This meta-analysis reviews 208 laboratory studies of acute psychological stressors and tests a theoretical model delineating conditions capable of eliciting cortisol responses. Psychological stressors increased cortisol levels; however, effects varied widely across tasks. Consistent with the theoretical model, motivated performance tasks elicited cortisol responses if they were uncontrollable or characterized by social-evaluative threat (task performance could be negatively judged by others), when methodological factors and other stressor characteristics were controlled for. Tasks containing both uncontrollable and social-evaluative elements were associated with the largest cortisol and adrenocorticotropin hormone changes and the longest times to recovery. These findings are consistent with the animal literature on the physiological effects of uncontrollable social threat and contradict the belief that cortisol is responsive to all types of stressors.

http://anthro.vancouver.wsu.edu/media/Course_files/anth-260-edward-h-hagen/acute-stressors-and-cortisol-responses-a-theoretical-integration-and-synthesis-of-laboratory-research-1.pdf

Acute stressors and cortisol responses: a theoretical integration and synthesis of laboratory research.

Moral emotions represent a key element of our human moral apparatus, influencing the link between moral standards and moral behavior This chapter reviews current theory and research on moral emotions We first focus on a triad of negatively valenced “self-conscious” emotions—shame, guilt, and embarrassment As in previous decades, much research remains focused on shame and guilt We review current thinking on the distinction between shame and guilt, and the relative advantages and disadvantages of these two moral emotions Several new areas of research are highlighted: research on the domain-specific phenomenon of body shame, styles of coping with shame, psychobiological aspects of shame, the link between childhood abuse and later proneness to shame, and the phenomena of vicarious or “collective” experiences of shame and guilt In recent years, the concept of moral emotions has been expanded to include several positive emotions—elevation, gratitude, and the sometimes morally relevant experience o

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Moral emotions and moral behavior

Major life stressors, especially those involving interpersonal stress and social rejection, are among the strongest proximal risk factors for depression. In this review, we propose a biologically plausible, multilevel theory that describes neural, physiologic, molecular, and genomic mechanisms that link experiences of social-environmental stress with internal biological processes that drive depression pathogenesis. Central to this social signal transduction theory of depression is the hypothesis that experiences of social threat and adversity up-regulate components of the immune system involved in inflammation. The key mediators of this response, called proinflammatory cytokines, can in turn elicit profound changes in behavior, which include the initiation of depressive symptoms such as sad mood, anhedonia, fatigue, psychomotor retardation, and social-behavioral withdrawal. This highly conserved biological response to adversity is critical for survival during times of actual physical threat or injury. However, this response can also be activated by modern-day social, symbolic, or imagined threats, leading to an increasingly proinflammatory phenotype that may be a key phenomenon driving depression pathogenesis and recurrence, as well as the overlap of depression with several somatic conditions including asthma, rheumatoid arthritis, chronic pain, metabolic syndrome, cardiovascular disease, obesity, and neurodegeneration. Insights from this theory may thus shed light on several important questions including how depression develops, why it frequently recurs, why it is strongly predicted by early life stress, and why it often co-occurs with symptoms of anxiety and with certain physical disease conditions. This work may also suggest new opportunities for preventing and treating depression by targeting inflammation.

/pdf/from-stress-to-inflammation-and-major-depressive-disorder-a-2ftmq57sq0.pdf

From Stress to Inflammation and Major Depressive Disorder: A Social Signal Transduction Theory of Depression

Disclosing information, thoughts, and feelings about personal and meaningful topics (experimental disclosure) is purported to have various health and psychological consequences (e.g., J. W. Pennebaker, 1993). Although the results of 2 small meta-analyses (P. G. Frisina, J. C. Borod, & S. J. Lepore, 2004; J. M. Smyth, 1998) suggest that experimental disclosure has a positive and significant effect, both used a fixed effects approach, limiting generalizability. Also, a plethora of studies on experimental disclosure have been completed that were not included in the previous analyses. One hundred forty-six randomized studies of experimental disclosure were collected and included in the present meta-analysis. Results of random effects analyses indicate that experimental disclosure is effective, with a positive and significant average r-effect size of .075. In addition, a number of moderators were identified.

Experimental Disclosure and Its Moderators: A Meta-Analysis

Coping, defined as action-oriented and intrapsychic efforts to manage the demands created by stressful events, is coming to be recognized both for its significant impact on stress-related mental and physical health outcomes and for its intervention potential. We review coping resources that aid in this process, including individual differences in optimism, mastery, self-esteem, and social support, and examine appraisal and coping processes, especially those marked by approach or avoidance. We address the origins of coping resources and processes in genes, early life experience, and gene-environment interactions, and address neural underpinnings of coping that may shed light on evaluating coping interventions. We conclude by outlining possible intervention strategies for improving coping processes.

/pdf/coping-resources-coping-processes-and-mental-health-3krtuts97e.pdf

Coping Resources, Coping Processes, and Mental Health

Objective To determine if inducing self-blame would lead to increases in shame and guilt as well as increases in proinflammatory cytokine activity and cortisol. Based on previous research and theory, it was hypothesized that induced shame would be specifically associated with elevations in proinflammatory cytokine activity. Materials and methods Healthy participants were randomly assigned to write about traumatic experiences in which they blamed themselves (N = 31) or neutral experiences (N = 18) during three 20-minute experimental laboratory sessions over 1 week. Tumor necrosis factor-alpha receptor levels (sTNFalphaRII), an indicator of proinflammatory cytokine activity, beta2-microglobulin, cortisol (all obtained from oral fluids), and emotion were assessed prewriting and postwriting. Results Participants in the self-blame condition showed an increase in shame and guilt as well as an increase in sTNFalphaRII activity when compared with those in the control condition. Cortisol and beta2-microglobulin levels were unaffected by the procedures. Those individuals in the self-blame condition reporting the greatest increases in shame in response to the task showed the greatest elevations in proinflammatory cytokine activity, while levels of guilt and general negative emotion were unrelated to cytokine changes. Conclusion These data suggest that inducing self-related emotions can cause changes in inflammatory products, and that shame may have specific immunological correlates.

https://wesfiles.wesleyan.edu/courses/PSYC-317-jwellman/Week%2012%20-%20Psychoneuroimmunology/Dickerson%20et%20al.,%202004.pdf

Kevin H. Kim

Papers

Immunological effects of induced shame and guilt.