Tryptophan-Niacin Relationships in Man Studies with Diets Deficient in Riboflavin and Niacin, Together with Observations on the Excretion of Nitrogen and Niacin Metabolites

Abstract
Controlled feeding of a diet which provided only 5.8 mg of niacin and 265 mg of tryptophan per 2300 calories to 15 subjects for from 38 to 87 weeks produced no clinical evidence of pellagra. Data from studies of niacin metabolites excreted in the urine of these subjects were compared with results obtained at the same time from 15 other subjects who received the experimental diet plus controlled amounts of tryptophan, niacin and lactalbumin. Another group of 9 subjects who ate the regular hospital diet, were observed simultaneously. Comparisons of the levels of N1-methylnicotinamide excreted at different levels of niacin and tryptophan intake showed that approximately 60 mg of tryptophan are equivalent to 1 mg of niacin. It is suggested that one “niacin equivalent” be considered as equal to either of these amounts. To simplify discussions of food values, the term “niacin ratio” is suggested as the number of niacin equivalents per 1000 calories. The niacin ratio of representative foods and of some experimental diets which have promoted pellagra are presented and compared to show the predictability of pellagragenic diets. From a comparison of the data obtained in this study with previously published information from other sources, it is estimated that the base line level for the development of pellagra is 8.8 niacin equivalents for the first 2000 calories, or part thereof, plus an additional 0.44 equivalents for each 100 calories above 2000. Tryptophan in lactalbumin appears to be as readily available for conversion to niacin derivatives as is L-tryptophan, itself. The nitrogen excretion data reported emphasize the length of time which it may take to achieve a steady state of urinary nitrogen excretion (24 weeks) after a major change has been made in the protein intake. This observation is consistent with experience on all previous Elgin projects. Data on urinary excretions of quinolinic acid could be only roughly related to the amounts of niacin and tryptophan in the diet; the results were not so consistent or as reliable as similar data obtained on N1-methylnicotinamide excretion. Urinary excretions of niacin and tryptophan were not directly related to the usual levels at which these were present in the diet. Data pertaining to the possibility that lysine or methionine added as supplements may inhibit the formation of niacin metabolites are presented and discussed. While attempting to correlate the effects of riboflavin deficiency on “pellagragenic” diets the following observations were made; (1) That a diet low in niacin and tryptophan did not cause any noticeable alterations in the previously reported course of ariboflavinosis; (2) that supplementation with vitamin B12 produced no changes in either the development or repair of ariboflavinosis and (3) confirmed a previous report that scrotal dermatitis was a consistent observation in ariboflavinosis in man. The withdrawal of folic acid, calcium pantothenate, pyridoxine, and vitamin B12 as supplements to the basal diet of 5 subjects for a period of 25 weeks had no noticeable effect on the subjects involved. One may assume that either the basal diet was not grossly deficient in these vitamins or that the previous 62 weeks of supplementation had created a large reserve. The level of excretion of N1-methylnicotinamide has been confirmed as an indicator of the ability of the organism to extract niacin derivatives from the diet and in this manner may prove to be a useful index of niacin-tryptophan availability.