An obesity gene that affects one in every six people could be partially treated thanks to a new study that's finally determined how it works. Researchers led by Rachel Batterham at University College London were looking into an obesity gene, known as FTO, and found that it caused people with a specific variation of it to maintain higher levels of ghrelin, a hunger-stimulating hormone, throughout their system. In people without the gene variation, ghrelin levels dropped after a meal — but in people with the specific gene variant, ghrelin levels remained high even after eating, keeping them hungry.
"It's a double hit."
Because ghrelin levels can be suppressed, the type of obesity caused by FTO could be mitigated. "Ghrelin (and therefore hunger) can be reduced by exercise like running and cycling, or by eating a high-protein diet," Batterham said in a statement. She also noted that drugs to suppress the hormone are already in development. However, her research team found one other effect of the FTO variation that they haven't determined a way to treat: it makes fatty foods appear more appealing. Between the reduced hunger suppression and the increased interest in fatty foods, Batterham says that people with the obesity-prone FTO variation "are biologically programmed to eat more ... it's a double hit."
The findings come nearly a month after the American Medical Association officially declared obesity to be a disease. The decision was a controversial one, leading some to worry that it would increase patients' reliance on medications and surgery to treat weight issues — though that may not be a problem under Batterham's suggested treatments. Her research team's findings, which were published today in The Journal of Clinical Investigation, say that more work still needs to be done to fully understand the mechanisms that cause FTO to alter the body. But even so, Batterham thinks that their study will have an immediate impact: "This arms us with some important new insights to help in the fight against the obesity pandemic."