Do genes play a role in ptsd? study of rwanda genocide survivors suggests yes

Do genes play a role in ptsd? study of rwanda genocide survivors suggests yes

A study of Rwandan Genocide survivors, some with and some without post traumatic stress disorder or PTSD, suggests that genetic factors influence the relationship between a person's "traumatic load", or the number of traumatic events he or she experiences, and their likelihood of developing PTSD.

You can read about the study by Dr Iris-Tatjana Kolassa, from the department of Clinical Psychology and Neuropsychology at the University of Konstanz in Germany, and other colleagues in Germany and Switzerland, in the 15 February print issue of the Elsevier journal Biological Psychiatry.

Although there is no exact official figure, estimates suggest that 1 in 5 of the population of Rwanda, or up to 1 million people lost their lives in the 1994 genocide, which occurred over about 100 days.

While it is not surprising that many survivors developed PTSD, an anxiety disorder that can occur when we experience or witness a life-threatening event such as abuse, natural disaster and war, not all of them did, and why that should be so is not clear, so Kolassa and colleagues decided to look for some answers by applying their knowledge of molecular genetics.

There is a general consensus among PTSD researchers that the greater a person's traumatic load, the higher the chance they will develop PTSD, but Kolassa and colleagues wanted to see if there is a genetic influence too.

For the study, they examined samples and medical records from 424 Rwanda genocide survivors living in the Nakivale refugee camp in southwestern Uganda, some with and some without PTSD.

As anticipated, they found a "dose-response" relationship between traumatic load and prevalence of lifetime PTSD, ie the higher the traumatic load, the higher the chance of developing PTSD.

But they also found something else: a variant of a gene that codes for the enzyme catechol-O-methyltransferase (COMT) appears to play a role in this relationship. (The variant is called the COMT Val158Met polymorphism and has already been implicated in previous studies that linked it to fear extinction.)

Carriers of the Met/Met version of the gene (ie they inherited Met from both parents) showed a high risk of developing PTSD independently of their traumatic load, whereas carriers who had at least one Val version of the gene, showed the expected dose-response relationship between traumatic load and risk of developing PTSD.

The COMT enzyme metabolizes the neurotransmitters norepinephrine and dopamine which are released during stress, and the researchers suggested that the Met/Met carriers had substantially lower activity of COMT enzyme, leaving them more vulnerable to PTSD independently of traumatic load.

Dr. John Krystal who edits Biological Psychiatry said he hoped molecular genetics studies like this will help us learn more about resilience so we can help people cope with stress at psychological, behavioral, and biological levels.

"We also would like a biological test to help us to identify people who are most vulnerable to the negative effects of stress so that we could target supportive services to these people," he added.

Kolassa was more cautious: she said we have to deal with many unanswered technical and clinical questions before we can start thinking about developing molecular genetic tests that predict patterns of stress response.

But she said she expects one day molecular genetics will play a key role in helping to prevent and treat PTSD.

"The Risk of Posttraumatic Stress Disorder After Trauma Depends on Traumatic Load and the Catechol-O-Methyltransferase Val158Met Polymorphism."

Iris-Tatjana Kolassa, Stephan Kolassa, Verena Ertl, Andreas Papassotiropoulos, Dominique J.-F. De Quervain.

Biological Psychiatry, Volume 67, Issue 4, 15 February 2010, Pages 304-308


Sources: Elsevier.

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Section Issues On Medicine: Psychiatry