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Sally S. Dickerson

Bio: Sally S. Dickerson is an academic researcher from Pace University. The author has contributed to research in topic(s): Rumination & Stressor. The author has an hindex of 24, co-authored 43 publication(s) receiving 8123 citation(s). Previous affiliations of Sally S. Dickerson include University of California, Berkeley & University of California, Irvine.

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TL;DR: 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.
Abstract: 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.

4,602 citations

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TL;DR: Support seeking was highest for diseases viewed as stigmatizing and was lowest for less embarrassing but equally devastating disorders, such as heart disease, and implications for social comparison theory and its applications in health care are discussed.
Abstract: More Americans try to change their health behaviors through self-help than through all other forms of professionally designed programs. Mutual support groups, involving little or no cost to participants, have a powerful effect on mental and physical health, yet little is known about patterns of support group participation in health care. What kinds of illness experiences prompt patients to seek each other's company? In an effort to observe social comparison processes with real-world relevance, support group participation was measured for 20 disease categories in 4 metropolitan areas (New York, Chicago, Los Angeles, and Dallas) and on 2 on-line forums. Support seeking was highest for diseases viewed as stigmatizing (e.g., AIDS, alcoholism, breast and prostate cancer) and was lowest for less embarrassing but equally devastating disorders, such as heart disease. The authors discuss implications for social comparison theory and its applications in health care.

698 citations

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TL;DR: It is demonstrated that acute threats to the social self increase proinflammatory cytokine activity and cortisol and that these changes occur in concert with shame, which support a stressor- and emotional response-specificity model for psychobiological and health research.
Abstract: Our program of research focuses on shame as a key emotional response to "social self" threats (i.e., social evaluation or rejection). We propose that shame may orchestrate specific patterns of psychobiological changes under these conditions. A series of studies demonstrates that acute threats to the social self increase proinflammatory cytokine activity and cortisol and that these changes occur in concert with shame. Chronic social self threats and persistent experience of shame-related cognitive and affective states predict disease-relevant immunological and health outcomes in HIV. Across our laboratory and longitudinal studies, general or composite affective states (e.g., distress) are unrelated to these physiological and health outcomes. These findings support a stressor- and emotional response-specificity model for psychobiological and health research.

576 citations

Journal ArticleDOI
TL;DR: Results suggest a subtle dysregulation in hypothalamic-pituitary-adrenal axis functioning in breast cancer survivors with persistent fatigue, which is associated with alterations in immunological parameters and serum cortisol levels.
Abstract: Approximately 30% of breast cancer survivors report persistent fatigue of unknown origin. We have previously shown that cancer-related fatigue is associated with alterations in immunological parameters and serum cortisol levels in breast cancer survivors. The current study examined the diurnal rhythm of salivary cortisol in fatigued and non-fatigued breast cancer survivors. Salivary cortisol measures were obtained from breast cancer survivors with persistent fatigue (n=13) and a control group of non-fatigued survivors (n=16). Participants collected saliva samples upon awakening and at 1200, 1700, and 2200 h on two consecutive days. Diurnal cortisol slope for each day was determined by linear regression of log-transformed cortisol values on collection time and analyzed using multi-level modeling. Fatigued breast cancer survivors had a significantly flatter cortisol slope than non-fatigued survivors, with a less rapid decline in cortisol levels in the evening hours. At the individual patient level, survivors who reported the highest levels of fatigue also had the flattest cortisol slopes. Group differences remained significant in analyses controlling for demographic and medical factors, daily health behaviors, and other potential confounds (e.g. depressed mood, body mass index). Results suggest a subtle dysregulation in hypothalamic-pituitary-adrenal axis functioning in breast cancer survivors with persistent fatigue.

263 citations

Journal ArticleDOI
TL;DR: It is suggested that inducing self-related emotions can cause changes in inflammatory products, and that shame may have specific immunological correlates.
Abstract: 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.

