Abnormal perfusion to the fetus can slow fetal growth and result in intrauterine growth restriction (IUGR).1 IUGR, or failure to reach one’s birth potential, is one of the most common complications during pregnancy and generally results from placental insufficiency.1 IUGR is generally not recognized before delivery, and treatment options for IUGR are limited, with early delivery being the most common.1 Preeclampsia is often a contributory cause of IUGR, and numerous studies indicate that individuals exposed to a preeclamptic pregnancy exhibit a higher body mass index and blood pressure during childhood and adult life.2 Individuals born with IUGR also demonstrate an increase in blood pressure later in life.3 This association forms the basis for the developmental origins of health and disease and indicates that adverse influences during fetal life that slow fetal growth program an individual for greater cardiovascular risk in later life.4,5 Article see p 2202 Experimental models of placental insufficiency provide proof of principle that IUGR induced by reduced uterine perfusion programs an increase in blood pressure and cardiovascular risk in later life.5 However, in this issue of Circulation , Gaillard et al6 provide a direct link between reduced uterine perfusion and IUGR with increased cardiovascular risk. Using a large, prospective, longitudinal cohort, Gaillard and colleagues report that an increase in third-trimester fetoplacental vascular resistance indicative of reduced perfusion was associated with a decrease in size at birth and a later increase in total fat mass and systolic blood pressure at 6 years of age.6 Thus, this study indicates that assessment of fetal growth characteristics via Doppler flow velocity waveforms in the umbilical artery not only may be indicative of IUGR but also may identify an individual at greater risk …