Numerous epidemiological studies report that birth weight is inversely associated with blood pressure, suggesting that slow growth during fetal life programs hypertension and increased risk for cardiovascular disease in later life. Different experimental models are used to provide proof of concept for the theory of developmental programming of cardiovascular disease, and studies in these different animal models are providing insight into the etiology of chronic disease programmed by an imbalance in nutrition during early life or exposure to maternal complications during pregnancy. Alterations in the regulatory systems key to the long-term control of blood pressure are implicated in the etiology of hypertension that results from adverse exposures during early development. Epigenetic processes are also implicated in the increased risk for programmed cardiovascular disease and the passage of programmed cardiovascular risk to the next generation. Sex, age, and early postnatal growth impact later programmed risk; programmed risk is also amplified in response to a secondary challenge that includes normal physiological processes such as pregnancy. Thus, this book will highlight how events during early life impact later cardiovascular health in a manner that is sex- and age-dependent and can be transmitted to the next generation.