200 citations


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5,269 citations

Journal ArticleDOI
TL;DR: 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.
Abstract: 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.

4,602 citations

Journal ArticleDOI
TL;DR: Analysis of 134 samples suggests that when weighting each study's contribution by sample size, perceived discrimination has a significant negative effect on both mental and physical health.
Abstract: Perceived discrimination has been studied with regard to its impact on several types of health effects. This meta-analysis provides a comprehensive account of the relationships between multiple forms of perceived discrimination and both mental and physical health outcomes. In addition, this meta-analysis examines potential mechanisms by which perceiving discrimination may affect health, including through psychological and physiological stress responses and health behaviors. Analysis of 134 samples suggests that when weighting each study's contribution by sample size, perceived discrimination has a significant negative effect on both mental and physical health. Perceived discrimination also produces significantly heightened stress responses and is related to participation in unhealthy and nonparticipation in healthy behaviors. These findings suggest potential pathways linking perceived discrimination to negative health outcomes.

2,741 citations

Journal ArticleDOI
TL;DR: Preliminary data from patients with inflammatory disorders, as well as medically healthy depressed patients, suggest that inhibiting proinflammatory cytokines or their signaling pathways may improve depressed mood and increase treatment response to conventional antidepressant medication.
Abstract: Recognition that inflammation may represent a common mechanism of disease has been extended to include neuropsychiatric disorders including major depression. Patients with major depression have been found to exhibit increased peripheral blood inflammatory biomarkers, including inflammatory cytokines, which have been shown to access the brain and interact with virtually every pathophysiologic domain known to be involved in depression, including neurotransmitter metabolism, neuroendocrine function, and neural plasticity. Indeed, activation of inflammatory pathways within the brain is believed to contribute to a confluence of decreased neurotrophic support and altered glutamate release/reuptake, as well as oxidative stress, leading to excitotoxicity and loss of glial elements, consistent with neuropathologic findings that characterize depressive disorders. Further instantiating the link between inflammation and depression are data demonstrating that psychosocial stress, a well-known precipitant of mood disorders, is capable of stimulating inflammatory signaling molecules, including nuclear factor kappa B, in part, through activation of sympathetic nervous system outflow pathways. Interestingly, depressed patients with increased inflammatory biomarkers have been found to be more likely to exhibit treatment resistance, and in several studies, antidepressant therapy has been associated with decreased inflammatory responses. Finally, preliminary data from patients with inflammatory disorders, as well as medically healthy depressed patients, suggest that inhibiting proinflammatory cytokines or their signaling pathways may improve depressed mood and increase treatment response to conventional antidepressant medication. Translational implications of these findings include the unique opportunity to identify relevant patient populations, apply immune-targeted therapies, and monitor therapeutic efficacy at the level of the immune system in addition to behavior.

2,679 citations

Journal ArticleDOI
TL;DR: This chapter addresses the psychological effects of social stigma by reviewing and organizing recent theory and empirical research within an identity threat model of stigma, which posits that situational cues, collective representations of one's stigma status, and personal beliefs and motives shape appraisals of the significance of stigma-relevant situations for well-being.
Abstract: This chapter addresses the psychological effects of social stigma. Stigma directly affects the stigmatized via mechanisms of discrimination, expectancy confirmation, and automatic stereotype activation, and indirectly via threats to personal and social identity. We review and organize recent theory and empirical research within an identity threat model of stigma. This model posits that situational cues, collective representations of one's stigma status, and personal beliefs and motives shape appraisals of the significance of stigma-relevant situations for well-being. Identity threat results when stigma-relevant stressors are appraised as potentially harmful to one's social identity and as exceeding one's coping resources. Identity threat creates involuntary stress responses and motivates attempts at threat reduction through coping strategies. Stress responses and coping efforts affect important outcomes such as self-esteem, academic achievement, and health. Identity threat perspectives help to explain the...

2,444 citations