For those of us who find that a new year means a new hole in the belt and a resolution to diet, genetics can be a comforting science. Where once we would have muttered something about metabolism to explain why our weight balloons over Christmas while others stay slim as ever, DNA has given us reason to hold up our heads as we suck in our stomachs. Since recent discoveries have shown how far genetic factors influence obesity, “big genes” have become the new big bones.

Comparisons between identical and non-identical twins have found that inherited factors account for about three quarters of the differences between people's waistlines, and new gene-hunting techniques have revealed some of the DNA variations responsible.

People who inherit one version of a gene called FTO are 70 per cent more likely to be obese than those who inherit another, and weigh, on average, 3kg more. Variations in another gene, MC4R, can tip the scales by an extra 1.5kg. This month scientists from deCODE Genetics and the international Giant consortium have discovered seven more genetic regions that influence body weight. These might not be the “genes for” love handles and double chins, but the message is clear. DNA, as well as diet, affects whether people get fat.

This is often taken to mean that obese people bear little responsibility for their shape. Rather than lacking the willpower to eat less and exercise more, perhaps their genes have forged thrifty, fat-prone bodies that burn calories reluctantly. If nature can trump nurture like this, the thinking goes, politicians and doctors are wrong to hector fat people about unhealthy lifestyles. They are just prisoners of their genes.

Such determinism is common in popular readings of genetic research, but it is founded on a misconception - that either genes or environment must be the dominant influence on physiology. In truth, they usually work together.

Many people with the “fat” version of FTO maintain a perfectly healthy weight because they eat well and take exercise. Changing lifestyles, too, must lie behind recent obesity trends: genes that predispose to weight gain have not become more common over the past decade, during which child obesity has increased by 7 per cent.

Most genes that affect health work by raising the risk of an outcome such as obesity, if the right environmental factors are present. Scientists on both sides of the nature versus nurture debate now accept that it is rare for either to act alone. The latest genetic research, however, suggests that the true extent of this interaction is more subtle and fascinating than was imagined. DNA does not just create predispositions that are triggered by environmental influences. It also affects the environmental influences to which we become exposed.

When the importance of genetics in obesity was first grasped, the mechanism of the effect was not known. The obvious hypothesis was that DNA alters metabolism, so that some people burn less energy and lay down more fat. As some of the genes involved have been pinpointed, however, it has become possible to work out what they do. And it turns out that most seem not to affect metabolism at all.

Of the seven variants identified this month, five are active in the brain. The implication is that they affect obesity not by changing people's energy balance, but their behaviour. Quite what these genes do exactly remains unknown. They might increase appetite or confer a sweet tooth. They might affect the brain's reward system - there is evidence that some obese people get less pleasure from food, not more, so eat more to feel satisfied.

Either way, the genetic roots of obesity seem to lie at least partly in the mind. Certain genes predispose people to enjoy a diet that can make them fat. Obesity is not the only aspect of human health in which nature seems to guide nurture in this way. The discovery of a DNA variant that can increase the risk of lung cancer by between 30 and 80 per cent points in the same direction.

Although it is still uncertain how it works, the strongest evidence indicates another behavioural effect. The gene does not appear to raise the chances of cancer directly, by making cells more likely to grow out of control. Rather, it may make people who try cigarettes more likely to become addicted, and smoke more heavily for more of their lives.

Insights of this sort have profound significance for the way we should think about the human genome, and its application to medicine. As we identify how variations in the genetic code affect disease and behaviour, we are learning about much more than the action of individual genes. Such research is illuminating the non-genetic factors that matter, too, and these will often be more useful as they are more amenable to change.

If genes affect obesity primarily by boosting appetite, that means we cannot lazily blame DNA for an expanding waistline. But it also shows that there is nothing in our biology to stop us from losing weight if we count calories and join a gym. The task might be harder for people with one genetic profile than another, but no gene compels us to have second helpings. Far from justifying fatalism, a fuller understanding of genetics can demonstrate just how much control we have over our health. Obesity and lung cancer might well be in your genes, but they're also in your head.

What's more, it is becoming clear that the dichotomy between nature and nurture was not the only sterile aspect of that great debate. The very terms are not clear cut. Is a gene that predisposes to obesity by means of appetite an aspect of nature or nurture? It is not just that these forces often work together. They can, at times, mean much the same thing.

Mark Henderson is science editor of The Times. His book, 50 Genetics Ideas You Really Need to Know, will be published in April by Quercus

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