Obesity is a major health concern and appropriate strategies need to be adopted to tackle obesity which itself brings about significant disability and premature deaths. Of increasing concern is the rise in the prevalence of childhood obesity - with concomitant increases in childhood type 2 diabetes and fatty liver disease. Although metabolic disorders arise from a complex interaction of many factors, including genetic, physiologic, behavioral, and environmental influences, the rates at which these diseases have increased suggest that environmental and behavioral influences, rather than genetic causes, are fuelling the epidemic. The developmental origins of health and disease (DOHaD) hypothesis highlights 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 not fully understood, this programming was generally considered an irreversible change in developmental trajectory. It has now been shown 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 DOHaD hypothesis as relates to obesity, critical windows of developmental plasticity and avenues to ameliorate the development of postnatal obesity following an adverse early life environment.