amounts for normal growth and development of primates. A report by Stegink and colleagues (1980) conclusively showed that D-methionine is poorly used by monkeys. That is in agreement with data from humans but in contrast with data from rats, chickens, pigs, and rabbits, in which D-methionine may be converted to L-methionine by an oxidase. Although no studies have used a pure amino acid mixture to titrate the exact lysine or methionine requirement, the addition of lysine to gluten or bread diets and of methionine to soy-isolate diets markedly improved protein potency (Table 4-2). In the case of methionine-supplemented soy protein, potency was not distinguishable from the reference. That addition of lysine alone to wheat protein did not make its potency equivalent to the reference suggests that a secondary and perhaps tertiary amino acid was limiting (Samonds and Hegsted, 1973; Ausman and Hegsted, 1980).


Human infants with phenylketonuria have a deficiency of the hepatic enzyme phenylalanine hydroxylase, which converts phenylalanine to tyrosine. Treatment for this condition is life-long restriction of dietary phenylalanine. Kerr et al. (1969a) fed a commercial formula low in phenylalanine to infant rhesus monkeys. Those maintained on the formula up to the age of 70 days developed lethargy, anemia, anorexia, diarrhea, hair depigmentation, dermatitis, and edema. Supplementation of the formula with phenylalanine ameliorated all the signs except dermatitis. The experiments suggest how difficult it might be to restrict phenylalanine in the diet of a phenylketonuric without producing evidence of protein deficiency.


Experimental studies with the vervet monkey (Cercopithecus aethiops) focused on the role of tryptophan and its neurotransmitter, 5-hydroxytryptamine, in aggression (Chamberlain et al., 1987). Monkeys were given amino acid mixtures that contained no tryptophan (T−), were nutritionally balanced (B), or had tryptophan in excess (T+). During competition for food, the T− solution increased aggression in male vervet monkeys whereas the T+ solution decreased aggression in both males and females. In a second study with these monkeys, Young et al. (1989) were able to show that the change in behavior (aggression) was inversely correlated with the amount of tryptophan and 5-hydroxyindoleacetic acid in the cerebrospinal fluid, adding further support to the idea that altered behavior in humans could be due to a decrease in 5-hydroxytryptamine. Of the common proteins fed, maize has the lowest ratio of tryptophan to total protein.


Taurine was first isolated in 1827 from ox bile (Hayes, 1985). Taurine ( γ-aminoethanesulfonic acid) is synthesized in liver and brain of all animals studied, but the synthetic system might be poorly developed in young or preterm infants of any species (Hayes, 1985), thereby necessitating an exogenous supply. Taurine is found in most cells, and it is suggested that it performs a wide variety of functions (Gaull, 1989). Initial observations centered on stabilization of the membranes of the central retinal tapetum (Hayes, 1985). It is also thought to play a role in the developing nervous system, conjugation of bile acids, brain osmoregulation, and platelet and muscle function. Infant monkeys fed soy-based human-infant formulas (lacking supplemental taurine) showed a depression in growth and an alteration in the ratio of glycine to taurine in conjugated bile acids (Hayes et al., 1980; Stephan et al., 1981). Indeed, in this latter study, infant cynomolgus monkeys showed no change in bile acid pool size during taurine depletion whereas bile acid pool size dropped from 89.0 to 73.0 μmol·BWkg−1 in the infant capuchin monkey under the same conditions. It is noteworthy that cynomolgus monkeys normally conjugated 84% of their bile acids with taurine, and taurine depletion decreased this value to 64%. In contrast, capuchin monkeys obligatorially conjugated 97% of their bile acids with taurine, independent of taurine status. Infant rhesus macaques fed a taurine-free diet exhibited a loss of visual acuity and retinal degeneration (Sturman et al., 1984; Neuringer and Sturman, 1987; Imaki et al., 1987). In a further study, Sturman et al. (1988) compared monkeys fed a liquid soy diet with those fed one supplemented with taurine at 70 μmol·dl−1, the amount in rhesus monkey milk. Taurine concentrations in 28 of 31 tissues measured were significantly increased (by 50-75%) over nonsupplemented concentrations. Further studies showed that by 12 months of age, infant rhesus monkeys were no longer dependent on an exogenous source of dietary taurine (Sturman et al., 1991; Neuringer et al., 1992). Collectively, those results suggest that it is important to provide an exogenous source of taurine for primates for the first year of life.


Given a high-quality “reference” protein, the efficiency of protein use in the growing rat is greater than 90%. That is to say, given 1 g of dietary protein, a growing rat will deposit more than 0.9 g in its carcass (Rand et al., 1981). Humans are not nearly as efficient; their efficiency of protein use is 50-70% (Rand et al., 1981). Cynomolgus monkeys (Macaca fascicularis) fed lactalbumin protein have an efficiency of 65% (Ausman et al., 1979). In one study, infant cebus monkeys fed lactalbumin were reported to

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