�By doing tests on mice federal official on a calorie restricted diet, US researchers take in discovered that ghrelin, a hormone that increases when people
don't eat, may defend against symptoms of depression or anxiety brought on by stress.
The research is the work of scientists lED by aged author Dr Jeffrey Zigman, assistant prof of inner medicine and psychiatry at the University of Texas (UT) Southwestern Medical Center in Dallas. It was published on-line on 15th June
2008 in the journal Nature Neuroscience.
"Our findings in mice suggest that chronic stress causes ghrelin levels to go up and that behaviors associated with depression and anxiety decrease
when ghrelin levels rise," aforesaid Zigman, adding that:
"An unfortunate side result, however, is increased food intake and body weight."
Lead author and instructor of psychiatry at UT Southwestern, Dr Michael Lutter, said:
"Our findings support the idea that these hunger hormones don't do just unitary thing; quite, they align an entire behavioral response to tenseness and
in all probability affect modality, stress and energy levels."
Scientists like Zigman and colleagues already knew that fasting causes the gut to produce ghrelin, which is involved in sending hunger signals to the
mental capacity, and this has lED them to suggest blocking ghrelin as an approach to weight control.
But this new subject shows that if you do that, it could interfere with the body's natural way of dealing with anxiety and natural depression.
For the study, Zigman and his team commit "wild type" (ie not genetically altered in whatever way) mice on a calorie restricted diet for 10 days, which lED to a
four-fold increase in their ghrelin levels. Stress tests involving mazes and forced swims showed that the calorie restricted mice had reduced
symptoms of anxiety and depression compared to control couterparts that had been allowed unrestricted access to food.
The researchers then bred genetically neutered mice whose bodies did not respond to ghrelin and federal official them a calorie restricted diet as well, but under
tenseness tests their depression and anxiety symptoms stayed high; there was no anti-depression or anti-anxiety effect as there had been in the dotty type
mice on the low nutritionist's calorie diet.
Finally, Zigman and colleagues did a third prove, this time to explore social tenseness where normal wild type and genetically altered mice were exposed to aggressive "bully" mice every mean solar day (an access often used to study parallels of depression in humans).
Under stress atmospheric condition both types of mice had raised ghrelin that lasted for up to four weeks after existence bullied for the final time, only the mice that had been genetically altered not to respond to gherlin showed more social shunning behaviour and ate less than the non-altered mice, suggesting they had more depression symptoms.
A possible explanation could be the survival reward that is gained from such an effect over countless generations of evolution where the main
priority is getting enough nutrient to avoid starving to death. Zigman suggested that hunter gatherers needed to remain becalm in order of magnitude to hunt
successfully (or they could end being someone else's meal). Perhaps ghrelin induced by hunger leading to anti-anxiety gave them the edge over
their competitors.
These findings might also explain what happens in conditions like anorexia nervosa aforementioned Lutter:
"We're very interested to see whether ghrelin discourse could help people with anorexia nervosa, with the idea organism that in a certain population,
calorie restriction and weight release could make an antidepressant effect and could be reinforcing for this illness."
Zigman, Lutter and colleagues bob Hope to continue with their research and look at the areas of the brain where ghrelin could be causation these
antidepressant-like effects.
"The orexigenic hormone ghrelin defends against depressive symptoms of continuing stress."
Michael Lutter, Ichiro Sakata, Sherri Osborne-Lawrence, Sherry A Rovinsky, Jason G Anderson, Saendy Jung, Shari Birnbaum, Masashi Yanagisawa,
Joel K Elmquist, Eric J Nestler & Jeffrey M Zigman
Nature Neuroscience Published online 15 June 2008.
DOI: 10.1038/nn.2139
Click here for
Abstract.
Sources: Nature Neuroscience press liberation and abstract.
Written by: Catharine Paddock, PhD
Copyright: Medical News Today
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