Stress Can Make Us Obese - How Can We Stop It From Doing So?

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Stress Can Make Us Obese - How Can We Stop It From Doing So?

http://www.medicalnewstoday.com/medicalnews.php?newsid=75788

New findings published in Nature Medicine online could offer hope to

millions of people who have become obese as a result of stress.

Professor Herbert Herzog, Director of the Neuroscience Research

Program at the Garvan Institute of Medical Research, together with

scientists from the US and Slovakia, 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). Basically, 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 town University (Washington D.C), 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 utilised and stored fat differently.

" Our findings suggest that we may be able to reverse or prevent

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, " says senior author of the Nature

Medicine paper, Professor Zofia Zukowska of town

University. " 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, " she said.

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. "

Stress-activated adipogenic pathway in fat tissue exaggerates diet-

induced obesity and metabolic syndrome.

Kuo, L.E., Kitlinska, J.B., Tilan, J.U., Li, L., Baker, S.B.,

, M.D., Lee, E.W., Burnett, M.S., Fricke, S.T., Kvetnansky,

R.K., Herzog, H. & Zukowska, Z.

Nature Medicine advance online publication, 1 July 2007

Link to article

The study was co-funded by the National Institutes of Health, the

American Heart Association, and the Slovak Research and Development

Agency.

About Garvan

The Garvan Institute of Medical Research was founded in 1963.

Initially a research department of St 's Hospital in Sydney,

it is now one of Australia's largest medical research institutions

with approximately 400 scientists, students and support staff.

Garvan's main research programs are: Cancer, Diabetes & Obesity,

Arthritis & Immunology, Osteoporosis, and Neuroscience. The Garvan's

mission is to make significant contributions to medical science that

will change the directions of science and medicine and have major

impacts on human health. The outcome of Garvan's discoveries is the

development of better methods of diagnosis, treatment, and

ultimately, prevention of disease.

http://www.garvan.org.au