Miller Gregory E, Chen Edith, Zhou Eric S
Department of Psychology, University of British Columbia (UBC), Vancouver, BC, Canada.
Psychol Bull. 2007 Jan;133(1):25-45. doi: 10.1037/0033-2909.133.1.25.
The notion that chronic stress fosters disease by activating the hypothalamic-pituitary-adrenocortical (HPA) axis is featured prominently in many theories. The research linking chronic stress and HPA function is contradictory, however, with some studies reporting increased activation, and others reporting the opposite. This meta-analysis showed that much of the variability is attributable to stressor and person features. Timing is an especially critical element, as hormonal activity is elevated at stressor onset but reduces as time passes. Stressors that threaten physical integrity, involve trauma, and are uncontrollable elicit a high, flat diurnal profile of cortisol secretion. Finally, HPA activity is shaped by a person's response to the situation; it increases with subjective distress but is lower in persons with posttraumatic stress disorder.
慢性应激通过激活下丘脑 - 垂体 - 肾上腺皮质（HPA）轴促进疾病发生的观点在许多理论中占据显著地位。然而，将慢性应激与HPA功能联系起来的研究结果相互矛盾，一些研究报告激活增加，而另一些则报告相反情况。这项荟萃分析表明，许多变异性可归因于应激源和个体特征。时间是一个特别关键的因素，因为激素活动在应激源出现时升高，但随着时间推移会降低。威胁身体完整性、涉及创伤且无法控制的应激源会引发皮质醇分泌的高而平稳的昼夜模式。最后，HPA活动受个体对情境的反应影响；它随主观痛苦增加，但在患有创伤后应激障碍的个体中较低。
