Degering Magdalena, Linz Roman, Puhlmann Lara M C, Singer Tania, Engert Veronika
Independent Research Group "Social Stress and Family Health", Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany.
Leibniz Institute for Resilience Research (LIR), Mainz, Germany.
Brain Behav Immun Health. 2023 Jan 31;28:100598. doi: 10.1016/j.bbih.2023.100598. eCollection 2023 Mar.
Exposure to excessive and long-term stress may result in dysregulation of the stress system, including the acute stress response. In particular, failure to downregulate stress-related reactivity may lead to prolonged stress responses and the accumulation of allostatic load. However, the contribution of altered acute cortisol recovery to chronic stress and associated health impairments has often been neglected. Addressing this lack of research, we explored whether recovery from - more so than reactivity to - acute stress captures the basal stress load of an individual. Using Piecewise Growth Curve Models with Landmark Registration, we analyzed cortisol reactivity and recovery slopes of 130 healthy participants exposed to a standardized psychosocial laboratory stressor. Reactivity and recovery were predicted by measures indicative of long-term stress and its downstream effects, including self-report questionnaires, diurnal cortisol indices [cortisol awakening response (CAR); diurnal cortisol slope], markers of pro-inflammatory activity (interleukin-6; high-sensitive C-reactive protein), and hippocampal volume (HCV). Among these measures, only an increased CAR was specifically and consistently associated with relatively impaired recovery. Since the CAR represents the physiological enhancement needed to meet the anticipated demands of the forthcoming day, this finding may highlight the contribution of cognitive processes in determining both CAR and acute stress recovery. Furthermore, greater cortisol reactivity covaried with smaller HCV, showing that increased acute reactivity translates to health-relevant downstream effects. The lack of further associations between long-term and acute stress measures may arise from biases in self-reported chronic stress and the rigorously health-screened study sample. Overall, our findings suggest that while cortisol stress recovery might not supersede reactivity as an indicator of the long-term stress load or associated health effects, recovery and reactivity have differential utility in describing individuals' allostatic states.
长期暴露于过度压力之下可能会导致应激系统失调，包括急性应激反应。特别是，无法下调与压力相关的反应性可能会导致应激反应持续时间延长和负荷过重。然而，急性皮质醇恢复改变对慢性压力及相关健康损害的影响常常被忽视。为填补这一研究空白，我们探究了急性应激恢复（而非应激反应性）是否能反映个体的基础应激负荷。我们使用带有地标配准的分段生长曲线模型，分析了130名健康参与者在接触标准化社会心理实验室应激源时的皮质醇反应性和恢复斜率。通过一系列指标来预测反应性和恢复情况，这些指标包括表明长期压力及其下游效应的测量值，如自我报告问卷、昼夜皮质醇指标[皮质醇觉醒反应（CAR）；昼夜皮质醇斜率]、促炎活性标志物（白细胞介素-6；高敏C反应蛋白）以及海马体积（HCV）。在这些测量指标中，只有CAR升高与恢复相对受损存在特异性且一致的关联。由于CAR代表了应对即将到来一天预期需求所需的生理增强，这一发现可能突出了认知过程在决定CAR和急性应激恢复方面的作用。此外，皮质醇反应性越高，HCV越小，这表明急性反应性增加会转化为与健康相关的下游效应。长期应激测量指标与急性应激测量指标之间缺乏进一步关联，可能是由于自我报告的慢性应激存在偏差以及研究样本经过严格的健康筛查。总体而言，我们的研究结果表明，虽然皮质醇应激恢复可能无法取代反应性，作为长期应激负荷或相关健康影响的指标，但恢复和反应性在描述个体的负荷状态方面具有不同的作用。
