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Revisiting the stress recovery hypothesis: Differential associations of cortisol stress reactivity and recovery after acute psychosocial stress with markers of long-term stress and health

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Degering,  Magdalena
Research Group Social Stress and Family Health, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Linz,  Roman       
Research Group Social Stress and Family Health, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Puhlmann,  Lara M.       
Research Group Social Stress and Family Health, MPI for Human Cognitive and Brain Sciences, Max Planck Society;
Leibniz Institute for Resilience Research (LIR), Mainz, Germany;

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Engert,  Veronika       
Research Group Social Stress and Family Health, MPI for Human Cognitive and Brain Sciences, Max Planck Society;
Institute of Psychosocial Medicine, Psychotherapy, and Psycho-Oncology, Jena University Hospital, Germany;

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Citation

Degering, M., Linz, R., Puhlmann, L. M., Singer, T., & Engert, V. (2023). Revisiting the stress recovery hypothesis: Differential associations of cortisol stress reactivity and recovery after acute psychosocial stress with markers of long-term stress and health. Brain, Behavior, & Immunity - Health, 28: 100598. doi:10.1016/j.bbih.2023.100598.


Cite as: https://hdl.handle.net/21.11116/0000-000C-8A99-C
Abstract
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.