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“Niacin” is a generic term for nicotinic acid and other derivatives with similar nutritional activity. Unlike most other vitamins, niacin can be synthesized from the amino acid tryptophan. Niacin is an essential component of the co-enzymes nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP), which are involved in many oxidation-reduction reactions. The major food sources of niacin are proteins containing tryptophan and numerous cereals, vegetables, and dairy products.

Historically, niacin deficiency occurred when corn, which is relatively deficient in both tryptophan and niacin, was the major source of calories. Currently, niacin deficiency is more commonly due to alcoholism and nutrient–drug interactions. Niacin deficiency can also occur in inborn errors of metabolism. Niacin in the form of nicotinic acid is used therapeutically for the treatment of hypercholesterolemia and hypertriglyceridemia. Daily doses of 3–6 g can result in significant reductions in levels of low-density lipoprotein (LDL) and very-low-density lipoproteins (VLDL) and in elevation of HDL. Clinical trials have shown, however, that when added to statins there is no benefit of niacin on cardiovascular events. Niacinamide (the form of niacin usually used to treat niacin deficiency) does not exhibit the lipid-lowering effects of nicotinic acid.


As with other B vitamins, early manifestations of niacin deficiency are nonspecific—anorexia, weakness, irritability, mouth soreness, glossitis, stomatitis, and weight loss. More advanced deficiency results in the classic triad of pellagra: dermatitis, diarrhea, and dementia. The dermatitis is symmetric, involving sun-exposed areas. Skin lesions are dark, dry, and scaling. The dementia begins with insomnia, irritability, and apathy and progresses to confusion, memory loss, hallucinations, and psychosis. The diarrhea can be severe and may result in malabsorption due to atrophy of the intestinal villi. Advanced pellagra can result in death.


In early deficiency, diagnosis requires a high index of suspicion and attempts to confirm niacin deficiency. Niacin can be measured in serum or plasma. The adult reference range is 0.50–8.45 mcg/mL. Low levels suggest niacin deficiency but may also be found in patients with generalized under-nutrition. In advanced cases, the diagnosis of pellagra can be made on clinical grounds.


Niacin deficiency can be effectively treated with oral niacin, usually given as nicotinamide (10–150 mg/day).

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