Electronic Thesis and Dissertation Repository

Thesis Format

Monograph

Degree

Doctor of Philosophy

Program

Psychology

Supervisor

Dozois, David JA

Abstract

Background: Cognitive theories posit that cognitive control deficits promote depression by reducing ability to self-regulate under stress. When activated by stress and accessible to working memory, negative cognitive content and structure (i.e., schemas), may interfere with cognitive control abilities, resulting in even greater declines in executive functioning. Moreover, burgeoning evidence indicates that social stress upregulates inflammation, resulting in a pro-inflammatory phenotype that drives depression pathogenesis. However, cognitive mechanisms underlying this process are not well understood. An objective of this study was to examine depression-related deficits in cognitive control and their association with poor self-regulation. Another purpose was to evaluate the role of cognitive vulnerability in determining stress-induced declines in cognitive control. This study was the first to investigate the role of cognitive control and cognitive vulnerability (content, structure, and rumination) in shaping both resting-state and stress-induced upregulation of pro-inflammatory cytokines. Method: A clinical sample of currently depressed (n=40), remitted depressed (n=69), and healthy control (n=57) participants completed measures of cognitive content (core beliefs, dysfunctional attitudes), self-schema structure, rumination, depressive symptoms, and a battery of affective cognitive control tasks assessing inhibition, updating, and shifting. Salivary levels of four pro-inflammatory cytokines (IL-8, IL-6, IL-1β, and TNF-α) and updating abilities were assessed before and after a laboratory social stress induction. Depressive symptoms were evaluated at 2-week and 6-month follow-up. Results: Depressed individuals evinced deficits in inhibition and updating, which were associated with rumination, but not in shifting. As hypothesized, core beliefs and self-schema structure predicted declines in updating abilities following stress, and several cognitive control and vulnerability variables were related to baseline and stress-induced changes in cytokines. A fairly consistent pattern of findings emerged whereby deficits in cognitive control were associated with greater resting-state and stress-induced inflammation among individuals with low, and not high, cognitive vulnerability. Moreover, greater inflammatory reactivity to the stressor predicted decreases in depressive symptoms at follow-up. Conclusion: Cognitive content and structure are important in determining stress-induced declines in cognitive control, and inflammation represents a biological pathway through which cognitive vulnerability and cognitive control may influence depression. Theoretical and clinical implications of findings and directions for future research are discussed.

Summary for Lay Audience

Background: Cognitive control refers to the ability to control the contents of current awareness. Theories of depression suggest that poor cognitive control interferes with emotion regulation during stress and that this promotes low mood. During stressful experiences, negative memories and thoughts may enter current awareness, further reducing cognitive control and resulting in poorer self-regulation, including ruminative thinking. Moreover, evidence indicates that social stress upregulates inflammation, which may promote depression. However, cognitive mechanisms underlying this process are not well understood. The current study examined cognitive control and rumination in individuals with current and past diagnoses of depression, as well as never-depressed individuals. Another goal was to examine the role of negative thinking in shaping declines in cognitive control under stress, and the role of cognitive control and negative thinking in influencing both resting-state and stress-induced upregulation of inflammation. Method: A total of 166 participants completed measures of negative thinking, rumination, depressive symptoms, and a battery of cognitive control tasks. Salivary levels of four inflammatory markers and cognitive control abilities were assessed before and after a laboratory social stress induction. Depressive symptoms were evaluated at 2-week and 6-month follow-up. Results: Depressed individuals showed deficits across several facets of cognitive control, and these were associated with rumination. Negative thinking predicted declines in cognitive control abilities following stress, and several cognitive control and negative thinking variables were related to baseline and stress-induced changes in inflammation. A fairly consistent pattern of findings emerged whereby deficits in cognitive control were associated with greater resting-state and stress-induced inflammation among individuals with low, and not high, negative thinking. Moreover, greater inflammatory reactivity to the stressor predicted decreases in depressive symptoms at follow-up. Conclusion: Negative thinking is important in determining stress-induced declines in cognitive control, and inflammation represents a biological pathway through which negative thinking and cognitive control may influence depression. Theoretical and clinical implications of findings and directions for future research are discussed.

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