Date of Award

Fall 10-24-2015

Document Type

Dissertation

Degree Name

Doctor of Philosophy in Clinical Psychology (PhD)

Department

Clinical Psychology

First Advisor/Committee Member

Amy H. Mezulis

Second Advisor/Committee Member

David G. Stewart

Third Advisor/Committee Member

Thane M. Erickson

Fourth Advisor/Committee Member

Sheila E. Crowell

Abstract

Vulnerability-stress models of depression posit risk for depression is characterized by the presence of underlying affective, biological, and cognitive vulnerabilities that become activated during life stress exposure. Extant research has shown heightened reactivity to stress across these vulnerability domains predicts depression; however, little is known whether the persistence of and failure to down-regulate these maladaptive stress responses conveys greater risk of depression than initial reactivity alone. The current study examined associations between the time course of responses to a laboratory stress induction and depressive symptoms. I hypothesized that prolonged maladaptive responses to the stressor across affective (state negative affect; NA), biological (respiratory sinus arrhythmia; RSA), and cognitive (rumination) domains would be most strongly associated with concurrent and prospective depressive symptoms, above and beyond trait vulnerabilities and initial reactivity to stress. I also expected these associations would be moderated by life stress exposure during the 8-week follow up period. The sample was comprised of 92 young adults ages 18-24 (M = 19.50; SD = 1.37), 72.9% of whom identified as Caucasian and 82.6% as female. Analyses indicated prolonged NA following the stressor was associated with concurrent (B = 8.11, p < .001), but not prospective (B = -0.74, p = .77) depressive symptoms. High NA during stress marginally interacted with life stress exposure to predict greater symptoms at follow up (B = 0.28, p = .15). RSA recovery from stress was not associated with symptoms concurrently (B = 2.2, p = .61) or prospectively (B = -1.08, p = .39) and did not interact with life stress exposure. Prolonged rumination about the stressor was also not associated with depressive symptoms concurrently (B = 0.70, p = .62) or at follow up (B = -1.42, p = .25) and was not moderated by life stress exposure. Although hypotheses were only partially supported, the current study’s findings provide important implications for understanding the role of recovery from stress in the development, maintenance, and treatment of depressive symptoms among young adults.

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