TABLE 9-5 Composition of Nonhuman-Primate Milk, Human Milk, and Human-Infant Formula

Constituent

Rhesusa

Infant Formulab

Human Milk

Baboonc

Lipids, %

4.6-5.4

3.6

4.6

4.6-5.8

Protein, %

2.3-2.5

1.5

1.3

1.5-1.7

Carbohydrate, %

7.8-8.1

7.2

7.1

7.4-7.7

GE, kcal·L-1

820-910

670

670

770-900

Calcium, mg·L-1

364-420

420

270

 

Magnesium, mg·L-1

31-33

45

34

 

Iron, mg·L-1

1.1-1.2

1.5, 12d

0.2-0.6

 

Zinc, mg·L-1

1.8-2.4

5.4

0.5-3.0

 

Copper, mg·L-1

0.5-1.2

0.5

0.2-0.4

 

Sodium, mg·L-1

82-96

150

184

 

Potassium, mg·L-1

242-276

560

470

 

aMature milk (Lönnerdal et al., 1984).

bSMA® (Wyeth-Ayerst).

cBuss (1968b).

dUnfortified/iron-fortified formula.

tions in caloric and nutrient intake. Thus, if self-fed, a nutritionally dilute formula might be consumed during some hours, and a thick, nutrient-dense diet at others. Other reports indicate that the vitamin D content of some human infant formulas may be too low to support normal bone growth in some nonhuman primates; the use of vitamin D supplement drops would be required. A variety of options for preparation of milk replacers that match the milk composition of many mammal species has been developed by commercial manufacturers.

Long-Term Consequences of Different Modes of Infant Feeding

Development of feeding regimens that produced satisfactory growth in artificially reared infant nonhuman primates led to studies of the long-term physiologic and metabolic consequences of early nutrition. Examples of long-term, carefully controlled studies include those focusing on effects of dietary taurine on development of visual and brain function (Hayes et al., 1980; Stephan et al., 1981; Sturman et al., 1984, 1988), the relationship of cholesterol intake and plasma lipoproteins, bile acid metabolism, and atherosclerosis (see Chapter 5), and the effect of marginal zinc deficiency on growth, immune function, and behavior (Hendrickx, 1984; Strobel and Sandstead, 1984; Golub et al., 1984, 1985, 1991; Haynes et al., 1985; Keen et al., 1989: Lonnerdal et al., 1990a, b; Liu et al., 1992; Polberger et al., 1996). Not only has important information regarding the specific nutrients being studied been obtained, but the studies provide important lessons for long-term management of nonhuman-primate research facilities and for conduct of primate research.

It is important to recognize that the composition of commercial infant formulas is only as good as our current knowledge of human infant nutrition. For example, taurine was not added to infant formulas until the 1980s, although it is a major free amino acid in human milk and has specific metabolic roles. In fact, nonhuman-primate studies were instrumental in gaining approval for taurine supplementation of human-infant formulas in the 1990s.

Another important consideration, despite the fact that formula rearing can lead to growth patterns similar to those of mother-reared infants, is that mode of feeding (natural vs formula) can lead to long-term differences in metabolism of nutrients and in health and development (Lucas, 1990). That is illustrated by a series of experiments performed on breast-fed and formula-fed baboons (Mott et al., 1982, 1985, 1990, 1993 a, b; Jackson et al., 1993; Lewis et al., 1988, 1993). Although many metabolic indices were similar in the two groups during infancy, plasma lipoprotein patterns, cholesterol levels and forms, arterial plaque formation, and bile acid conjugation were considerably different in both juvenile and adult baboons. This metabolic “imprinting” suggests that infant nonhuman primates that have been artificially reared might respond to some study conditions quite differently from animals that have been breast-fed.

Furthermore, even though growth and development of infant nonhuman primates fed diets marginally deficient in single nutrients appear to be normal, subtle, less apparent impairments can have long-term consequences. For example, the marginally zinc-deficient pregnant rhesus monkey can deliver an infant that is apparently normal but has defects in immune function and in behavior that are not overcome by consumption of a zinc-sufficient diet (Golub et al., 1984; Haynes et al., 1985). The association of such signs with a prenatal or early postnatal nutritional insult is particularly difficult to diagnose because marginal zinc deficiency usually does not affect plasma zinc concentration or other potential indicators of zinc status.



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