Until recently, obesity was considered the product of interactions between genotype and lifestyle. However, recent work suggests that the genetic heritability of adiposity has been over-estimated, whilst epidemiological studies show that although many genes are associated with nutritional status, the effect of each is very small. A polygenic basis of obesity risk may arise through bet-hedging of numerous traits to accommodate diverse unpredictable environments, rather than through systematic local adaptation. Such 'fragmentation' of the genetic component of metabolism across multiple alleles may be a necessary pre-requisite for complementary enhancement of phenotypic plasticity. The inter-generational component of obesity refers to phenotypic effects transmitted across generations, arising from exposure to maternal, familial and environmental niches during development. Inter-generational transfers of somatic capital (height, lean mass) may respond to ecological conditions through a slow-response damping system, through the influence of maternal phenotype on offspring growth and body composition. The primary traits subject to inter-generational effects may be physique and life history strategy, with adiposity both aiding and responding as a flexible risk management strategy. The biological processes that underpin the offspring's developmental plasticity appear sensitive to the obesogenic niche. Through this sensitivity, diverse environmental factors can induce excess weight gain from childhood onwards.