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Stress May Cause Illness By Changing Genes

A new study suggests that acute psychological stress, which is known to increase the risk of physical and mental illness, may do so by altering the control of genes.

A report on the study, thought to be the first to show that stress alters the methylation of DNA and thus the activity of certain genes, appeared online in the journal Translational Psychiatry on 14 August.

Researchers from the Ruhr-Universitšt Bochum (RUB), together with colleagues from Basel, Trier and London, looked at gene segments that are known to be involved with the control of biological stress.

One of the most important discoveries in genetics is epigenetics, or the "second code" that regulates gene activity.

Research is beginning to show that epigenetic changes could be involved in the development of some chronic diseases such as cancer or depression.

While the genome, the genetic code or DNA, for making a human being is more or less fixed once the sperm fertilizes the egg, it is the epigenome that decides how the blueprint is interpreted.

Think of the genome as being the construction manual for making all the proteins the body needs, and the epigenome as the construction or maintenance guy reading the manual: sometimes he will have off days when he is tired and makes mistakes, or just interprets the instructions differently.

Cells function by making proteins. Which proteins they produce depends on the cell type, which is set by genes, and the environment, which influences how the epigenome reads the genes. One way this happens is via methyl groups (CH3) that attach to sections of DNA: these can remain in place for quite a while, even after the cell divides.

Previous studies have shown that psychological trauma in early life and highly stressful events are associated with long-term methylation changes to DNA.

But what the researchers in this study wanted to find out was whether this also happens after acute psychological stress: for instance such as that experienced during a job interview.

For their study, they looked at two genes: one for the oxytocin receptor (OXTR), and one for the nerve growth factor Brain-Derived Neurotrophic Factor (BDNF).

The OXTR is a docking site in the central nervous system for the neurotransmitter oxytocin, a chemical messenger that has been dubbed the "love" or "trust hormone" or "anti-stress hormone".

BDNF plays an important role in the development and cross-linking of brain cells.

The researchers invited 76 participants in their sixties to undergo two types of stressful event: one was to to take part in a mock job interview, and the other was to solve arithmetic problems under observation. Both these tests are commonly used to produce stress under lab conditions.

The participants gave blood samples before the tests, and also twice afterwards: one ten minutes after (post-test), and another 1.5 hours after (follow-up). From these the researchers could measure the amount of DNA methylation in the two genes.

They found that the BDNF gene remained unaffected by any of the stress tests.

But the OXTR gene showed methylation changes. There was an increase in methylation in a section of the OXTR gene in the post-test measure: this suggests the cells formed fewer receptors.

And then in the follow-up measure 1.5 hours after the test, methylation in the OXTR gene dipped below the pre-test level: this suggests the cells produced too many receptors.

The researchers conclude:

"The results suggest a dynamic regulation of DNA methylation in OXTR - which may in part reflect changes in blood cell composition - but not BDNF after acute psychosocial stress."

Senior and corresponding author Gunther Meinlschmidt, is professor and Head of the Research Department of Psychobiology, Psychosomatics and Psychotherapy at the LWL University Hospital in RUB. He told the press the study shows:

"Epigenetic changes may well be an important link between stress and chronic diseases."

"We hope to identify more complex epigenetic stress patterns in future and thus to be able to determine the associated risk of disease. This could provide information on new approaches to treatment and prevention," he added.

Funds from the German Research Foundation and the Swiss National Science Foundation helped pay for the study.

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