Danielson Carla Kmett, Hankin Benjamin L, Badanes Lisa S
Department of Psychiatry & Behavioral Sciences, 67 President Street, Medical University of South Carolina, Charleston, SC 29425, United States.
Department of Psychology, 2155 South Race Street, University of Denver, Denver, CO 80208, United States.
Psychoneuroendocrinology. 2015 Mar;53:170-8. doi: 10.1016/j.psyneuen.2015.01.001. Epub 2015 Jan 12.
Parental Posttraumatic Stress Disorder (PTSD), particularly maternal PTSD, confers risk for stress-related psychopathology among offspring. Altered hypothalamic-pituitary-adrenal (HPA) axis functioning is one mechanism proposed to explain transmission of this intergenerational risk. Investigation of this mechanism has been largely limited to general stress response (e.g., diurnal cortisol), rather than reactivity in response to an acute stressor. We examined cortisol reactivity in response to a laboratory stressor among offspring of mothers with a lifetime diagnosis of PTSD (n=36) and age- and gender- matched control offspring of mothers without PTSD (n=36). Youth (67% girls; mean age=11.4, SD=2.6) participated in a developmentally sensitive laboratory stressor and had salivary cortisol assessed five times (one pre-stress, one immediate post-stress, and three recovery measures, spaced 15min apart). Results were consistent with the hypothesis that offspring of mothers with PTSD would exhibit a dysregulated, blunted cortisol reactivity profile, and control offspring would display the expected adaptive peak in cortisol response to challenge profile. Findings were maintained after controlling for youth traumatic event history, physical anxiety symptoms, and depression, as well as maternal depression. This finding contributes to the existing literature indicating that attenuated HPA axis functioning, inclusive of hyposecretion of cortisol in response to acute stress, is robust among youth of mothers with PTSD. Future research is warranted in elucidating cortisol reactivity as a link between maternal PTSD and stress-related psychopathology vulnerability among offspring.
父母创伤后应激障碍(PTSD),尤其是母亲的PTSD,会使后代出现与压力相关的精神病理学风险。下丘脑-垂体-肾上腺(HPA)轴功能改变是被提出用以解释这种代际风险传递的一种机制。对这一机制的研究在很大程度上局限于一般应激反应(如昼夜皮质醇),而非对急性应激源的反应性。我们研究了终生诊断为PTSD的母亲的后代(n = 36)以及年龄和性别匹配的无PTSD母亲的对照后代(n = 36)在实验室应激源刺激下的皮质醇反应性。青少年(67%为女孩;平均年龄 = 11.4,标准差 = 2.6)参与了一项对发育敏感的实验室应激源测试,并对唾液皮质醇进行了五次评估(一次应激前、一次应激后即刻,以及三次恢复测量,间隔15分钟)。结果与以下假设一致,即患有PTSD的母亲的后代会表现出皮质醇反应性失调、迟钝的特征,而对照后代会在应对挑战时表现出预期的适应性皮质醇反应峰值。在控制了青少年的创伤事件史、身体焦虑症状、抑郁以及母亲的抑郁后,这些发现依然成立。这一发现为现有文献提供了补充,表明HPA轴功能减弱,包括对急性应激时皮质醇分泌不足,在患有PTSD的母亲的青少年后代中很常见。未来有必要进行研究以阐明皮质醇反应性作为母亲PTSD与后代压力相关精神病理学易感性之间的联系。