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Psychosocial stress is a ubiquitous phenomenon in our society. While acute stress responses are necessary and adaptive, excessive activation of neurobiological stress systems can predispose an individual to far-reaching adverse health outcomes. Living in a complex social environment, experiencing stress is not limited to challenges humans face individually. Possibly linked with our capacity for empathy, we also display the tendency to physiologically resonate with others’ stress responses. This recently identified source of stress raises many interesting questions. In comparison to the wealth of studies that have advanced our understanding of sharing others’ affective states, the physiological resonance of stress has only recently begun to be more closely investigated. The aim of the current paper is to review the existing literature surrounding the emerging area of “stress contagion”, “empathic stress” or “stress resonance”, as it has been variably called. After a brief introduction of the concepts of stress and empathy, we discuss several key studies that paved the way for the merging of empathy with the concept of physiological resonance. We then delineate recent empirical studies specifically focusing on the physiological resonance of stress. In the final section of this review, we highlight differences between these studies and discuss the variability in terminology used for what seems to be the same phenomenon. Lastly, potential health implications of chronic empathic stress are presented and possible mechanisms of physiological stress transmission are discussed.

This article seeks to address the prevailing issue of how to measure specific process components of psychobiological stress responses. Particularly the change of cortisol secretion due to stress exposure has been discussed as an endophenotype of many psychosomatic health outcomes. To assess its process components, a large variety of non-compartmental parameters (i.e., composite measures of substance concentrations at different points in time) like the area under the concentration-time curve (AUC) are utilized. However, a systematic evaluation and validation of these parameters based on a physiologically plausible model of cortisol secretion has not been performed so far. Thus, a population pharmacokinetic (mixed-effects SDE) model was developed and fitted to densely sampled salivary cortisol data of 10 males from Montreal, Canada, and sparsely sampled data of 200 mixed-sex participants from Dresden, Germany, who completed the Trier Social Stress Test (TSST). Besides the two major process components representing (1) stress-related cortisol secretion (reactivity) and (2) cortisol elimination (recovery), the model incorporates two additional, often disregarded components: (3) the secretory delay after stress onset, and (4) deviations from the projected steady-state concentration. The fitted model (R2 = 99%) was thereafter used to investigate the correlation structure of the four individually varying, and readily interpretable model parameters and eleven popular non-compartmental parameters. Based on these analyses, we recommend to use the minimum-maximum cortisol difference and the minimum concentration as proxy measures of reactivity and recovery, respectively. Finally, statistical power analyses of the reactivity-related sex effect illustrate the consequences of using impure non-compartmental measures of the different process components that underlie the cortisol stress response., Comment: 49 pages, 10 figures, 4 tables

The prevalence of psychosocial stress in Western societies is constantly on the rise. Its influence on social decision-making, however, remains poorly understood. Whereas, it is known that stress triggers psychological and physiological defense mechanisms, indications of such patterns in social decisions are ambivalent. We sought to elucidate the underlying mechanisms of stress-induced social decisions. We recruited 145 men, who were individually exposed to either a psychosocial stressor or a control condition, while primed with affiliation by interacting either with members of an in- or an out-group. We found that stressed participants were less trusting and engaged in less costly punishment compared to the non-stressed control group. Interacting with out-group members led to less reciprocity and more spiteful punishment. There was no interaction between stress and the affiliation conditions in any of the used social-decision-making paradigms. Lastly, while stress-reactive cortisol levels had no effect on trust behavior, higher baseline cortisol was correlated with greater trust. Our findings suggest that previous ambiguities in data reported on the influence of stress on social decisions, namely tend-and-befriend behavior may have arisen through critical social confounds in the induction of stress. When controlling for potential social confounds, stress may trigger fight-or-flight behavior as indicated by increased social anxiety. These findings highlight the considerable context-dependence of psychosocial stress and its effects on social behavior.

