Cortisol’s role in obesity not clearcut
By Clementine Wallace
NEW YORK (Reuters Health) – 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
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
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
“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.