The obesity epidemic has seen the incidence of obesity and overweight almost double in Western societies and the trend is mirrored in developing nations that are transitioning to first-world economies. Obesity is strongly associated with the co-morbidities of type 2 diabetes, hypertension and heart disease and represents an enormous burden to the health care system. Of even more concern is the rise of over 40% over the last 20 years in the prevalence of childhood obesity - with concomitant increases in childhood type 2 diabetes. Metabolic disease results from a complex interaction of many factors, including genetic, physiologic, behavioral, and environmental influences. The recent rate at which these diseases have increased suggests that environmental and behavioral influences, rather than genetic causes, are fuelling the present epidemic. In this context, the developmental origins of health and disease (DOHaD) hypothesis has highlighted the link between the periconceptual, fetal and early infant phases of life and the subsequent development of adult obesity and related metabolic disorders. Although the mechanisms are yet to be fully elucidated, this programming has generally been considered an irreversible change in developmental trajectory. Recent work suggests that, at least in animal models, developmental programming of postnatal obesity is potentially reversible by nutritional or targeted therapeutic interventions during the period of developmental plasticity. This talk will focus on the developmental origins of obesity, critical windows of developmental plasticity and possible avenues to ameliorate the development of postnatal obesity following an adverse early life environment.