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Human obesity results from prolonged caloric imbalance, where energy intake exceeds energy expenditure over a period of months to years. It is presumed to occur as a consequence of complex interactions between environmental and heritable factors, although the search for which specific metabolic factors or genes persist has been challenging and remains incomplete. Despite a relatively high heritability of common forms of obesity which represents between 40 to 70 % of the obese population, the identification and conformation of definitive genetic or epigenetic obesogenic variants that when activated may contribute to a susceptibility for excess weight gain have been difficult to confirm. The incidence of obesity, overweight conditions, and their close association with hypertension in the US is increasing at alarming if not epidemic proportions throughout much of Western culture and society in recent history. Despite marked advances in nutrition knowledge and practice, pharmacotherapeutic management, and life-style modifications, approximately one third of the US population is now overweight, and the resulting predicted increases in the cost of medical management of overweight and obese conditions and their commonly associated pathophysiologic sequalae are becoming burdensome to public health and to the medical community. The development of obesity in most humans typically develops gradually over a duration of months to years but occurs more rapidly in onset in most commonly studied genetic models of obesity, where it usually follows the expression of an autosomal recessive genetic trait. In humans garden variety obesity is typically attributed to a combination of incompletely defined genetically linked traits and environmental factors.

Can epigenetic expression contribute to the development of an obese phenotype?