improvement was noted with oral administration of D-calcium pantothenate at 1-3 mg·BW_kg^-1·d^-1. Complete recovery was noted when supplements of both calcium pantothenate and liver powder were included in the diet, so a simultaneous deficiency of nutrients other than pantothenic acid is likely to have occurred. Greenberg (1970), citing unpublished studies, reported a dramatic response to 3 mg of calcium pantothenate per animal per day. Those are the only studies describing pantothenic acid deficiency in nonhuman primates.

Semipurified diets with calcium pantothenate at about 22-23 mg·kg^-1 DM(equivalent to pantothenic acid at 1920 mg·kg^-1 DM) have been fed to rhesus monkeys (Kark et al., 1974) and to squirrel monkeys (Rasmussen et al., 1979) without signs of deficiency. These latter studies do not provide the basis for estimating minimum pantothenic acid requirements, and the concentrations used exceed the minimum pantothenic acid requirements reported for other species in the National Research Council nutrient requirement series.

Niacin (also known as nicotinic acid) is a component of the coenzymes nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP), which play a part in metabolic oxidation-reduction and dehydrogenase reactions, serving as electron receptors or hydrogen donors (Jacob and Swenside, 1996; Cervantes-Laurean et al., 1999). Although niacin is widely distributed in natural foodstuffs, it is bound and largely unavailable in grains, such as wheat and corn (Jacob and Swenside, 1996). Niacin supplements are commonly added to diets as nicotinic acid or nicotinamide.

Estimating the niacin requirement is complicated by the ability of many mammals to synthesize niacin from a dietary excess of the amino acid tryptophan. That ability has been identified in some primate species (Tappan et al., 1952; Banerjee and Basak, 1957). Thus, to some extent the niacin requirement is related to the tryptophan supply in the diet. Deficiencies of a number of other nutrients—including vitamin B₆, riboflavin, iron, and copper—can inhibit the conversion of tryptophan to niacin (van Eys, 1991).

Niacin deficiency has been studied in rhesus monkeys (Macaca mulatta) by Tappan et al. (1952), Belavady et al. (1968), and Belavady and Rao (1973). The deficiency syndrome was characterized by weight loss, alopecia, anemia, skin hyperpigmentation, anorexia, chronic gastritis, and diarrhea. Declines in serum albumin and blood pyridine nucleotide concentrations and development of chronic atrophic gastritis and atrophic necrotizing enterocolitis were also observed.

Tappan et al. (1952) reported that deficiency signs in rhesus monkeys weighing 1.4-3.2 kg and fed purified diets containing 7% protein from casein were ameliorated by weekly administration of 10-35 mg of niacin (equivalent to about 0.7-1.8 mg·BW_kg^-1·d^-1)or 1-4g of D,L-tryptophan. A weekly dose of 5 mg of niacin was not adequate to reverse deficiency signs, and 30-35 mg of niacin per week was more effective than 10 mg. Intermediate dosages were not tested. Belavady et al. (1968) reported that niacin deficiency in rhesus monkeys was reversed by giving animals 25 mg of niacin per day in the first week and 10 mg per day for 3 more weeks; lower dosages were not tested. The animals weighed 6.0-11.0 kg. Belavaday and Rao (1973) induced niacin deficiency by supplementing the diet of rhesus monkeys with 1.5 g of leucine (a niacin antagonist) per day. That resulted in reduced synthesis of nicotinamide