constitutes a substantial part of the diet. Bound niacin, found in maize, is not assimilated in the GI tract unless it has been previously treated with alkali, as when tortillas are prepared. Corn protein is also deficient in tryptophan. The high incidence of pellagra in India among people who eat millet with a high leucine content has led to the hypothesis that amino acid imbalance may contribute to deficiency. Deficiencies of protein and many B vitamins commonly accompany primary niacin deficiency.