Prenatal and Childhood Stressors Promote Chronic Disease in Later Life

Abstract

There is a pandemic of chronic disease that is widespread across the globe. Low birthweight, as a result of slow fetal growth, is associated with increased rates of chronic disease including coronary heart disease and related disorders, stroke, hypertension, obesity, and type 2 diabetes. These associations extend across the entire range of birthweight. People who were small at birth have elevated risks for later disease because they have reduced functional capacity in specific organs, altered settings of hormones and metabolism, or harmful responses to adverse influences in the postnatal environment. People born at the high end of the birthweight scale who put on weight rapidly during infancy and early childhood also have elevated risks for chronic disease. The most common chronic diseases are the consequences of developmental plasticity, the biological process by which one genotype can give rise to a range of different physiological or morphological phenotypes in response to environmental stressors during development. This is often referred to as programming.

Slow growth in infancy and rapid weight gain after the age of one year further increase the risk of later disease. Slow fetal growth is the product of the mother’s body composition and diet before and during pregnancy, together with her metabolism. The placenta is complicit in the growth of the fetus and hence in the programing of disease. The vulnerability for adult-onset chronic disease can be firmly entrenched during prenatal stages but can also arise independently during childhood when individuals remain plastic, providing the underpinnings for harm from adverse childhood experiences that progress to chronic conditions and mental disorders.