According to this ‘thrifty phenotype’ hypothesis, an increased risk of diabetes following low birth weight could be attributed to poor pancreatic development interacting with excess body weight in later life. An alternative hypothesis, focusing on life-course plasticity, proposed that low birth weight babies responded to their low level of nutritional intake in early life through alterations in growth and metabolism, which impact on subsequent obesity risk ( Hales and Barker, 1992). Nevertheless, it became extremely influential, and is still widely cited today. This hypothesis was somewhat abstract, with no discussion of when such cycles of feast and famine might have occurred. Those experiencing more frequent famines were assumed to have undergone selection for thriftier genes. In the 1960s, the ‘thrifty genotype’ hypothesis suggested that populations varied genetically in their predisposition to store energy, on account of differential ancestral exposure to ‘cycles of feast and famine’ ( Neel, 1962). Previous evolutionary approaches to human obesity, hence relevant to adiposity in general, have been dominated by two hypotheses, each focusing on the concept of thrift. Although diverse phenotypic traits differ between obese and non-obese individuals, it remains unclear which differences are causal in its development. Its causes remain subject to vigorous debate, owing to the fact that the energy balance equation is a ‘truism’ and hence offers no explanatory framework for why excess weight gain occurs ( Wells and Siervo, 2011). Obesity is a nebulous concept, defined using statistical criteria rather than explicit diagnosis of a metabolic pathology ( Cole et al., 2000 Garrow and Webster, 1985). Obesity confounds the standard medical model of disease, which developed historically to address biological pathogens and can be more difficult to apply to other forms of ill health. This scenario can be attributed in part to the persisting poor understanding of what exactly obesity is. 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.ĭespite seemingly compelling evidence that obesity is bad for human health, both public health efforts to reduce its prevalence and clinical efforts to treat it have had only modest success. The disease component of obesity might lie not in adipose tissue itself, but in its perturbation by our modern industrialized niche. ![]() 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 sensitivity of numerous metabolic pathways to ecological cues makes our species vulnerable to manipulative globalized economic forces. 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. However, phenotypic variation in age, sex, ethnicity and social status is further associated with different strategies for storing and using energy. The large number of individual alleles associated with adipose tissue illustrates its integration with diverse metabolic pathways. ![]() Importantly, many relevant ecological cues act on growth and physique, with adiposity responding as a counterbalancing risk management strategy. ![]() 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. Because obesity is associated with diverse chronic diseases, little attention has been directed to the multiple beneficial functions of adipose tissue.
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