Dual-hormone stress reactivity predicts downstream war-zone stress-evoked PTSD

Robert A Josephs; Adam R Cobb; Cynthia L Lancaster; Han-Joo Lee; Michael J Telch

doi:10.1016/j.psyneuen.2017.01.013

Dual-hormone stress reactivity predicts downstream war-zone stress-evoked PTSD

Psychoneuroendocrinology. 2017 Apr:78:76-84. doi: 10.1016/j.psyneuen.2017.01.013. Epub 2017 Jan 19.

Authors

Robert A Josephs¹, Adam R Cobb², Cynthia L Lancaster², Han-Joo Lee³, Michael J Telch⁴

Affiliations

¹ Department of Psychology, University of Texas at Austin, Austin, TX 78712, USA; Institute for Mental Health Research, University of Texas at Austin, Austin, TX 78712, USA; Clinical Neuroendocrinology Laboratory, University of Texas at Austin, Austin, TX 78712, USA.
² Department of Psychology, University of Texas at Austin, Austin, TX 78712, USA; Institute for Mental Health Research, University of Texas at Austin, Austin, TX 78712, USA.
³ Department of Psychology, University of Texas at Austin, Austin, TX 78712, USA; Laboratory for the Study of Anxiety Disorders, University of Texas at Austin, Austin, TX 78712, USA.
⁴ Department of Psychology, University of Texas at Austin, Austin, TX 78712, USA; Institute for Mental Health Research, University of Texas at Austin, Austin, TX 78712, USA; Laboratory for the Study of Anxiety Disorders, University of Texas at Austin, Austin, TX 78712, USA. Electronic address: Telch@austin.utexas.edu.

PMID: 28178580
DOI: 10.1016/j.psyneuen.2017.01.013

Abstract

Background: The crucial role of the hypothalamic-pituitary-adrenal axis (HPA) in stress-related homeostasis suggests dysregulated HPA involvement in the pathogenesis of post-traumatic stress disorder (PTSD), yet most studies examining linkages between HPA axis measures and PTSD have yielded null findings. One untested explanation for this inconsistency is a failure to account for simultaneous adrenal and gonadal influence. Here we tested the singular and interactive effects of cortisol (C_R) and testosterone (T_R) reactivity as moderators of war-zone stress evoked PTSD emergence in the war-zone.

Methods: U.S. soldiers (N=120) scheduled for deployment to Iraq completed pre-deployment measures of C_R and T_R stress reactivity to a CO₂ inhalation challenge. Once deployed, monthly assessments of exposure to traumatic war-zone stressors and PTSD symptoms were collected via a web-based assessment system.

Results: Cortisol hypo-reactivity potentiated the pathogenic impact of war-zone stressors only in soldiers for whom the CO₂ challenge did not elevate testosterone, suggesting that the dual hormone stress reactivity profile of blunted cortisol and testosterone may confer increased risk for PTSD emergence by potentiating the pathogenic effects of war-zone stressors.

Conclusions: Findings underscore the utility of assessing both HPA and HPG stress reactivity when assessing PTSD vulnerability and may help inform efforts for enhanced soldier screening and inoculation to war-zone stressors.

Keywords: Cortisol; Military; PTSD; Stress-reactivity; Testosterone; War-zone assessment.

Publication types

Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

Adult
Female
Humans
Hydrocortisone / analysis*
Hypothalamo-Hypophyseal System / physiopathology*
Iraq War, 2003-2011
Male
Military Personnel*
Pituitary-Adrenal System / physiopathology*
Saliva / chemistry
Stress Disorders, Post-Traumatic / diagnosis*
Stress Disorders, Post-Traumatic / physiopathology
Testosterone / analysis*

Substances

Testosterone
Hydrocortisone