Obesity is growing at alarming rates worldwide, and the biggest culprit is overeating. In a study of brain circuits that control hunger and satiety, Yale School of Medicine researchers have found that molecular mechanisms controlling free radicals -- molecules tied to aging and tissue damage -- are at the heart of increased appetite in diet-induced obesity.No hope, no hope.
Published Aug. 28 in the advanced online issue of Nature Medicine, the study found that elevating free radical levels in the hypothalamus directly or indirectly suppresses appetite in obese mice by activating satiety-promoting melanocortin neurons. Free radicals, however, are also thought to drive the aging process.
"It's a catch-22," said senior author Tamas Horvath, the Jean and David W. Wallace Professor of Biomedical Research, chair of comparative medicine and director of the Yale Program on Integrative Cell Signaling and Neurobiology of Metabolism. "On one hand, you must have these critical signaling molecules to stop eating. On the other hand, if exposed to them chronically, free radicals damage cells and promote aging."
"That's why, in response to continuous overeating, a cellular mechanism kicks in to suppress the generation of these free radicals," added lead author Sabrina Diano, associate professor of Ob/Gyn, neurobiology and comparative medicine. "While this free radical-suppressing mechanism -- promoted by growth of intracellular organelles, called peroxisomes -- protects the cells from damage, this same process will decrease the ability to feel full after eating."
Except for one thing.
You can stop wasting your money at Whore Foods buying antioxidants.
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