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April 25, 2013 Volume 34, No. 28

Some people might be genetically predisposed to inactivity, scientist says


MU researchers might have discovered “lazy” genes, which may explain why some people hate exercise.

Most American adults are inactive, meaning they do not meet the federally recommended standard of 30 minutes of moderate activity five days a week. Of 5,700 MU employees who recently took the Healthy For Life wellness assessment, 46 percent were deemed overweight, 40 percent were inactive and 30 percent were being treated for high blood pressure.

These days, more scientists are connecting inactivity to weight gain and high blood pressure, both of which place people at risk for developing coronary heart disease, various cancers, type 2 diabetes and hypertension.

But perhaps people’s inactivity is not their fault. Perhaps their genes are to blame.

New research by Frank Booth, professor of biomedical sciences in the College of Veterinary Medicine, and Michael Roberts, a postdoctoral fellow, indicate that genes may predispose people to embrace or avoid exercise. The scientists published a paper this month based on mice experiments that could mean that genetics play a role in exercise motivation, even in humans.

The research builds on the discovery in recent years of a fat gene, or FTO, and its variants. The fat gene aided food storage in the prehistoric ancestors of Homo sapiens, a necessity for survival during food scarcity. FTO, discovered by scientists in 2007, gave ancient carriers an edge in surviving short famines.

In today’s world of rampant inactivity, the fat gene loses much of its purpose. Booth finds this ironic. “The same genes that were selected for survival when people had to forage for their food may now shorten survival in the absence of sufficient physical activity,” he said in the 2012 summer issue of MIZZOU magazine.
In the MU study, published April 3 in the American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, Booth and Roberts measured running-wheel use by rats during a six-day period. They bred the top 26 runners with one another and the bottom 26 rats with one another. They repeated the process through 10 generations. They discovered that descendants of the top exercisers ran 10 times more than the descendants of the “couch potato” rats.

Afterward, the scientists studied in each rat the levels of mitochondria in muscle cells, compared body composition and conducted thorough genetic evaluations through RNA deep sequencing.

“While we found minor differences in the body composition and levels of mitochondria in muscle cells of the rats, the most important thing we identified were the genetic differences between the two lines of rats,” Roberts said. Out of more than 17,000 different genes in one part of the brain, Booth and Roberts have identified 36 genes that may play a role in people cleaving to inactivity.

“We have shown that it is possible to be genetically predisposed to being lazy,” Booth said. 

“This could be an important step in identifying additional causes for obesity in humans, especially considering dramatic increases in childhood obesity in the United States,” he said. 

Booth and colleagues plan future studies on “lazy” genes, including whether carriers are predestined to inactive lives. 

For a few years, a similar Calvinistic debate involved the fat gene. Sixty percent of people of European and African descent, and nearly half of those of Asian descent are believed to be FTO carriers. 

That may sound depressing, but recent studies show that fat gene carriers who are inactive have only a 10 percent greater chance of becoming overweight or obese than a noncarrier, Booth said in the MIZZOU article. 

Moreover, a November 2011 study published in PLoS One found that patients who performed as little as one hour of moderate to intense activity a week subverted the fat gene by 30 percent. 

Perhaps there is similar hope for the lazy-gene carrying couch potato.