GENETICS

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“Many of your clients will be

concerned about their weight and may wish to blame it on their ‘bad genes. But what are bad genes?”

in human history we have access to food 24 hours a day seven days a week. The first group, those with ‘good gene variants’ will burn off their energy efficiently protecting them from metabolic disease, however, the second group, those with ‘bad gene variants’ will continue to store extra energy very efficiently causing them to be overweight and ultimately leading to metabolic disease. This idea is known as the ‘thrifty gene hypothesis’ (Neel 1962).

My research is concerned with what we call ‘complex genetics’, that is characteristics that cannot be explained by one thing, whether that’s one gene or one environmental factor such as diet or exercise regime. We must look at the influence of many genes and many lifestyle choices, and importantly how they interact with each other. Completing this task is many decades away, however, we can turn the question around now and ask how one particular gene and one environmental factor influence a complex characteristic, and how they interact with each other.

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I am interested in how much exercise people do and how this interacts with genetics to alter the amount of fat that people store. Put another way, I want to ask, ‘Is exercise as good for all of us?’ To do this we take a candidate gene led approach, where we start off with a gene of known function that could plausibly be involved in our characteristic of interest.

For example, exercise increases levels of the catecholamines, adrenaline and noradrenaline, in the blood. The effects of the catecholamines are mediated by a gene known as the β-adrenergic receptor 2 (ADrB2 for short). Amongst the processes controlled by ADrB2 is lipolysis (the burning of fat). Crucially, ADrB2 is part of the 0.1% of the genome that varies between individuals.

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CONTACT US: 020 7492 2622 health&movement@citylit.ac.uk www.citylit.ac.uk

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