Evolutionary and developmental perspectives add considerably to our understanding of the aetiology of
obesity and its related disorders. One pathway to obesity represents the maladaptive consequences of an
evolutionarily preserved mechanism by which the developing mammal monitors nutritional cues from its
mother and adjusts its developmental trajectory accordingly. Prediction of a nutritionally sparse environment
leads to a phenotype that promotes metabolic parsimony by favouring fat deposition, insulin resistance,
sarcopenia and low energy expenditure. But this adaptive mechanism evolved to accommodate
gradual changes in nutritional environment; rapid transition to a situation of high energy density results in
a mismatch between predicted and actual environments and increased susceptibility to metabolic disease.
This pathway may also explain why breast and bottle feeding confer different risks of obesity. We discuss
how early environmental signals act through epigenetic mechanisms to alter metabolic partitioning, glucocorticoid
action and neuroendocrine control of appetite. A second pathway involves alterations in fetal
insulin levels, as seen in gestational diabetes, leading to increased prenatal fat mass which is subsequently
amplified by postnatal factors. Both classes of pathway may coexist in an individual. This developmental
approach to obesity suggests that potential interventions will vary according to the target population.
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