Iron deficiency reduces the efficacy of tryptophan as a niacin precursor.

A niacin-deficient purified amino acid diet that contained adequate (40 mg/kg) or deficient (10 or 15 mg/kg) iron was used to assess the growth promoting efficacy of tryptophan as a niacin precursor. Basal diets contained 1400 mg/kg tryptophan, a level that was established as meeting the requirement for tryptophan per se in diets containing excess nicotinic acid. Chicks fed the iron-deficient diets had markedly lower hemoglobin concentrations than those fed the iron-adequate diets. Regardless of iron level, chicks exhibited linear growth responses to either nicotinic acid or tryptophan supplementation. Using multiple-linear regression of weight gain on supplemental tryptophan or nicotinic acid intake, the efficiency (wt:wt) of tryptophan conversion to niacin activity (i.e., tryptophan slope divided by nicotinic acid slope) was a mean of 1.77% (56:1) for chicks fed the iron-deficient diet. This was significantly (P < 0.05) lower than the 2.39% (42:1) efficiency calculated for chicks fed the iron-adequate diet. Thus, iron deficiency reduced tryptophan utilization (for NAD synthesis) but had no effect on nicotinic acid utilization. The results suggest that pellagra in populations having endemic anemia and protein-energy malnutrition may be due not only to inadequate intakes of bioavailable niacin but also to inadequate intakes of bioavailable iron.