Genes Tied to Belly Size Also Linked to Heart Disease

TUESDAY, Feb. 14, 2017 (HealthDay News) -- Gene variants that raise a person's odds of being "apple-shaped" may be linked to heightened risks of heart disease and type 2 diabetes, a large study suggests.

Many previous studies have hinted that a large waistline can be particularly unhealthy, compared to carrying your weight around the hips and thighs ("pear-shaped"). This new research suggests that people who carry weight at the belly tend to have higher rates of diabetes and heart disease.

These types of studies do not prove a cause-and-effect link, said Dr. Kirk Knowlton, director of cardiovascular research at Intermountain Medical Center Heart Institute in Salt Lake City.

But, the new findings "go a step further," said Knowlton, who was not involved in the study.

The new findings give "considerably more weight" to the evidence that excess belly fat, by itself, contributes to diabetes and heart disease, he said.

That's because study took a different approach to the question: Researchers looked at whether gene variants that predispose people to abdominal obesity were also tied to the risks of diabetes and heart disease -- and whether that seemed to be independent of other factors, such as overall body weight.

That was, in fact, the case.

The findings were published Feb. 14 in the Journal of the American Medical Association.

Dr. George Davey Smith, of the University of Bristol in England, wrote an editorial that accompanied the study.

"This study suggests waist-hip ratio influences diseases outcome," Smith said, "and that this is independent of body mass index."

The findings do not prove that shedding belly fat would cut a person's risk of diabetes or heart disease, Smith pointed out. But, he said, they do suggest it would.

For the study, researchers at Harvard University and Massachusetts General Hospital in Boston focused on 48 gene variants that had already been linked to waist-to-hip ratio. From that, they developed a genetic "risk score."

The researchers then applied the score to more than 400,000 adults who'd taken part in several previous health studies.

To help zero in on the role of belly fat, the genetic risk score was adjusted for people's body mass index -- a measure of weight in relation to height.

In the end, the study found, waist size mattered.

Based on the genetic scores, each standard deviation in waist-to-hip ratio raised the risk of heart disease by 46 percent. The risk of type 2 diabetes rose by 77 percent.

People with a genetic predisposition toward a large waist also tended to have higher blood sugar, blood pressure and triglyceride levels -- all risk factors for diabetes or heart disease.

It all offers "pretty strong evidence" that excess abdominal fat directly contributes to diabetes and heart disease, said study lead author Connor Emdin, of Mass General's Center for Genomic Medicine.

That assumes that people with the culprit gene variations first develop abdominal obesity, and that is what raises their risk of the two diseases.

But the findings do not definitively prove that, according to Emdin.

It's still possible, he said, that the genes that contribute to abdominal obesity also feed the development of diabetes and heart disease -- through mechanisms other than extra belly fat.

Still, everyone agreed on what the findings imply: Preventing or shedding excess weight around the middle could help ward off two major diseases.

"This is something we should be paying attention to," Knowlton said.

And even though genes can make some people vulnerable to abdominal obesity, that does not mean it's destiny.

It's clear, Emdin said, that diet, exercise and other lifestyle habits make a difference.

More information

The American Heart Association has more on weight and heart disease.


SOURCES: Connor Emdin, D.Phil., Center for Genomic Medicine, Massachusetts General Hospital, Boston; Kirk Knowlton, M.D., director, cardiovascular research, Intermountain Medical Center Heart Institute, Salt Lake City; George Davey Smith, M.D., D.Sc., professor, clinical epidemiology, University of Bristol, U.K.; Feb. 14, 2017, Journal of the American Medical Association

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