Abstract

This chapter presents the hypothesis that chronic diseases in adulthood have origins in the fetal and early postnatal period. The fetal programming hypothesis holds that, in response to undernutrition during critical periods of growth and development, the structure and function of organs and tissues are “programmed,” or permanently altered in ways that predispose individuals to chronic disease in later life, most notably diabetes and cardiovascular disease (CVD). The predisposition may take the form of increased susceptibility to chronic disease risk factors, such as atherogenic diets, excess energy intake, and reduced physical activity. Rates of fetal growth retardation remain relatively high in developing countries, while at the same time, rapid socioeconomic changes are accompanied by an increase in sedentary activity and a transition to higher energy density diets. Thus, today's older children and adults in developing countries are more likely than those in earlier decades to be small at birth, but subsequently exposed to more environmental and behavioral risk factors for chronic disease during their childhood and adult years. Evidence to support the fetal programming hypothesis was accumulated at a rapid rate over the past decade.

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