Josephs Robert A, Cobb Adam R, Lancaster Cynthia L, Lee Han-Joo, Telch Michael J
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.
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.
Psychoneuroendocrinology. 2017 Apr;78:76-84. doi: 10.1016/j.psyneuen.2017.01.013. Epub 2017 Jan 19.
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) and testosterone (T) reactivity as moderators of war-zone stress evoked PTSD emergence in the war-zone.
U.S. soldiers (N=120) scheduled for deployment to Iraq completed pre-deployment measures of C and T stress reactivity to a CO inhalation challenge. Once deployed, monthly assessments of exposure to traumatic war-zone stressors and PTSD symptoms were collected via a web-based assessment system.
Cortisol hypo-reactivity potentiated the pathogenic impact of war-zone stressors only in soldiers for whom the CO 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.
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.
下丘脑 - 垂体 - 肾上腺轴（HPA）在应激相关的内环境稳定中起关键作用，这表明HPA轴失调参与创伤后应激障碍（PTSD）的发病机制，但大多数研究HPA轴指标与PTSD之间联系的研究均未得出明确结果。对于这种不一致，一种未经检验的解释是未能考虑肾上腺和性腺的同时影响。在此，我们测试了皮质醇（C）和睾酮（T）反应性作为战区应激诱发PTSD出现的调节因素的单一和交互作用。
计划部署到伊拉克的美国士兵（N = 120）在部署前完成了对吸入一氧化碳挑战的C和T应激反应的测量。一旦部署，通过基于网络的评估系统每月收集创伤性战区应激源暴露和PTSD症状的评估数据。
仅在一氧化碳挑战未使睾酮升高的士兵中，皮质醇低反应性增强了战区应激源的致病影响，这表明皮质醇和睾酮反应迟钝的双激素应激反应模式可能通过增强战区应激源的致病作用而增加PTSD出现的风险。
研究结果强调了在评估PTSD易感性时同时评估HPA和HPG应激反应性的实用性，并可能有助于为加强士兵对战区应激源的筛查和预防工作提供信息。
