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Having the ‘obesity gene’ doesn’t hinder ability to lose weight, study finds

“Genetics may influence weight,” writes John Mathers, the study’s senior author, “but it doesn’t dictate what you can do about it.”

More than 100 human gene variants have been identified as possibly playing a role in whether someone becomes overweight or obese.

People with a gene variant that puts them at greater risk of being overweight or obese can successfully shed excess pounds by using the same kind of weight-loss programs as other people, according to a study published this week in the journal BMJ.

The study also found that no single weight-loss approach worked better for them than any other one.

“This is important news for people trying to lose weight since it means that diet, physical activity or drug-based weight loss plans will work just as well in those who carry the FTO gene,” writes John Mathers, the study’s senior author and the director of the Human Nutrition Research Center at Newcastle University in the U.K., in an essay published on The Conversation website.

“Genetics may influence weight,” he added, “but it doesn’t dictate what you can do about it.”

A greater risk

More than 100 human gene variants have been identified as possibly playing a role in whether someone becomes overweight or obese. The one with the strongest association with obesity, however, is a variant of the gene FTO. People who carry this variant are 70 percent more likely to be obese than those without it.

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But are they also more likely to have trouble losing weight?

To examine that question, Mathers and his colleagues conducted a systematic review and meta-analysis of the eight large randomized controlled studies on weight loss. Those studies, which used various approaches to diet, physical activity or drugs to induce weight loss, contained individual data — including the existence of the FTO variant — for more than 9,500 people.

After pooling the data from all the studies (and testing it for potential bias or confounding factors), they looked at whether the FTO variant made a difference in how much the studies’ participants weighed and how much they responded to the weight-loss treatment. They also looked to see if that response was affected by age, gender, ethnic background or initial weight.

“We were surprised to discover that having the FTO gene had no effect on weight loss,” writes Mathers. “The weight loss interventions were just as effective in people with the risk version of this gene as in everyone else. And our finding appears to be universal — it applies to men and women, to younger and older people, and to Caucasians and Black Americans.”

Limitations and implications

The meta-analysis comes with several caveats. Although it used data from eight large randomized clinical trials, the overall number of participants was still low for this kind of analysis. In addition, most of the participants were white and came from North America and Europe, which limited the researchers’ ability to determine differences between ethnic and racial groups. In addition, the meta-analysis focused only on the FTO variant. “The effect of other obesity related genes … on weight loss remains to be determined,” write Mathers and his colleagues.

Still, the study’s findings are important, for they suggest that personalized approaches to losing weight are not as effective as societal ones — approaches that, say, discourage the consumption of sugary foods and that promote walking and biking.

“If we are to turn back the tide of obesity, an understanding of how diet and lifestyle interact with the genome might help some people, particularly those with rare conditions that cause devastating levels of weight gain in early life,” acknowledges Alison Tedstone, chief nutritionist for Public Health England, in an editorial that accompanies the study.

But, she adds, “it is increasingly evidence … that the idea that personalized interventions based on the genome will yield population benefit, may not pay off, at least in the short term. Given that obesity and poor diet are leading causes of morbidity in Britain [and in the U.S.], a rebalancing of research towards whole systems approaches including environmental drivers may be of greater benefit to the population in the long term.”

FMI: You can read both the study and the editorial on the BMJ website. You can read Mathers’ essay at The Conversation.