Deficiency of niacin is characterized by severe metabolic disorders in the skin and digestive organs. The first signs to appear are loss of appetite, retarded growth, weakness, digestive disorders and diarrhea. Burroughs et al. (1950) observed these signs of niacin deficiency in rations that were calculated to contain less than 15 mg of niacin per g of diet. However, the weanling pigs supplied with the same rations plus an additional 60 mg of niacin daily grew and developed normally. Cartwright et al. (1948) reported that pigs fed a low-protein diet without niacin developed a moderately severe, normocytic anemia that could be relieved by supplementation of niacin or protein. When fed this same low-protein diet but with supplemental niacin, the pigs did not develop significant anemia. Niacin deficiency is found in both human and animal populations that are overly dependent on foods (particularly corn) low in available niacin and its precursor tryptophan.
Niacin is one of the B vitamins that would be expected to be deficient for typical swine diets, particularly when corn, which is low in available niacin and tryptophan, is fed. Wide variation has been observed in the severity of clinical signs of niacin deficiency in pigs with similar breeding and environmental backgrounds. Occasionally, animals appear to thrive with no niacin, and other animals appear to vary in their requirement (Cunha, 1977). During gestation and lactation, it was not possible to produce niacin deficiency with sows fed a purified diet with either 18% or 26.1% casein (Ensminger et al., 1951). Evidently the diet contained enough tryptophan to supply niacin needs, or the duration of the experiment was not sufficient for the animals to develop a niacin deficiency.
Signs of niacin deficiency include poor appetite, decreased growth rate (Illus. 1), stomatitis, normocytic anemia and achlorhydria, followed by diarrhea, occasional vomiting and an exfoliate type of dermatitis and hair loss (Cunha, 1977). Nervous system degenerative changes are reported to occur in the ganglion cells in the posterior root with extensive chromatolysis in the dorsal root (Wintrobe et al., 1945). Powick et al. (1947b) and Braude et al. (1946) observed deficiency symptoms that were similar but not identical to those reported by Cunha (1977).
