Not everyone who has personally experienced, or has been exposed to, severe trauma develops posttraumatic stress disorder (PTSD). The risk-resilience equation is complex and, as we are becoming increasingly aware, includes both genetic predictors and environmental stressors, starting in early childhood. For example, as Binder and colleagues (
1) first showed, FKBP5, a gene influencing activity of the hypothalamic-pituitary-adrenal axis, together with exposure to childhood trauma but not adult stressors, predicted the development of PTSD in a low-income, urban African American sample. There is much to be understood about the etiology of PTSD and equally there is much to be learned about developing new treatment options and improving the rates of response to the current first-line treatment for PTSD: cognitive behavioral therapy (CBT).
- Binder E.B.
- Bradley R.G.
- Liu W.
- Epstein M.P.
- Deveau T.C.
- Mercer K.B.
- et al.
Association of FKBP5 polymorphisms and childhood abuse with risk of posttraumatic stress disorder symptoms in adults.
JAMA. 2008; 299: 1291-1305
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- Association of FKBP5 polymorphisms and childhood abuse with risk of posttraumatic stress disorder symptoms in adults.JAMA. 2008; 299: 1291-1305
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Accepted: April 9, 2013
Received: March 28, 2013
Published by Elsevier Inc.
ScienceDirectAccess this article on ScienceDirect
- The Brain-Derived Neurotrophic Factor Val66Met Polymorphism Predicts Response to Exposure Therapy in Posttraumatic Stress DisorderBiological PsychiatryVol. 73Issue 11
- PreviewThe most effective treatment for posttraumatic stress disorder (PTSD) is exposure therapy, which aims to facilitate extinction of conditioned fear. Recent evidence suggests that brain-derived neurotrophic factor (BDNF) facilitates extinction learning. This study assessed whether the Met-66 allele of BDNF, which results in lower activity-dependent secretion, predicts poor response to exposure therapy in PTSD.