Niacin is a generic term used to describe nicotinic acid and nicotinamide (niacinamide), both of which can provide the activity of vitamin B3. Niacin is not a true vitamin as it can be synthesised in humans from the essential amino acid tryptophan. However there is a large variation in the rate of production between individuals. Low intakes of tryptophan necessitate inclusion of niacin into the diet. Because the conversion of tryptophan to niacin requires riboflavin and pyridoxal phosphate, deficiencies of vitamin B2 or vitamin B6 can cause a vitamin B3 deficiency. In many cereals, nicotinic acid is bound to other components forming non-absorbable compound called niacytin. In Mexico and Central America, corn is treated with lime in order to release the nicotinic acid. Deficiency of niacin produces pellagra, which is common in developing nations where the population subsists on cereal grains, particularly corn, which is low in tryptophan. Pellagra causes dermatitis, dementia and diarrhoea.
Niacin is needed in humans because it forms part of the coenzyme nicotinamide adenine dinucleotide (NAD+) and nicotinamide adenine dinucleotide phosphate (NADP+). These coenzymes function as electron carriers, and when attached to appropriate enzymes function as dehydrogenases by accepting hydrogen atoms to become reduced to NADH + H+ and NADPH + H+, respectively. Unlike FAD and FNM, NAD+ and NADPH+ are not bound to their enzymes and so can transport electrons. The NADPH+ coenzyme functions in synthesis pathways where it provides reducing power, and can also recycle oxidised glutathione (GSSG) back to reduced glutathione (GSH). Nicotinic acid at high dose has a pharmacological effect to dilate blood vessels in humans. This can result in a flushing effect on skin that is accompanied by itching and burning. However, this action is not shared by nicotinamide, which can be used in its place in dietary preparations. In high doses, nicotinamide can lower blood cholesterol levels but may negatively affect blood glucose levels.