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obesity gene

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According to US researchers, a defective gene linked to obesity appears to affect impulse control and food choices.

This could explain why people with the gene have so much trouble maintaining a healthy weight as they age.

Middle-aged and older people with obesity-associated variants of the FTO gene tend to gain weight, according to researchers from the National Institutes of Health. Moreover, scans detected reduced function in brain regions that govern impulsivity and perception of food texture and taste, the researchers found.

“Sure enough, people who carry one or two copies of the FTO variant show increased intake of high-calorie or fatty food as they age,” said senior author Dr. Madhav Thambisetty, chief of clinical and translational neuroscience at the National Institute on Aging’s Laboratory of Behavioral Neuroscience.

“There may be a common biological factor underlying both the risk for obesity during aging as well as obesity-related behavior like your ability to resist impulse eating,” Madhav Thambisetty said.

Many studies have tied certain versions of the FTO gene to chronic obesity, but doctors have struggled to determine why the gene affects a person’s risk of obesity, said Ruth Loos, director of the genetics of obesity and related metabolic traits program at the Icahn School of Medicine at Mount Sinai in New York City.

Middle-aged and older people with obesity-associated variants of the FTO gene tend to gain weight

Middle-aged and older people with obesity-associated variants of the FTO gene tend to gain weight

“These types of studies are important to disentangle the mechanism of why FTO is associated with obesity, but it’s only one piece of a huge puzzle,” Ruth Loos said.

In the US, more than one-third of adults aged 65 and over are obese, according to background information in the study.

About 45% of people in this study had at least one copy of the pro-obesity FTO variant, Dr. Madhav Thambisetty said, which tracks with the white population in the US. About 16% of people had two copies of the gene, which confers an even greater risk of obesity.

The study focused on nearly 700 participants, including 69 people who agreed to annual PET scans to gather additional information regarding their brain structure and function. At the start of the study, average age was 46. All were participating in the Baltimore Longitudinal Study of Aging, one of the longest running studies of human aging in North America.

They first confirmed that body mass index increased in those with one or two copies of the FTO gene variant. They then compared brain PET scans of patients with the FTO variant with scans of non-carriers, looking for differences in brain function over time.

They found people with the gene variant had reduced function in their medial prefrontal cortex, a region thought to be important in controlling impulses and response to the taste and texture of food.

In a final step, the team reviewed data gathered on participants’ personality and diet. The group at increased genetic risk for obesity showed a greater tendency to impulsivity as well as a greater intake of fatty foods during aging.

The effect appears to increase with the number of copies.

“We see a dose effect, where these changes in impulsivity or a preference for fatty foods increase with multiple copies of the gene,” Dr. Madhav Thambisetty said.

The findings are published May 27 in the journal Molecular Psychiatry.

If these results pan out in additional studies, they mean that people who have a greater genetic risk of obesity face an uphill battle to maintain a healthy weight.

However, a genetic predisposition to obesity does not mean one is doomed to obesity.

“You may be genetically susceptible, but by living a healthy lifestyle you can overcome your genetics,” Ruth Loos said.

“You are not destined to be obese.”

Dr. Madhav Thambisetty agreed, noting that previous studies have shown that people can overcome the obesity risk posed by the FTO gene through regular exercise.

An international group of scientists have solved the mystery of a genetic flaw which greatly increases the risk of obesity in one in six people.

A version of an obesity gene, called FTO, had been linked to a bigger belly, but the reason why was uncertain.

A study, published in The Journal of Clinical Investigation, showed FTO gene made fatty foods more tempting and altered levels of the hunger hormone, ghrelin.

Obesity experts said drugs targeting ghrelin might reduce weight gain.

There is a strong family link with obesity, and a person’s genetic code is thought to play a major role in the risk of them becoming overweight.

People have two copies of the FTO gene – one from each parent – and each copy comes in a high and a low-risk form. Those with two-high risk copies of the FTO gene are thought to be 70% more likely to become obese than those with low-risk genes.

But no-one knew why.

FTO gene made fatty foods more tempting and altered levels of the hunger hormone, ghrelin

FTO gene made fatty foods more tempting and altered levels of the hunger hormone, ghrelin

A team, led by researchers at University College London, tested two groups of men. All were a normal weight, but one group had the high-risk FTO genes and the other was low risk.

The first tests looked at levels of the hormone ghrelin either side of a meal in 10 men from each group.

Levels of the hormone, which makes people hungry, did not fall as far in the high-risk patients after the meal. Their ghrelin levels also began to climb more quickly.

In separate tests, a series of brain scans after a meal showed further differences between the two groups. Men with the high-risk genes found pictures of high-fat foods more appealing than the low-risk men.

Dr. Rachel Batterham, the head of the centre for obesity research at University College London, said: “Their brain is set up to be particularly interested in anything to do with high-calorie food.”

She said they were “biologically programmed to eat more”.

Dr. Rachel Batterham said understanding how FTO affected the odds of becoming overweight would help patients.

She said exercise such as cycling was an excellent way to lower ghrelin levels and there was a significant amount of research from pharmaceutical companies working on the hormone.

Dr. Rachel Batterham added: “Also protein meals do lower ghrelin more, so anything that suppresses ghrelin is more likely to be effective in FTO patients.”

The FTO mutations were probably life-saving at one point in human history when piling on the pounds in the summer would help people survive the winter.