colitis, and often anemia (Barnard et al., 1988). Seventeen male and 22 female adult Saguinus mystax were offered a commercial canned (60.3% moisture) marmoset diet at 120 g·day-1. The diet contained 23.4% crude protein (CP, dry basis) and 4.74 kcal gross energy (GE) per g of dry matter (DM), and was supplemented 3 days per week (20 ml per supplemented day) with a preparation (78.7% moisture) containing 14.2% CP (dry basis) and GE at 4.11 kcal·DMg-1. Ingredients in the commercial diet included water, ground wheat, whole egg, soy grits, sucrose, brewer’s rice, dried skimmed milk, vegetable oil, dehydrated alfalfa meal, dicalcium phosphate, iodized salt, and brewer’s dried yeast. The supplement contained water, wheat germ, honey, grape juice, and Biozyme®. On those days when only the commercial canned product was offered, average consumption was 172 g·BWkg-1·day-1, providing 12.0 g of protein and 290 kcal GE·BWkg-1·day-1. When the supplement was available, consumption of the commercial diet decreased to 110 g·BWkg-1·day-1, providing 10.2 g of protein and 185 kcal GE·BWkg-1·day-1. The tamarins preferred the supplement and, when offered, consumed it prior to consumption of the canned diet. The tamarins lost weight and exhibited alopecia and chronic diarrhea.

During 3 months of feeding a pelleted diet (10.3% moisture), formulated to contain 26.2% protein (dry basis) and 4.78 kcal GE·DMg-1, mean food intake was 82 g·BWkg-1· day-1, providing protein at 19.3 g and GE at 335 kcal·BWkg-1 ·day-1, and the marmosets gained an average of 56 g. The pelleted diet contained rice gel, glucose, soybean meal, dried apple pomace, high fat milk solids, casein, beet pulp, soy oil, soy lecithin, and mineral and vitamin premixes. Evidence of WMS abated, and hematologic and serum-biochemistry profiles were no longer consistent with those of protein-calorie deficiency. The authors concluded that the tamarins appeared physically unable to consume sufficient amounts of the high-moisture canned diet and supplement to meet apparent protein and energy requirements for prevention of WMS. Because some of the pathophysiologic signs exhibited during consumption of the commercial diet and supplement resemble those of gluten intolerance, and these signs disappeared when the pelleted diet containing no gluten source was fed, it may be appropriate to consider the possibility of a multifactorial nutritional disease. The issue of callitrichid nutrition and food sensitivity has been explored further by Gore et al. (2001).


Although pathologic protein excess is more rare in monkeys than in other species, such as the rat, monkeys can develop pathologic changes in the kidney, which sometimes lead to terminal renal failure (Burek et al., 1988). It is common practice in all species, including humans, to limit protein intake to prolong the preterminal period in renal disease (Bourgoignie, 1992). It has not been shown in humans that a high-protein diet will compromise an otherwise healthy kidney.

Bourgoignie et al. (1994) monitored renal function in 14 baboons that had been subjected to right nephrectomy and 20-30% infarction in the left kidney and that had been fed either 8% or 25% protein diets. Hemodynamic and metabolic characteristics were measured every 4 months for 5 years. Modest proteinuria developed after the kidney infarction, and hypertension after the nephrectomy. There was no difference in these measures between the monkeys fed 8% and 25% protein diets and no progression of the proteinuria or hypertension during the 60 months. Inulin clearance and glomerular filtration rate were significantly greater in baboons fed the 25% than the 8% protein diet throughout the study. The results suggest that within the 5-year experimental period excess protein was not detrimental to kidney function in the absence of other disease.

In humans, it has been clearly shown that excess dietary protein increases urinary calcium loss (see Chapter 6) and thus calcium requirements. There are no data on calcium requirements of nonhuman primates relative to different dietary protein intakes. Therefore, the conservative approach is to keep dietary protein within reasonable bounds.


Soy protein can have biologic effects other than those that depend strictly on protein quality. Fitch et al. (1964) reported reduced iron absorption and later anemia in rhesus monkeys fed a diet of soy isolate. Ausman et al. (1977) also reported anemia when infant squirrel monkeys were fed a protein-limiting diet based on soy isolate but not when they were fed lactalbumin. It was unclear which aspect of the soy protein was responsible for the anemia, although phytic acid in soybean meal has been shown to chelate iron and reduce its availability. A slightly lower digestibility of soy-protein was observed when diets containing soy-protein concentrate, casein, or lactalbumin were fed to Callithrix jacchus and Saguinus fuscicollis (Flurer et al., 1985).

Protein sources are often carriers of potentially harmful or beneficial non-amino-acid components in the primate diet. Examples are saturated fat and cholesterol in red meat and fiber in grains. Raw soybeans have harmful concentrations of trypsin inhibitor, which, when incorporated into the diet, interfere with protein digestion in all species and are associated with pancreatic hypertrophy and cancer in rodents (McGuinness et al., 1980, 1982). Heat treatment of soybean meal or isolating soy protein decreases trypsin

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