Developmental Hypertension, Nephrogenesis, and Mother's Milk

ompelling epidemiologic and experimental evidence indicates that early-life experiences shape risk for dis- ease in later life. Infants who are born smaller, reflect- ing a slower growth trajectory in utero, experience higher inci- dences of hypertension, obesity, diabetes, and renal disease as adults (1). Birth weight is a crude surrogate for the broad spectrum of specific adverse events that may impair fetal growth in humans; therefore, experimental models have been developed to probe postnatal outcomes after specific interven- tions that are relevant to human pregnancy, including nutrient deficits and placental insufficiency (2). Attention continues to focus primarily on fetal growth, a period of biologic plasticity in which environmental insults can permanently "program" the fetus and thereby alter the postnatal phenotype by a num- ber of different mechanisms. Impaired growth during critical periods of organ development may have an impact on disease risk by permanently reducing the number of functional units, for