Early Life Nutrition and Developmental Programming of Obesity - Evidence from Animal Models and Potential Strategies for Intervention (#4)
Obesity is a world-wide epidemic associated with significant morbidity and mortality which costs billions of dollars per year and is a major cause of non-communicable chronic diseases 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, behavioural and environmental influences, the rates at which these diseases have increased suggest that environmental and behavioural influences, rather than genetic causes, are fuelling the epidemic. The developmental origins of health and disease (DOHaD) hypothesis has highlighted the link between the early life nutritional environment and the later development of adult obesity and related metabolic disorders. Although the mechanisms are not yet fully understood, this developmental programming was generally considered an irreversible change in life course trajectory. It has now been shown that, at least in animal models, developmental programming of postnatal obesity and related disorders is potentially reversible by nutritional (e.g. dietary methyl donors) or targeted therapeutic interventions (e.g. leptin, growth hormone) during the period of early life developmental plasticity. This presentation 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 nutritional environment.