Stress induced Obesity
Professor Herbert Herzog, Director of the Neuroscience Research Program at
Australia-based Garvan Institute of Medical Research, together with scientists
from the US and Slovakia, have done obesity research which have shown that
neuropeptide Y (NPY), a molecule the body releases when stressed, can
‘unlock’ Y2 receptors in the body’s fat cells, stimulating the cells to grow in
size and number. By blocking those receptors, it may be possible to prevent
fat growth, or make fat cells die.
“We have known for over a decade that there is a connection between chronic
stress and obesity,” said Professor Herzog. “We also know that NPY plays a
major role in other chronic stress-induced conditions, such as susceptibility
to infection. Now we have identified the exact pathway, or chain of molecular
events, that links chronic stress with obesity.”
“There is not much we can do about the increased levels of NPY caused by
stress, but we can do something about the damage it causes. If we can
interfere before it causes fat to amass, it could have a major impact on
cardiovascular disease, diabetes, and cancer (which all have links with
obesity). When we have a stress reaction, NPY levels rise in our bodies,
causing our heart rate and blood pressure to go up, among other things.
Stress reactions are normal, unavoidable, and generally serve a useful
purpose in life. It’s when stress is chronic that its effects become damaging,”
he said.
Scientists at Georgetown University (Washington DC), part of this
collaborative study, have found a direct connection between stress, a high
calorie diet and unexpectedly high weight gain. Stressed and unstressed
mice were fed normal diets and high calorie (high fat and high sugar, or so
called comfort food) diets. The mice on normal diets did not become obese.
However, stressed mice on high calorie diets gained twice as much fat as
unstressed mice on the same diet. The novel and unexpected finding was
that when stressed and non-stressed animals ate the same high calorie
foods, the stressed animals utilized and stored fat differently.
“Our findings suggest that we may be able to reverse or fidn treatments for
obesity caused by stress and diet, including the worst kind of obesity; the
apple-shaped type, which makes people more susceptible to heart disease
and diabetes,” said Professor Zofia Zukowska, the senior author of paper
published in Nature Medicine. “Using animal models, in which we have either
blocked the Y2 receptor, or selectively removed the gene from the abdominal
fat cells, we have shown that stressed mice on high calorie diets do not
become obese. Even more surprisingly, in addition to having flatter bellies,
adverse metabolic changes linked to stress and diet, which include glucose
intolerance and fatty liver, became markedly reduced. We do not know yet
exactly how that happens, but the effect was remarkable,” said Professor
Zukowska.
Professor Herzog believes that these research findings will have a profound
effect on the way society will deal with the obesity epidemic. “There are
millions of people around the world who have lived with high levels of stress for
so long their bodies think it’s ‘normal’. If these people also eat a high fat and
high sugar diet, which is what many do as a way to reduce their stress, they
will become obese. Until now, the pharmaceutical industry has focused on
appetite suppressants with only moderate success. Our hope is that in the
near future pharmaceutical companies, using the results of our research, will
develop antagonists against the Y2 receptor that will bring about a reduction
in fat cells.” . This could be a good approach in finding a treatment for obesity
and the key to obesity prevention.
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