There are a number of substances that fall into the grey area between essential and nonessential dietary compounds. Vitamin D is a classic example of this, as in reality vitamin D is a steroid hormone synthesised in the skin through the action of ultraviolet light on cholesterol. Another vitamin that can be synthesised in humans is niacin, also sometimes designated vitamin B3. Niacin is actually a generic name for the two compounds niacinamide and nicotinic acid, both of which share similar biochemical activity. The main physiological roles of niacin include incorporation into the structures of the important cellular coenzymes nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADPH). The NAD coenzyme is pivotal in cellular energy production and the NADPH coenzyme is pivotal in synthesis reactions. Inadequate intakes of dietary niacin have been shown to result in the deficiency disease pellagra, which is fatal if not reversed through supply of adequate niacin.
However, niacin can be synthesised in the body from the amino acid L-tryptophan. Pellagra then is actually a multi-nutritional disease because as well as requiring a deficient intake of dietary niacin to develop, low intakes of L-tryptophan must also be present. In addition, as pyridoxine (vitamin B6) is required for the conversion of L-tryptophan to niacin, low intakes of this vitamin can also be a factor. Some suggestions have also been made that high intakes of L-leucine may exacerbate the problems caused by low intakes of niacin, because high intakes of dietary L-leucine may decrease the conversion of L-tryptophan to niacin. Thus pellagra is in reality a multi-nutritional disease with a number of dietary factors all contributing to the development of the metabolic changes that result in deficiency symptoms. The interactive effects of L-leucine, L-tryptophan and pyridoxine on niacin metabolism have been investigated in man in order to identify the role they play in the formation of niacin.
In one study1, researchers performed a number of metabolic studies that lasted for 35 days each. In the studies healthy men consumed a basal diet containing 8 mg of niacin, 1 mg of pyridoxine and either 245, 548, or 845 of L-tryptophan each day. For the first 15 days of the 35 day study period the basal diet was followed with no changes. In the next 15 days, 10 grams of L-leucine was ingested in addition to the basal diet, and in the last 15 days 20 mg of pyridoxine was ingested in addition to the basal diet. There was no significant changes to the urinary excretion of the niacin metabolites N1-methyl nicotinamide, N1-methyl-2-pyridone 5-carboxamide or quinolinic acid during the study. However, the proportion of L-tryptophan converted to niacin increased with higher intakes of L-tryptophan. From this the authors concluded that the ratio of L-tryptophan to niacin conversion was around 72 to 1 in healthy subjects. Vitamin B6 and L-leucine therefore may only affect niacin metabolism in severely malnourished subjects.
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