Developmental Origins of Health and Disease
In 1989, David Barker, M.D., Ph.D., F.R.S., reported the relationship between birth weight and death rates from coronary heart disease in both men and women in Hertfordshire, UK. He showed that among adults who had been born in the birth weight range of 5 to 9 pounds, more men and women died of heart disease when they were born on the lighter end of that range than on the heavier end. He also showed that being born above 9.5 pounds carried a particularly high risk for heart disease. These data initiated a new field of medicine, known as the Developmental Origins of Health and Disease (DOHAD). Research in this field has since demonstrated that stresses experienced in the womb – virtually all of which have roots in the social and physical environment — alter the structures of organs in the fetus, thus changing the expression of regulatory genes throughout the lifetime. Together, these two processes lead to vulnerability for disease in later life.
Developmental origins are now understood to underlie most, if not all, chronic disease. Among the fetal stressors that are known to increase a person’s disease risk in adult life are under- or over-nutrition from the time of that person’s conception, and even — interestingly — prior; high levels of stress hormone in the mother; and low oxygen in the womb. Such factors and others, including maternal exposure to the kinds of social stresses associated with poor housing and unemployment, are now known to play a role not only in adult cardiovascular disease, but also diabetes, and even osteoporosis. In other words, the environmental conditions affecting our mothers while pregnant with us very much predict our disease experience as adults. And the effects are intergenerational, still measurable two generations later.
It is the metaphorical “perfect storm” of disease predisposition: high calorie malnutrition, great reductions in physical activity, and a trans-generational effect of environmental exposures, all contribute to a high vulnerability for diseases among large segments of the population.
Importantly, these risks are in large part socially determined, meaning that we can organize our communities in ways that prevent population exposures that would otherwise create health problems for our offspring — and their offspring, as well. Moreover, the implications for health care economics are enormous. There are clear results from this research that suggest numerous opportunities for preventive factors, such as access to nutritious food options and a sense of stress or security resulting from the relative safety of one’s neighborhood. Indeed, Barker and colleagues have reported that two-thirds of adult-onset diabetes could be eliminated in a single generation by eliminating the developmental influences on the disease.
The possibility of such a public health triumph leads us to consider whether there are ways to alter the trajectory of these current chronic disease epidemics through purposeful, integrated alterations to our social environment. Unaltered, the current trajectory is frightening: the health of the next generation will be largely determined by the body compositions and diets of today’s girls and young women, both of which are influenced by any number of environmental and socio-structural factors. There is a desperate need for effective population-level strategies to improve the life circumstances of today’s “mothers in the making.” This means we need to focus not just on the biology of individuals but, importantly, the social, economic, and physical environments that substantially influence how biology plays out.