Cortisol’s role in obesity not clearcut

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It is simplistic to suggest that lowering cortisol levels will promote weight loss, as some television ads claim, according to researchers at the Oregon Health and Science University in Portland.

In their study, published in the Journal of Clinical Investigation, the scientists show that the hormone isn’t the major factor involved in weight gain and fat distribution, and might actually come into play at a secondary level.

“There’s no question that this pathway is involved in metabolism, but the mechanism is more complex than just cortisol ‘causing’ obesity,” Dr. Malcolm Low, from the OHSU Center for The Study of Weight Regulation and Associated Disorders, told Reuters Health.

Cortisol, the active form of cortisone, is a hormone involved in a variety of different bodily functions, from the immune system to the regulation of blood sugar and liver function.

When treating inflammations such as asthma, patients might have to take high doses of cortisone, which can lead to weight gain. On the flip side, obese people usually have elevated cortisol blood levels.

“This has probably led to the general misconception that says: cortisol is responsible for obesity and should be lowered to loose weight,” said Low. “You hear this argument very often, and it’s promoted by manufacturers of anti-obesity cortisol reducing supplements.”

In their experiments, Low and his team worked on mice lacking a gene—the proopiomelanocortin (POMC) gene—which when absent is known to cause obesity. The goal was to figure out if weight gain results from POMC’s absence in the brain or from its absence in peripheral tissues.

Their findings showed that the primary site for POMC weight regulation is the brain, and suggested that abnormal cortisol levels might actually result from defects of this control route.

“Cortisol is a concomitant resultant rather than a direct cause,” said Low. “In this paper, we show that administering small quantities of cortisone increases body weight in mice lacking POMC, but not in normal mice.”

What happens in mice is pretty similar to what happens in humans, added Low.

SOURCE: Journal of Clinical Investigation, February 2006.

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