The intrauterine environment plays a critical role in childhood growth. Infants exposed to acute malnutrition in early pregnancy are more likely to be obese in later life. Similarly, children exposed to hyperglycemia in utero are also more likely to develop insulin intolerance and obesity during childhood. The mechanisms underlying these changes are not understood. However, animal experiments suggest that severe overnutrition or undernutrition during pregnancy may affect hypothalamic development, or pancreatic beta-cell development. The effects of cigarette smoking on childhood growth can best be explained by the increased risk of intrauterine growth retardation. In contrast, alcohol ingestion during pregnancy leads to a syndromic decrease in childhood head circumference, stature, and weight. The effects of cocaine are most likely multifactorial, since cocaine ingestion tends to covary with tobacco use, alcohol use, opiate use, and low socioeconomic status. The most striking effects of the intrauterine environment on childhood growth are seen in children with intrauterine growth retardation. These children remain significantly lighter and shorter than their peers. Efforts to reverse intrauterine growth retardation have been disappointing, and at times risky. However, caloric supplementation in undernourished populations may be of significant benefit. The use of growth hormone promises to reduce some of the height deficits in children with intrauterine growth retardation. However, to date there is no evidence suggesting changes in final height in children with intrauterine growth retardation who receive growth hormone.