20 April 2009

Its Not 'All in your Head'


Child abuse has been found to cause epigenetic changes to the victim. In the study by scientists from the Singapore Institute for Clinical Sciences, the Douglas Mental Health University Institute and the McGill University, researchers analysed brain samples from three groups of deceased: suicide victims with a history of child abuse, suicide victims with no history of child abuse and people who had died of other causes (control group). The researchers studied samples from the hippocampus, a region involved in stress response regulation.

It was found that in the brain samples of the suicide victims with a history of child abuse, there was a difference in the expression of the NC3R1 gene, as compared to the other two groups of people. This difference was not a genetic change, but rather an epigenetic one. Epigenetics refers to the expression of genes by DNA methylation. Epigenetics can be changed by the environment, particularly in the more vulnerable stages of development, such as in utero and during early childhood.

The NC3R1 gene affects the part of the brain that deals with stress. The hypothalamic-pituitary-adrenal (HPA) function is a response to stress that increases the risk of suicide. This is where the researchers found the differing epigenetic expression in the suicide victims who suffered child abuse. They have also found that there are treatments that reverse the epigenetic changes by DNA methylation.

This research is a step forward in understanding the effect that abuse and other situations have on children at a biological level. It has far-reaching consequences. Maybe one day scientists will be able to reverse the biological effects of abuse or other adverse incidents. As co-investigator Moshe Szyf said, "Now we are starting to understand the biological implications of such psychological abuse."

By 42028947

References:

Paddock, Catharine. PhD. "Child Abuse Causes Lifelong Changes To DNA Expression And Brain." Medical News Today: Health News. 23 Feb. 2009. 14 Apr. 2009 .

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