Intrauterine growth retardation can result from a variety of environmental or genetic influences on fetal growth.1 The sequelae of intrauterine growth retardation resulting from impairment of nutrient flow from mother to fetus are well known and include low birth weight with sparing of brain growth, polycythemia, and hypoglycemia resulting from decreased storage fuels and defective gluconeogenesis. Despite the generally held assumption that nutritionally related intrauterine growth retardation (either maternal malnutrition or impaired uteroplacental blood flow) represents a serious pathologic insult to the fetus, the available data suggest that the vast majority of infants with intrauterine growth retardation have normal development without significant differences in IQ or neurologic scores from normal infants.2

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