Infant iron deficiency anemia (IDA) occurs spontaneously in monkey populations as it does in humans, providing a model for understanding effects on brain and behavior. A set of 34 monkey infants identified as IDA (hemoglobin <11 g/dL) over a 5-year period at the California National Primate Research Center (CNPRC) was compared to a set of 57 controls (hemoglobin >12 g/dL) matched for age and caging location. The infants had participated in a Biobehavioral Assessment conducted at 3-4 months of age at CNPRC that included measures of behavioral and adrenocortical response to a novel environment. IDA males differed from control males in two factors ("activity", "emotionality") derived from observational data taken on the first and second day of the exposure to the novel environment. In the male infants, IDA was associated with less restriction of activity in the novel environment on both days and less emotionality on the second day (p<.05). IDA males also displayed less response to approach by a human (human intruder test) than did control males. IDA females did not differ from controls. Adrenocortical response was not significantly affected. These findings may be relevant to functional deficits in human infants with IDA that influence later behavior.
Human studies have shown that iron deficiency and iron deficiency anemia in infants are associated with behavioral impairment, but the periods of brain development most susceptible to iron deficiency have not been established. In the present study, rhesus monkeys were deprived of iron by dietary iron restriction during prenatal (n = 14, 10 μg Fe/g diet) or early postnatal (n = 12, 1.5 mg Fe/L formula) brain development and compared to controls (n = 12, 100 μg Fe/g diet, 12 mg Fe/L formula) in behavioral evaluations conducted during the first four months of life in the nonhuman primate nursery. Iron deficiency anemia was detected in the pregnant dams in the third trimester and compromised iron status was seen in the prenatally iron-deprived infants at birth, but no iron deficiency was seen in either the prenatally or postnatally iron-deprived infants during the period of behavioral evaluation. Neither prenatal nor postnatal iron deprivation led to significant delays in growth, or gross or fine motor development. Prenatally deprived infants demonstrated a 20% reduced spontaneous activity level, lower inhibitory response to novel environments, and more changes from one behavior to another in weekly observation sessions. Postnatally deprived infants demonstrated poorer performance of an object concept task, and greater emotionality relative to controls. This study indicates that different syndromes of behavioral effects are associated with prenatal and postnatal iron deprivation in rhesus monkey infants and that these effects can occur in the absence of concurrent iron deficiency as reflected in hematological measures.
These data indicate that an inadequate intake of iron from the diet during pregnancy in rhesus monkeys can lead to compromised hematologic status of the neonate without indications of growth retardation or impaired neurologic function at birth.
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