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Perinatal sex hormones and risk of breast and prostate cancers in adulthood.

Fetal origins of adult disease, such as cardiovascular diseases and diabetes, have been suggested by ecologic and individual-level studies (1). Fetal and placental growth is influenced by maternal nutrition, function of the placenta, and the hormonal, metabolic, or circulatory environment of the maternal-placental-fetal unit (2). Various biologic mechanisms—for example, effects on cell numbers, alteration of gene expression, selective survival or "natural selection" of particular clones of cells, effects on structure and function of organs, and upor down-regulation of hormone receptors— have been proposed to explain the putative long-term effects of perinatal conditions on selected organs (2). The link between perinatal variables and the risk of adult chronic diseases, if it existed, would have profound public health implications (1). In the area of cancer research, there has been increasing interest among epidemiologists as well as experimental scientists in the potential effects of the intrauterine environment on the risk of breast and prostate cancers. Mammary and prostate glands undergo the early phases of organ development, growth, and cell differentiation during the fetal period (3, 4), when the process of carcinogenesis in these organs may first begin (5). Many of the epidemiologists who have reported the associations between preand perinatal characteristics and subsequent risk of breast and prostate cancers have hypothesized that exposure to high concentrations of sex hormones during the fetal period might explain the associations (6-10). Both the breast and prostate depend on sex hormones for their growth and physiologic functioning. Thus, sex hormones may be a reasonable candidate for a mediating factor in the reported associations. However, it would be a formidable task to unequivocally demonstrate in humans that preand perinatal conditions influence the risk of developing breast or prostate cancer several decades later, let alone the biologic mechanisms of such effects. Major difficulty arises from the long putative induction period spanReceived for publication August 25, 1999, and accepted for publication May 26, 2000.