Life stress and cortisol reactivity: An exploratory analysis of the effects of stress exposure across life on HPA-axis functioning.
Life stress and cortisol reactivity: An exploratory analysis of the effects of stress exposure across life on HPA-axis functioning.
复制标题
生活压力和皮质醇反应性：对生活中压力暴露对HPA轴功能影响的探索性分析。
DOI：
10.1017/s0954579419001779
复制
发表时间：
2021-03
影响因子：
3.3
通讯作者：
Simpson JA
中科院分区：
文献类型：
--
作者：
Young ES;Doom JR;Farrell AK;Carlson EA;Englund MM;Miller GE;Gunnar MR;Roisman GI;Simpson JA
应激经历影响生物应激系统，如下丘脑-垂体-肾上腺（HPA）轴。生活压力可能会改变下丘脑轴的调节，并与较差的身心健康有关。然而，对于不同发育时期遇到的应激源对成年期急性应激反应的相对影响，我们所知甚少。在这项研究中，我们利用一个高风险出生队列（N = 112） 37年的纵向数据，探讨了应激暴露对皮质醇反应性的影响的三种模型。累积压力模型表明，在整个生命周期中积累的压力会导致反应性失调，而生物嵌入模型则暗示幼儿期是一个关键时期。敏化模型假设失调只会发生在儿童早期和同时的压力很高的时候。所有的模型都预测了反应性的改变，但没有预测其确切形式。我们发现了累积效应和生物嵌入效应的支持。然而，当相互比较时，早期生活压力预示着37岁时比累积生活压力更迟钝的皮质醇反应。另外的分析显示，童年中期的压力暴露也预示着更迟钝的皮质醇反应。
Stressful experiences affect biological stress systems, such as the hypothalamic–pituitary–adrenal (HPA) axis. Life stress can potentially alter regulation of the HPA axis and has been associated with poorer physical and mental health. Little, however, is known about the relative influence of stressors that are encountered at different developmental periods on acute stress reactions in adulthood. In this study, we explored three models of the influence of stress exposure on cortisol reactivity to a modified version of the Trier Social Stress Test (TSST) by leveraging 37 years of longitudinal data in a high-risk birth cohort (N = 112). The cumulative stress model suggests that accumulated stress across the lifespan leads to dysregulated reactivity, whereas the biological embedding model implicates early childhood as a critical period. The sensitization model assumes that dysregulation should only occur when stress is high in both early childhood and concurrently. All of the models predicted altered reactivity, but do not anticipate its exact form. We found support for both cumulative and biological embedding effects. However, when pitted against each other, early life stress predicted more blunted cortisol responses at age 37 over and above cumulative life stress. Additional analyses revealed that stress exposure in middle childhood also predicted more blunted cortisol reactivity.