Early Origins of Cardiometabolic Disease

This chapter discusses the developmental origins of health and disease (DOHaD) and their implications for public health. It summarizes the epidemiological evidence in humans linking low birth weight, infant and childhood growth, adult body mass index (BMI), and maternal weight and nutrition to cardiometabolic risk factors in later life. It describes what is meant by developmental programming and considers alternative explanations for the epidemiological associations. It then evaluates the effects of interventions in pregnancy, infancy, and childhood on later cardiovascular risk and concludes with the public health implications and potential economic benefits of early life interventions. Forsdahl (1977) discovered that Norwegian counties with the highest infant mortality in 1896–1925 experienced the highest death rates from coronary heart disease in the mid to late twentieth century. He suggested that poverty in childhood caused permanent damage, perhaps due to a nutritional deficit, that resulted in lifelong vulnerability to an affluent lifestyle and high fat intake. A decade later, Barker and Osmond (1986) found a similar phenomenon in the United Kingdom. Using archived birth records from the county of Hertfordshire, they found that lower birth weight and lower weight at age one year were associated with an increased risk of death from coronary heart disease and stroke in adulthood (Barker and others 1989; Osmond and others 1993). Mortality approximately doubled from the highest to the lowest extremes of birth weight or infant weight (figure 3.1). Barker and others (1989) concluded that processes linked to growth and active in prenatal or early postnatal life strongly influence the risk of adult coronary heart disease. The association between lower birth weight and increased risk of coronary heart disease has been replicated in many different populations (Andersen and others 2010; Forsen and others 1999; Huxley and others 2007; Leon and others 1998; Stein and others 1996) (figure 3.2). The association is linear and graded across the whole range of birth weight, with an upturn at extremely high birth weight (figure 3.1). The association is independent of adult socioeconomic status, making confounding an unlikely explanation (Leon and others 1998). Studies that include gestational age data indicate that restricted fetal growth, rather than preterm delivery, is associated with coronary heart disease (Leon and others 1998).