Study Finds Gene Methylation a Marker of PTSD Vulnerability

from Psychiatric News Alert: The Voice of the American Psychiatric Association and the Psychiatric Community
This journal article may provide an important new piece to the puzzle of trying to understand PTSD vulnerability and resiliency factors. It could bring us closer to biological testing for PTSD vulnerability which could eventually be used to screen applicants for high PTSD risk occupations such as combat or first responders. Read this Psychiatric News Alert below. The link to the scientific article is Biological Psychiatry.

Researchers have long sought biological factors to help them understand the development of psychiatric illnesses, information that often depends on patient self-reports. Now a team of scientists has studied 122 combat veterans and found different epigenetic patterns in those who developed posttraumatic stress disorder (PTSD) and those who did not. 

Cytosine methylation of the NR3C1-F promoter was lower in in peripheral blood mononuclear cells among combat veterans with PTSD and was “inversely correlated with clinical markers and symptoms associated with PTSD,” said Rachel Yehuda, Ph.D. (shown above), a professor of psychiatry and neuroscience at Icahn School of Medicine at Mt. Sinai in New York, and colleagues.“NR3C1-1F promoter methylation was also associated with three functional measures of glucocorticoid activity that have been associated with PTSD in combat veterans,” they explained in their report published online February 19 in Biological Psychiatry.

These epigenetic changes may represent one mechanism by which environmental exposures, such as combat, lead to changes in neuroendocrine function and thus help differentiate combat-exposed veterans who are likely to develop PTSD from those who are not, concluded the researchers.

To read more about recent research on the biology of PTSD, see the Psychiatric News articles, “Fear Extinction Requires Multipronged Intervention” and “9/11 Tragedy Spurs Advances in PTSD Research.”