Date Awarded
2024
Document Type
Thesis
Degree Name
Master of Science (M.Sc.)
Department
Psychology
Advisor
Meghan E Quinn
Committee Member
Josh A Burk
Committee Member
Janice L Zeman
Abstract
Social stressors are common emotion-eliciting interactions that increase feelings of social exclusion, evaluative threat, or rejection (Denson et al., 2009). The Social Signal Transduction Theory of Depression postulates social stressors can upregulate proinflammatory activity, which increases risk for depressive symptoms (Slavich & Irwin, 2014). However, not all individuals who experience social stress will show increased proinflammatory responses. Past literature has found that the use of isolated coping strategies, following social stress, may be associated with proinflammatory activity. Additionally, because lower cortisol responses to social stress result in mild proinflammatory responses, it may be that effective coping is particularly needed to regulate a proinflammatory response under stress when cortisol is blunted. We hypothesized that processing coping strategies, effortful actions to manage the stressor, predict a lower proinflammatory response. In contrast, we hypothesized that expression coping strategies, actions that signal an emotional state, predict greater proinflammatory activity. In addition, we expected stronger relationships between each coping strategy category and proinflammatory reactivity in participants with low cortisol responses to social stress. One hundred and ninety undergraduate participants were randomly assigned to a laboratory-based social stress or control condition. Participants were then asked to report on their use of coping strategies during the control/stress induction. Saliva samples were collected before and after exposure to the control/stress induction. Samples were assayed for cortisol and inflammatory markers (Interleukin (IL)-6, IL-1β, and Tumor Necrosis Factor (TNF)-α). We found that greater processing predicted greater increase in TNF-α and IL-1β under social stress. Additionally greater expression predicted a decrease in TNF-α and IL-6. The interaction between cortisol and coping measures did not predict a change in inflammation. Because our study did not demonstrate expected relationships, we discussed implications for future research, including methods to improve the measurement of coping and inflammatory markers under social stress. One hundred and ninety undergraduate participants were randomly assigned to a laboratory-based social stress or control condition. Salivary cortisol was collected throughout the experimental conditions. Inflammatory markers (Interleukin (IL)-6, IL-1β, and Tumor Necrosis Factor (TNF)-α) were collected before and after exposure to the conditions. Participants were then asked to report on their use of coping strategies. We found that greater processing and lower expression predicted greater change in TNF-α under social stress. However, we did not observe the same relationships for the IL-1β or IL-6. The interaction between cortisol and coping measures did not predict a change in inflammation. Although our study did not demonstrate expected relationships, we discussed methods to improve the measurement of coping and inflammatory markers under social stress.
DOI
https://dx.doi.org/10.21220/s2-td9k-0j90
Rights
© The Author
Recommended Citation
Al-Bizri, Mona, "Regulating Under Social Stress: Coping, Cortisol, And Cytokine Reactivity" (2024). Dissertations, Theses, and Masters Projects. William & Mary. Paper 1717521871.
https://dx.doi.org/10.21220/s2-td9k-0j90
