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01st Apr 2019

Despite the ubiquity of the modern ‘obesogenic’ environment, we have not uniformly developed obesity. On the contrary, there is considerable variation in weight gain, which is observable from early infancy. In fact, it is not uncommon for siblings to vary considerably in their weight, even when they live in the same household. Obesity risk is about far more than just the environment we are exposed to. Genetic susceptibility to the environment is thought to explain some of the variation in adiposity. Nearly 100 twin studies have established that weight is a highly heritable trait (50-90%), and ~1000 common genetic variants (single nucleotide polymorphisms) have been discovered. Individual differences in appetite have been implicated as one of the mechanisms through which genes influence adiposity, so-called ‘Behavioural Susceptibility Theory’ (BST). BST hypothesises that individuals who inherit a set of genes that confer greater responsiveness to food cues (wanting to eat in response to the sight, smell or taste of palatable food), and lower sensitivity to satiety (fullness), are more vulnerable to overeating in response to the modern food environment, and therefore to developing obesity. At the same time, our environment is not simply an ‘exposure’ – we select and shape our environment to suit our preferences, many of which have some genetic basis (called gene-environment correlation). This talk summarises the interplay between genes, appetite and the home family environment in early weight gain, using data from Gemini and TEDS – two large, population-based British twin birth cohorts set up to study genetic and environmental influence on health and development.

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