The evolution of human adiposity and obesity: where did it all go wrong?
Because obesity is associated with diverse chronic diseases, little attention has been directed to the multiple beneficial functions of adipose tissue. Adipose tissue not only provides energy for growth, reproduction and immune function, but also secretes and receives diverse signaling molecules that coordinate energy allocation between these functions in response to ecological conditions. Importantly, many relevant ecological cues act on growth and physique, with adiposity responding as a counterbalancing risk management strategy. The large number of individual alleles associated with adipose tissue illustrates its integration with diverse metabolic pathways. However, phenotypic variation in age, sex, ethnicity and social status is further associated with different strategies for storing and using energy. Adiposity therefore represents a key means of phenotypic flexibility within and across generations, enabling a coherent life-history strategy in the face of ecological stochasticity. The sensitivity of numerous metabolic pathways to ecological cues makes our species vulnerable to manipulative globalized economic forces. The aim of this article is to understand how human adipose tissue biology interacts with modern environmental pressures to generate excess weight gain and obesity. The disease component of obesity might lie not in adipose tissue itself, but in its perturbation by our modern industrialized niche. Efforts to combat obesity could be more effective if they prioritized 'external' environmental change rather than attempting to manipulate 'internal' biology through pharmaceutical or behavioral means.
Childhood Nutrition Research Centre, UCL Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK. Jonathan.Wells@ucl.ac.uk
Jonathan C K
JC
Wells
D000273:Adipose Tissue / Q000473:pathology; D050154:Adiposity / Q000235:genetics*; D005075:Biological Evolution; D004777:Environment; D020022:Genetic Predisposition to Disease; D006801:Humans; D009765:Obesity / Q000235:genetics* / Q000473:pathology*