have an efficiency of 65% (Samonds and Hegsted, 1973) measured by weight gain. In a second study, lactalbuminfed monkeys showed efficiencies of 43% measured by weight gain or 47% measured by nitrogen balance (Ausman et al., 1986). Finally, when infant squirrel monkeys were fed lactalbumin or casein, their efficiencies of protein use were 28.8 and 37.4%, respectively; this suggests that the animals were extremely inefficient users of the protein provided (Ausman et al., 1979). In all species, efficiency drops as protein quality is decreased.

PROTEIN DEFICIENCY

Beginning in the 1960s, several laboratories worldwide were engaged in studies of protein and calorie malnutrition, using the monkey as a model in which to produce the human diseases of kwashiorkor and marasmus (Oftedal, 1991). Protein deficiency and its sequelae are easily produced in several primate models. The studies have been reviewed by Knapka et al. (1995). Biochemical and clinical signs of protein deficiency include decreased total serum protein and albumin concentrations, decreased plasma amino acid concentrations, decreased serum transferrin concentrations, alopecia, anemia, edema, altered hormone and enzyme concentrations, abnormal neural cytochemistry, and pathologic alterations in several organs.

In some of the studies, the investigators studied pure protein deficiency, pure caloric deficiency, or a combination of the two. Samonds and Hegsted (1978) found that a 33% caloric restriction in the face of an otherwise adequate diet with added proteins, minerals, and vitamins produced a small but otherwise apparently “healthy” monkey. When the caloric restriction was combined with a protein-deficient diet, the resulting animals appeared no worse than either group alone; that suggests that in the face of an energy deficit protein was not “burned” for calories, as implied by several short-term studies in humans (Calloway, 1981; Garza et al., 1976; Calloway and Margen, 1971). The same experimental paradigm was repeated in infant squirrel monkeys fed protein-deficient, calorie-deficient, and protein and calorie-deficient diets (Gallina et al., 1987; Ausman et al., 1989). Again, the double-deficient animals appeared no worse than the others. The observations made on these squirrel and cebus monkeys appeared to be restricted to serum biochemical measurements, food intake, body weight, and appearance. The authors could make no judgments about body composition; rates of protein synthesis, turnover, or degradation; or any other index of protein and calorie metabolism. See Chapter 9 for further discussion of caloric restriction and health.

Alopecia and weight loss in a colony of western lowland gorillas over a 3-year period was ascribed to a dietary protein deficiency, based on findings of hypoalbuminemia, low serum amino acid and protein concentrations, and the positive response to dietary protein supplementation (Mundy et al., 1998).

PROTEIN FOR PREGNANCY AND LACTATION

Protein requirements for pregnancy and lactation have not been systematically studied. The protein requirement for infant monkeys is presumed to be the amount provided in the mother’s milk. The protein concentration in mature nonhuman-primate milk is 7-22% of GE (Oftedal, 1984, 1991). Studies of infant squirrel monkeys show that mean protein requirements for maximal growth approximate 18% of ME calories (Ausman et al., 1985b), which is similar to what is found in squirrel monkey milk (Buss and Cooper, 1972).

It is clear that protein deficiency in the pregnant nonhuman primate can have untoward effects on the offspring. When pregnant rhesus monkeys were fed diets containing 3.4% ME calories as protein, neonatal mortality was 40-50% (Riopelle et al., 1975a, 1976; Kohrs, 1976). If the diet provided protein at 0.4-0.5 g·BWkg-1·day-1, infants had reduced birth weights (Kohrs 1976; Novy, 1981) and decreased head circumferences for several months after birth (Kohrs et al., 1980). Maternal protein intakes of at least 1 g·BWkg-1·day-1 were associated with normal prenatal linear growth; normal birth weight; normal skeletal maturity and measurements; and normal post-natal food intake (Riopelle et al., 1975b, 1976; Cheek et al., 1976; Riopelle and Favret, 1977).

PROTEIN-CALORIE MALNUTRITION IN YOUNG PRIMATES

Nutritional requirements per unit body weight are highest for the young of any species, and growing children or growing animals exhibit the most serious clinical and biochemical evidence of malnutrition when fed diets deficient in essential nutrients. Studies of malnutrition conducted with young rats and pigs have not proved relevant to the pathogenesis of the malnourished human child, primarily because the animals grow more rapidly and have shorter periods between weaning and puberty (Coward and Whitehead, 1972). A closer relationship between higher primates and humans in growth patterns suggests that nonhuman primates would be more realistic experimental models.

Nonhuman-primate models of protein-calorie malnutrition (PCM) could provide a means to study biochemical and physiologic responses to a primary deficiency of either protein or energy and could replicate the related clinical



The National Academies | 500 Fifth St. N.W. | Washington, D.C. 20001
Copyright © National Academy of Sciences. All rights reserved.
Terms of Use and Privacy Statement