Do these genes make me look fat?

We ask geneticist Dr Colin Moran to explain more about his research into how genetic make-up can influence the effects of exercise from person to person.

ore and more the barriers that define traditional research disciplines are being broken down. I trained as a geneticist but have spent most of my research life working with physiologists, sports scientists and nutritionists as they become increasingly intrigued by what genetics can tell them about their areas of interest.

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The spread of genetics into other areas of research has come on the back of the Human Genome Project. This was launched in 1986 with the first draft published fifteen years later. The (sequence) data generated by this project is like a recipe for building a human and shows that we are 99.9% similar to each other. This makes sense, as we are all humans, not cats, not dogs, not flowers, not bacteria and more similar to each other than to other forms of life. However, as technology improves and we sequence more and more individuals what is becoming clear is that the interesting bit is the 0.1%. This gives us different potential and contributes, along with the environment, to making us unique individuals. It gives us blue eyes or brown eyes, blonde hair or dark hair, makes us tall or short, fat or thin. It is this last one that interests me: I want to understand the influence of certain genes and exercise on obesity.

Obesity is on the increase, not just in the USA (Figure 1), but is a global epidemic. 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’?

Genes (or more correctly ‘gene variants’ as we all share the same genes although for 0.1% of them we have different versions of them) that cause fat to stick to your clients thighs? Gene variants that force them to eat too much and shy away from exercise? That’s not as ridiculous as you might think. Imagine 200 years ago (Figure 2) in what we will call a ‘good environment’ for metabolic health, i.e. one in which there is not enough food and most people do some form of manual labour. First of all, take a group of individuals with modern day ‘good gene variants’, they will struggle to get enough energy from the little food that they get as their bodies burn it off so successfully, they will struggle to survive. Now take a group of individuals with modern day ‘bad gene variants’, they will get enough energy from the little food that they get and any extra their bodies will store very efficiently to be used only in times of hardship, they will find it much easier to survive. Now transport these two groups forward 200 years to our modern obesogenic environment, where for the first time

Gene environment interactions

Year 1809 ‘good’

gene

variants ‘bad’

gene variants

Year 2009 ‘good’

gene

variants ‘bad’

gene variants

Figure 1. Data from the Centres for Disease Control (CDC) Behavioural Risk Factor Surveillance System (BRFSS) showing changes in adult obesity rates in the USA by state.

24 ‘bad’ environment high risk

Figure 2. Example of how gene-environment interactions may alter the risk of metabolic disease.

‘good’ environment lowish risk lowish risk low risk

The rEPs Journal 2009;15(Dec):24-26