Fetal Growth Restriction and Long-Term Cardiovascular Risk

Abstract

> What’s done is done. > > —Lady Macbeth to Macbeth (Act 3, Scene 2) The theory of fetal programming, known alternatively as the developmental origins of health and disease hypothesis, the fetal origins of adult disease concept, or simply the thrifty phenotype, posits that the maternal uterine environment to which a fetus is exposed can have substantial and long-lasting effects on the health of the individual, throughout childhood and beyond. Indeed, alterations in the maternal milieu comprising the early fetal environment have been implicated in the development of a wide variety of postnatal disturbances, ranging from neuropsychiatric and neurodevelopmental disorders1,2 to the metabolic syndrome and diabetes mellitus3,4, to endocrinologic dysfunction5,6, and to lung cancer.7 See Article by Sarvari et al First reported by Barker et al,8,9 this thrifty phenotype states that a hostile maternal environment engenders a process of fetal change that is adaptive during the initial time of fetal stress but leads to a permanent programming that later proves maladaptive over the long term. Barker’s original assertion,8–10 based on the observations of low birth weight babies in England and Wales in the 1920s and 1930s, focused on the adverse cardiovascular outcomes experienced by these small fetuses, including long-term increased risk of coronary heart disease, type 2 diabetes mellitus, stroke, and hypertension. To this day, however, specific mechanisms linking fetal growth restriction (FGR) with these poor long-term cardiovascular outcomes remain speculative, with a variety of …