PTSD: The Serotonin System Influences Vulnerability and Treatment
Philadelphia, PA, 17 June, 2010 - There is a great deal of interest in factors that contribute to the vulnerability to developing post-traumatic stress disorder, or PTSD. One factor that appears to contribute to the heritable vulnerability to PTSD is a variation in the gene that codes for the serotonin transporter, also known as the serotonin uptake site.
Having a shorter version of the serotonin transporter gene appears to increase one’s risk for depression and PTSD after exposure to extremely stressful situations. This same gene variant increases the activation of an emotion control center in the brain, the amygdala.
More recently, scientists began focusing on factors contributing to resilience to the impact of stress exposure. Could the same gene that contributes to the vulnerability to PTSD be implicated in the recovery from PTSD?
In their new study appearing in Biological Psychiatry, Dr. Richard Bryant and colleagues assessed whether serotonin transporter genotype predicted a change in patients’ PTSD severity following treatment. Specifically, patients with PTSD were classified according to their genotype, and they received eight weeks of cognitive behavior therapy. Approximately one-third of patients do not respond to this treatment, and this study has now demonstrated that there may be a genetic basis for not responding to this therapy.
Dr. Bryant explained: “Patients with PTSD who carried the short allele of the serotonin transporter gene promoter responded more poorly to treatment than other PTSD patients. This study highlights that the serotonin system is implicated in responding to cognitive behavior therapy.”
The recent focus on personalized medicine has emphasized the impact of variation in genes that influence the responses to medications. This study supports the reasoning that genetic variation would also influence the response to psychotherapeutic or rehabilitative treatments.
Dr. John Krystal, Editor of Biological Psychiatry, noted, “While this study identifies a potential predictor of poor treatment response, it also may help to identify groups of individuals who respond relatively favorably to treatment. It is interesting this ‘good outcome’ group is a group that is also more resilient, i.e., less likely to develop PTSD or depression, after stress.”
Although further research is necessary, this initial finding indicates that PTSD treatments may need to be modified to accommodate patients’ genetic profiles.
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Notes to EditorsThe article is “Preliminary Evidence of the Short Allele of the Serotonin Transporter Gene Predicting Poor Response to Cognitive Behavior Therapy in Posttraumatic Stress Disorder” by Richard A. Bryant, Kim L. Felmingham, Erin M. Falconer, Laarnie Pe Benito, Carol Dobson-Stone, Kerrie D. Pierce, and Peter R. Schofield. Bryant, Felmingham, Falconer, and Pe Benito are affiliated with the Brain Dynamics Centre, Westmead Millennium Institute, Westmead Hospital, Westmead, Australia. Bryant, Felmingham, and Falconer are also from the School of Psychology, University of New South Wales, Sydney, Australia. Dobson-Stone, Pierce, and Schofield are with the Prince of Wales Medical Research Institute, Randwick, Australia. Dobson-Stone and Schofield are also affiliated with the School of Medical Science, University of New South Wales, Sydney, Australia. The article appears in Biological Psychiatry, Volume 67, Issue 12 (June 15, 2010), published by Elsevier.
The authors’ disclosures of financial and conflicts of interests are available in the article.
John H. Krystal, M.D. is Chairman of the Department of Psychiatry at the Yale University School of Medicine and a research psychiatrist at the VA Connecticut Healthcare System. His disclosures of financial and conflicts of interests are available here. Full text of the article mentioned above is available upon request. Contact Maureen Hunter at firstname.lastname@example.org to obtain a copy or to schedule an interview.
About Biological Psychiatry This international rapid-publication journal is the official journal of the Society of Biological Psychiatry. It covers a broad range of topics in psychiatric neuroscience and therapeutics. Both basic and clinical contributions are encouraged from all disciplines and research areas relevant to the pathophysiology and treatment of major neuropsychiatric disorders. Full-length and Brief Reports of novel results, Commentaries, Case Studies of unusual significance, and Correspondence and Comments judged to be of high impact to the field are published, particularly those addressing genetic and environmental risk factors, neural circuitry and neurochemistry, and important new therapeutic approaches. Concise Reviews and Editorials that focus on topics of current research and interest are also published rapidly.
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