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August 7, 2009 at 5:12 am #1242Pat QuigleyMember
doi:10.1016/j.psyneuen.2007.04.001
Copyright © 2007 Elsevier Ltd All rights reserved.
Changes in cortisol and DHEA plasma levels after psychotherapy for PTSD
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Miranda Olffa, , , Giel-Jan de Vriesa, Yener Güzelcana, b, Johanna Assiesc and Berthold P.R. Gersonsa
aCenter for Psychological Trauma, Department of Psychiatry, Academic Medical Center/de Meren, University of Amsterdam, Tafelbergweg 25, 1105 BC Amsterdam, The Netherlands
bMental Health Care Department of ‘s Hertogenbosch and Department of Psychiatry, Academic Medical Center, University of Amsterdam, , Amsterdam, The Netherlands
cDepartment of Psychiatry, Academic Medical Center/ de Meren, Amsterdam, The Netherlands
Received 15 November 2006; revised 30 March 2007; accepted 4 April 2007. Available online 13 June 2007.
Summary
Post-traumatic stress disorder (PTSD) has been associated with dysregulation of the neuroendocrine system. In this study we examine the effects of psychotherapy in 21 PTSD patients, with and without coexisting depression, on the levels of six stress-related hormones: cortisol, dehydroepiandrosterone (DHEA), and dehydroepiandrosterone-sulfate (DHEA-S), prolactin, thyrotropin (TSH) and free thyroxin (fT4). The results show that after brief eclectic psychotherapy (BEP) significant changes occurred in levels of cortisol and DHEA. Responders showed an increase in cortisol and DHEA levels, while in non-responders both hormone levels decreased. Differences were only found after controlling for depressive symptoms. In conclusion, effective psychotherapy for PTSD may alter dysregulations in the Hypothalamus–pituitary–adrenal (HPA)-axis, but comorbid depressive symptoms should be taken into account.Keywords: Post-traumatic stress disorder; Psychotherapy; Hypothalamus–pituitary–adrenal (HPA) axis; Hypothalamus–pituitary–thyroid (HPT) axis; Cortisol; TSH; Depression
Article Outline
1. Introduction
2. Methods
2.1. Subjects
2.2. Psychological instruments
2.3. Hormones
2.4. Psychotherapy
2.5. Statistical analysis
3. Results
3.1. Subjects
3.2. Change in clinical measures
3.3. Change in hormone levels
3.3.1. Cortisol
3.3.2. DHEA
4. Discussion
Role of the funding sources
Conflict of interest
Contributors
Acknowledgements
References
Table 1.
Sample description (N=21).View Within Article
Table 2.
Clinical variables before and after treatment.View Within Article
Table 3.
Untransformed mean hormone levels and standard deviations before and after treatment together with effect sizes (Cohen’s d).View Within Article
Table 4.
Effect of time, response to treatment and depressive symptoms on six HPA- and HPT-axis hormone levels.η2: Partial squared η; Covariates added to the model to control for background variables: cortisol: no covariates; TSH: body mass index (r=0.40); fT4: body mass index (r=−.32); Prolactin: no covariates; DHEA: age (r=0.38); DHEA-S: age (r=0.45).
†p<0.05.
‡p<0.01.
View Within Article
Parts of this paper have been presented at the 20th Annual Meeting of International Society for Traumatic Stress Studies. New Orleans, 2004.
Corresponding author. Tel.: +31 20 5662356; fax: +31 20 6919019.
Psychoneuroendocrinology
Volume 32, Issue 6, July 2007, Pages 619-626 -
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