The time-honoured defence of the overweight — “It’s my metabolism, doctor” — has gained a degree of respectability today.

Some people, it seems, really are programmed by their genes to bulk up. It would have come as no surprise to William Sheldon, the American psychologist who divided the human race into skinny ectomorphs, shapely and well-muscled mesomorphs, or soft and tubby endomorphs.

But outcomes in life are seldom preordained. Obesity genes may influence why some people, given a similar lifestyle, get fatter than others, but they are not the whole answer.

One could speculate that in the distant past, in hunter-gatherer societies, the ability to build fat conferred a survival advantage that enabled some people to survive famines. Studies of the diabetes-prone and endomorphic Pima Indians of Arizona suggest possessing this “thrifty” gene is now a serious handicap.

Human beings who evolved when activity was unavoidable and food was scarce now have to live in an era when food is plentiful and activity all too easily avoided. It is this “obesogenic” environment that has given the genes predisposing to overweight and obesity a chance to express themselves. Eventually, should plenty become the norm, these genes will cease to provide any survival advantage and will become less common.

But that will take centuries, if not millennia. In the shorter term, the aim must be to use the knowledge to sharpen the focus on what works in cutting weight.

The variations found in the FTO gene do not immediately suggest a way forward. The gene has an unknown function and was originally found in mice with fused toes. How variations in this gene affect the risk of obesity and diabetes in humans is anybody's guess. They don’t make the mice fat.

The chances are that the gene will be found to be linked to some pathway that determines appetite, satiety or glucose metabolism. It may, alternatively, predispose those who carry it to be less active, though that is less likely.

It joins other interesting recent discoveries in the pathology of obesity such as the hormones leptin and ghrelin. It may one day be the target of a drug designed to modify its effects, or of a genetic test designed to identify those at extra risk of becoming overweight.

But the important point is that it will be only one piece in the obesity jigsaw. Many people carry it without becoming overweight. Even those who do carry a double copy weigh in, on average, at only a few kilograms more than those who don’t.

As an excuse for being obese, therefore, it lacks complete conviction. What matters is not what we are born with, but what we make of ourselves: and that depends upon our ability to balance calorie intake and expenditure.

Less food and more exercise is the sovereign remedy, though experts still argue over which is the more important. An unlucky genetic inheritance may be taken as a plea in mitigation, but it is not a defence.

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