It is suggested that acute stress shifts behavioral control from goal-directed, model-based toward habitual, model-free strategies. Recent findings indicate that interindividual differences in the cortisol stress response influence model-based decision-making. Although not yet investigated in humans, animal studies show that chronic stress also shifts decision-making toward more habitual behavior. Here, we ask whether acute stress and individual vulnerability factors, such as stress reactivity and previous exposure to stressful life events, impact the balance between model-free and model-based control systems. To test this, 39 male participants (21-30 years old) were exposed to a potent psychosocial stressor (Trier Social Stress Test) and a control condition in a within-subjects design before they performed a sequential decision-making task which evaluates the balance between the two systems. Physiological and subjective stress reactivity was assessed before, during, and after acute stress exposure. By means of computational modeling, we demonstrate that interindividual variability in stress reactivity predicts impairments in model-based decision-making. Whereas acute psychosocial stress did not alter model-based behavioral control, we found chronic and acute stress to interact in their detrimental effect on decision-making: subjects with high but not low chronic stress levels as indicated by stressful life events exhibited reduced model-based control in response to acute psychosocial stress. These findings emphasize that stress reactivity and chronic stress play an important role in mediating the relationship between stress and decision-making. Our results might stimulate new insights into the interplay between chronic and acute stress, attenuated model-based control, and the pathogenesis of various psychiatric diseases.

Item does not contain fulltext Most psychosocial stress studies assess the overall cortisol response without further identifying the temporal dynamics within hormone levels. It has been shown, however, that the amplitude of anticipatory cortisol stress levels has a unique predictive value for psychological health. So far, no "best practice" in how to investigate the anticipatory cortisol stress response has emerged. The goal of the current research was to develop a protocol that would allow for a sensitive and easy-to-implement laboratory-based investigation into anticipatory cortisol stress levels. We initially tested 26 healthy men in either an anticipation- or stress-only condition of the Trier Social Stress Test (TSST) to map the distinct timelines of anticipatory and reactive cortisol release profiles (study 1). Subsequently, we administered the TSST to 50 healthy men such that the cortisol responses to anticipatory and reactive stress components could be dissociated (study 2). In both studies we sampled saliva cortisol at high frequency (at baseline, during 10min of anticipation and during and after 10min of acute stress) and the current mood state pre- and post-stress. We found anticipatory responder rates of 20% and 40%, with peak anticipatory cortisol levels between 14 and 20min after onset of anticipation. Visible changes in reactive cortisol levels occurred only after the termination of the acute stressor. We conclude that the best practice to detect a maximum number of anticipatory responders in the TSST would be to extend the anticipation phase to 15min. In doing so, the anticipatory cortisol peak could be captured at a time-point of the actual stressor that is uninfluenced by reactive cortisol levels. Overall, we could reveal several features of anticipatory responders. Most importantly, there was a positive correlation between anticipatory and reactive stress responses. There was no association between anticipatory cortisol and alpha-amylase as well as subjective-psychological stress responses. Future studies will have to determine whether the anticipatory responders differ with respect to various stress-sensitive parameters like sex, personality, psychological wellbeing or chronic stress.

Animal models and human studies using paradigms designed to stimulate endogenous oxytocin release suggest a stress-buffering role of oxytocin. We here examined the involvement of stress-induced peripheral oxytocin secretion in reactivity and recovery phases of the human psychosocial stress response. Healthy male and female participants (N=114) were subjected to a standardized laboratory stressor, the Trier Social Stress Test. In addition to plasma oxytocin, cortisol was assessed as a marker of hypothalamic-pituitary-adrenal (HPA-) axis activity, alpha-amylase and heart rate as markers of sympathetic activity, high frequency heart rate variability as a marker of vagal tone and self-rated anxiety as an indicator of subjective stress experience. On average, oxytocin levels increased by 51% following psychosocial stress. The stress-induced oxytocin secretion, however, did not reduce stress reactivity. To the contrary, higher oxytocin secretion was associated with greater cortisol reactivity and peak cortisol levels in both sexes. In the second phase of the stress response the opposite pattern was observed, with higher oxytocin secretion associated with faster vagal recovery. We suggest that after an early stage of oxytocin and HPA-axis co-activation, the stress-reducing action of oxytocin unfolds. Due to the time lag it manifests as a recovery-boosting rather than a reactivity-buffering effect. By reinforcing parasympathetic autonomic activity, specifically during stress recovery, oxytocin may provide an important protective function against the health-compromising effects of sustained stress.