For those of us who have a tendency to put on a few extra pounds it is always tempting to reach for biological reasons why our body shapes might not be our fault. We all know slim people who seem to do nothing but eat and slob out in front of the television, and others whose second helpings go straight to the waist, however much they exercise. It often appears that diet and lifestyle cannot be all that matter.

The traditional excuse was always “big bones”, but this has now been joined by others with more scientific credentials. It has long been suspected that genetics are involved and in April scientists published details of the first gene to be directly linked to obesity. People who inherit one version of the FTO gene rather than another are 70 per cent more likely to be obese, and weigh an average of 3kg more. Big bones might not exist, but “big genes” are taking their place.

A study published this week, indeed, has shown that genetics is becoming the explanation of choice for people who become seriously obese. Research at the University of Warwick into people seeking weight-loss surgery found that all these patients saw their bodies as naturally “fat-prone”, often invoking genes or family history.

Another factor over which individuals have little control will be popularised by another item from the week’s research news: viruses. A study at Louisiana State University (LSU) showed that exposure to adenovirus36 (Ad36), which normally causes coughs and colds, can induce stem cells from fat tissue to become fully fledged fat cells. Though the findings applied only in the laboratory, they matched observations that 30 per cent of obese people carry the virus, compared with only 11 per cent of the lean. Fat could now be blamed on germs, as well as genes.

Neither explanation is to be sniffed at. Though the evidence for Ad36’s role is not yet conclusive, the LSU team has made a compelling case, with epidemiological, animal and cell studies that point the same way.

Two other adenoviruses have been linked to weight gain, and it is looking plausible that infection can contribute. That genetics plays a part is even more certain. Twin and family studies show that obesity is at least partially heritable, and if FTO is the first common gene with an effect to be identifed, it is unlikely to be the last.

Both channels of research promise benefits, in the shape of screening, to identify people at high risk of obesity, and drugs or vaccines that might assist weight loss. They may also help to lift the stigma of obesity, the perception that it is the result of not one but two deadly sins, gluttony and sloth.

Yet if less controllable factors can affect body shape, their influence should not be exaggerated. While people with a particular genetic profile are at higher risk of gaining weight, it must be remembered that there are very many people with “fat” FTO genes who are slim.

Equally, even if the influence of Ad36 is confirmed, most obese people are not infected and plenty of svelte people will be. Except in rare cases, such as Prader-Willi syndrome, obesity is not caused directly by genes. It is probably never “caught” as an infection. These are risk factors, which have an effect only in concert with the environment.

For the vast majority of people – genetically predisposed, virally infected or not – a simple equation still applies. Consume more calories than you burn off and you will put on weight. While genetic insights and antivirals might one day help people to control their weight, even those who might benefit from such advances can do plenty about their problems now.

Blaming genes and viruses will not help anybody to lose weight or lower their risk of hypertension and diabetes. The low-tech solution of improving diets and lifestyles is very much the best one.

Mark Henderson is the Science Editor of The Times