Niacin is a generic term for nicotinic acid and nicotinamide, both of which are substrates for the synthesis of nicotinamide nucleotide coenzymes, NAD and the phosphorylated derivative of NADP (Powers, 1999). The major metabolic role of NAD(P) is as a coenzyme in oxidation and reduction reactions. Niacin is therefore of crucial importance in intermediary metabolism and requirement is related to energy expenditure (Department of Health, 1991). Deficiency of niacin results in pellagra, which is fatal if untreated.

Quantitation of dietary niacin must take into account the dual source of the vitamin, the vitamin nicotinic acid and the amino acid tryptophan. Niacin in food is quantified as niacin equivalents (NE). Dietary sources are listed in Table 3.2 but meat is a rich source of both tryptophan and niacin.

High intake of tryptophan results in greater efficiency of conversion to niacin.

Oestrogens reduce the rate of tryptophan metabolism, so where pellagra is common, twice as many women as men are affected. However, before puberty and after menopause there are no sex differences. It is generally believed that 1 NE is equivalent to 60 mg of tryptophan or 1 mg dietary niacin.

The mean observed requirement for niacin to prevent or cure pellagra, or to normalise the urinary excretion of N-methyl nicotinamide (NMN) and its onward metabolite methyl pyridone carboxamide (MPCX), in experimental subjects maintained on niacin-deficient diets and in energy balance, is 5.5mg/4.2MJ (1000kcal). A coefficient of variation of 10% gives an RNI of 6.6mg/4.2MJ (i.e. plus 2SD) and an LNRI of 4.4mg/4.2MJ. A summary of niacin requirements is given in Table 3.1.

Niacin deficiency causes pellagra and occurs in parts of India and the African continent. Pellagra is frequently associated with the 'hungry season', strong sunshine and with diets of mainly maize and millet. The clinical features of pellagra are dermatitis, diarrhoea and dementia. Pellagra is occasionally found in malnourished alcoholic patients and it has been found associated with the intake of mycotoxins from the mould Fusarium. Pellagra occurs in Hartnup's disease, an autosomal recessive disorder with impaired absorption of several amino acids including tryptophan (Thurnham, 2000).

Classic pellagra responds dramatically to nicotinamide or niacin given at a dose of 100-300mg/day in three doses. In addition to niacin, it is usual to give riboflavin and pyridoxine and a diet high in calories and protein. Mental changes disappear within 24-48hours but dermal lesions may take 3-4weeks. A dose of 40-200mg niacin/day can be used to treat the symptoms of Hartnup's disease. Doses of 1-2g/day of niacin are used to manage patients with hypertriglyceri-daemia and/or hypercholesterolaemia. However, nicotinic acid, but not nicoti-namide, in excess of 200 mg causes vasodilation of cutaneous blood vessels. Higher doses cause vasodilation of other blood vessels and a transient drop in blood pressure (Thurnham, 2000).

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