Most of us have never heard of ghrelin (pronounced GRELL-in). The hormone has made headline news because a study published [this week] has explained how it interacts with FTO (fat mass and obesity-associated protein), the gene that researchers first linked to obesity in 2007. Here’s a closer look at the details of the new discovery.
While only one in six people possess the FTO gene (which makes them up to 70% more likely to become obese), until today’s announcement scientists had not linked the gene and the “hunger hormone” conclusively in the human body. Japanese scientists described the actions of ghrelin first.
They reported their findings about the substance, which the stomach and gut manufacture, in the journal Nature in December 1999. In the early 2000s, following their report, the hormone prompted a great deal of research into ghrelin’s role in making people hungry, slowing their metabolism, actually decreasing the body’s ability to burn fat, and causing dieters to regain weight previously lost. Ghrelin also at least partly explains to the success of gastric bypass in decreasing hunger and promoting weight loss.
Led by London senior authors Rachel Batterham and Dominic J. Withers from University College and Fernando O. Zelaya of Kings College, working with colleagues from Germany and Japan, the current research team studied blood samples from obese and nonobese men at mealtime. They combined these results with both the volunteers’ brain MRIs and cell-level studies of ghrelin production. The finding doesn’t explain everything about the complex phenomenon of obesity, but it excites many scientists because it’s an excellent step in the right direction.
In future, drugs developed to decrease or block ghrelin may help the nearly 20% who have the FTO gene to lose weight. Some such pharmaceuticals are already in the development pipeline. Two new weight control drugs, Qsymia and Belviq, which may affect the ghrelin/FTO relationship, have recently entered the market.
Ghrelin antagonists, on the other hand, may be useful not only in preventing eating disorders, but also in boosting appetite for cancer and heart failure patients. As such, the study even has implications for improving life during the process of aging.
Dr. David Cummings, an endocrinologist at the University of Washington and Department of Veterans Affairs, Seattle and first author of an important early study published in the New England Journal of Medicine, has speculated on the possible origin of grhelin:
“A powerful mechanism to increase appetite and decrease metabolism when weight loss occurs is likely to have evolved because our species was subjected to periods of famine, and the threat to survival came from starvation, not overnutrition. People with an array of genes that promoted gluttonous consumption in times of plenty and efficient storage of fat might survive and pass on those genes, while the finicky eaters would die.”
The high-caloric, very palatable food of the our developed world–and the fact that all it takes to acquire it is a short trip to the supermarket–may explain why grhelin is not a bonus in the 21st century, and why obesity is becoming such a prevalent health hazard.
The research also gives further impetus to anti-obesity campaigns such as “Let’s Move,” begun by First Lady Michelle Obama in 2011. Recent studies have shown that in the United States, two of every three people are overweight, and half of this group are clinically obese. The American Medical Association voted to label obesity as a “disease” at its annual convention several weeks ago.
Based in Chicago, Sandy Dechert has been covering women’s healthcare for Examiner.com since the webzine’s official startup. She began investigating the H7N9 human influenza on the day the Chinese announced it and has also followed the 2012-2013 American seasonal influenza since its inception. Ms. Dechert has also reported on the fungal meningitis outbreaks, other top women’s health stories of 2012, and the creation and progress of the Affordable Care Act of 2010.