Early Programming of Later Health and Disease: Factors Acting During Prenatal Life Might Have Lifelong Consequences

A slow rate of intrauterine or prenatal growth isknown to be a major risk factor for severalnoncommunicable diseases, including coronaryheart disease and type 2 diabetes (1–7). A small body size at birth, markers of which include a low birth weight, thinness, and shortness at birth, is commonly recognized as a manifestation of slow prenatal growth. However, it is not the small body size per se that is the underlying problem, but what it stands for. Programming describes the process when events during critical periods of development may change structure and function of the organism (8). Fetal malnutrition can influence prenatal growth and consequently program later health. Also, other factors, e.g., stress, can influence prenatal growth. Causes of severe prenatal stress include natural and human disas-ters, such as famines, earthquakes, and terrorist attacks. Studies on the effects on birth outcomes in term deliveries after the World Trade Center attacks in 2001 showed that birth weight in the offspring was significantly lower for those who lived close to the event site (9). Interestingly, fetal programming can also occur without any marked effect on birth size. This has been shown in the Dutch Hunger Winter study, findings from which suggested that malnutrition—and stress—during prenatal life have a long-term effect by increasing the risk of coronary heart disease and type 2 diabetes in later life. These effects also depend upon timing of the exposure (10). In this issue of Diabetes, Li et al. (11) report on the long-term health consequences of exposure to the Chinese famine in early life, with a focus on risk for impaired glucose regulation. The study offers a unique opportunity to study the early programming of health and disease as a consequence of a natural disaster, the Chinese famine