Less than a hundred years ago, thousands of Americans were dying from pellagra, induced by long-term vitamin B3 deficiency, and no one even knew the cause. Only toward the mid 20th century it was established that the missing link was a diet based on foods low in vitamin B3 and tryptophan, usually corn or sorghum-based (it is still killing people in some underdeveloped areas of the world as we speak).

The B3/tryptophan connection stems from body's ability to make the vitamin out of this essential amino acid; however, at the conversion rate of about 1-to-60, relatively large doses of tryptophan are needed if it is to be a major B3 source for the body, hence this route is not efficient with tryptophan-deficient diets.

The two main forms of vitamin B3 are niacin (also nicotinic acid, or nicotinate) and its primary metabolite, niacinamide (nicotinic acid amide, or nicotinamide, formerly vitamin B4). While it is water-soluble vitamin, some forms can get stored by the liver to some extent, which makes prolonged high-intake supplementation potentially toxic to this organ.

Among important functions of vitamin B3 are:

ü as a precursor key cellular coenzymes (NAD, nicotinamide adenine dinucleotide, and its reduced form NADH, as well as nicotinamide adenine dinucleotide phosphate, or NADP, and its reduced form, NADPH), it is a vital part of the cellular energy production; it is also involved in the related blood sugar regulation

ü assists in the production of steroid hormones

ü stimulates production of gastric juices and hydrochloric acid

In very high, therapeutic doses, niacin can inhibit breakdown of fats in adipose tissue sufficiently to significantly lower production of VLDL (very low-density lipoproteins) and ("bad" LDL) cholesterol by the liver. It also lowers triglycerides and, probably, lipoprotein(a), while rising "good" HDL cholesterol. In fact, niacin is the most effective pharmacological agent for fighting dyslipidemia.

These effects, however, are by-product of the niacin-to-niacinamide conversion, thus not born out by the latter. Another form of vitamin B3, inositol hexaniacinate (comprising six molecules of niacin and one of inositol), is as effective as niacin in correcting dyslipidemia, but without significant side-effects7. It clinical use in the U.S. is, unfortunately, infrequent and its effectiveness questioned, due to relatively small amount of research data (it is not patentable, so no large studies have been financed).

Niacin is more stable than either thiamin (B1) or riboflavin (B2), thus its losses during food processing, storage and preparation are lower.

Prolonged B3 deficiency may cause a number of symptoms, from indigestion, halitosis and canker sores to insomnia and depression. Severe vitamin B3 deficiency brings on pellagra which, if untreated, usually kills in 4-5 years. For this to occur, diet needs to be low in both, niacin and proteins, since the body, as mentioned, can make niacin from amino acid tryptophan.

Large doses of niacin (~100mg and more at once, or 35mg or more daily), can cause release of histamine which, among other effects, can cause skin flushing sensation. Niacinamide does not produce this side-effect, but is more likely be toxic to the liver in high doses.

Niacin DRI (Dietary Reference Intakes, the most recent set of dietary recommendations set by the government) for an average healthy adult female is 14mg a day, and 16mg for a male.

Best natural food sources of vitamin B3 are liver, whole grains, potatoes and brewer's yeast. R

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