Prenatal Origin of Childhood Overweight, Obesity and Insulin Resistance, with Special Emphasis on Maternal Diabetes, Excessive Weight, Nutrition and Hormone Imbalances

Overweight in childhood, adolescence and adulthood is now a world-wide epidemic. A variety of preventive and therapeutic measures are being developed with partial success. Since the pioneering studies of D.J. Barker linking maternal famine in pregnancy to long—term undesirable effects on the offspring—the “metabolic syndrome” that stems from long-lasting epigenetic changes, it became evident that there are many undesirable events which affect in-utero fetal growth and development. They often persist postnatally, through childhood and adulthood. The purpose of this review is to discuss the prenatal factors that may have long term effects on postnatal weight gain and obesity that are important contributors to the “obesity” epidemic. These prenatal undesired factors are pregestational and gestational diabetes, pre-pregnancy maternal obesity, excessive weight gain in pregnancy, placental dysfunction and maternal hormonal imbalances. They may affect fetal growth, generally causing excessive growth (macrosomia) and sometimes diminished growth (small for gestational age). These prenatal conditions are associated with epigenetic changes that may contribute to insulin resistance and subsequent metabolic alterations leading to increased food intake, overweight, and obesity. Studies also demonstrate that increased exposure in pregnancy to teratogens, like endocrine disruptors and cigarette smoking, may also affect prenatal and postnatal growth and adiposity. However, many the studies demonstrating the role of these factors are often weakened, as they mainly demonstrate associations and do not sufficiently consider possible confounding factors such as postnatal age, nutrition and lifestyle. Better understanding of these prenatal factors may support more effective prevention and management strategies for childhood overweight and obesity.