Aspects of fetoplacental nutrition in intrauterine growth restriction and macrosomia

Newborn birth weights have been steadily increasing throughout much of the developed world.1-3 However, the numbers of the two extremes, small fetuses that have suffered some form of intrauterine growth restriction (IUGR) and large or macrosomic fetuses, remain constant, and within some populations are actually increasing. IUGR and large-for-gestational-age (LGA) fetuses and newborns are at increased risk for fetal and neonatal morbidity and mortality.7, 8 IUGR is an important and relatively common problem in obstetrics, which may represent impaired placental insufficiency and associated placental nutrient transport function. In developed countries, 3-7% of newborns are classified as IUGR, 9 the causes of which include, but are not limited to, maternal malnutrition, maternal hypertension and idiopathic placental insufficiency. These fetuses are at increased risk of hypoxia, hypoglycemia and acidemia and also spontaneous preterm delivery. Interest in IUGR has increased recently by retrospective epidemiological, clinical follow-up and animal studies, 13, 14 that indicate increased susceptibility to adulthood metabolic disorders such as obesity, insulin resistance, type 2 diabetes mellitus and cardiovascular disease, particularly hypertension, in IUGR offspring.15-18 Furthermore, follow-up studies of infants who displayed abnormal umbilical artery Doppler flow velocity waveforms, commonly associated with IUGR, have demonstrated a lower IQ at 3 and 5 years of age. At the other end of the spectrum, the number of macrosomic, LGA births among certain minorities, delivered at term or ≥ 41 weeks, has increased.