Date of Award

2016

Document Type

Dissertation

Degree Name

Doctor of Philosophy in Clinical Psychology (PhD)

Department

Clinical Psychology

First Advisor/Committee Member

Amy Mezulis

Second Advisor/Committee Member

Thane Erickson

Third Advisor/Committee Member

David G. Stewart

Abstract

This study examined the relationships between stress, negative affect, rumination, and somatic symptoms among older adolescents. The following hypotheses were investigated: 1) greater number of life stressors would predict greater somatic symptoms, 2) rumination would moderate the relationship between stressors and somatic symptoms, 3) negative affect would also moderate the relationship between stressors and somatic symptoms, and 4) a three-way interaction between stress, rumination and negative affect would significantly predict somatic symptoms. Participants were 363 (71.1% female) university students with a mean age of 19.06 years (SD=2.06 years) who completed eight weekly online questionnaires, assessing levels of rumination and negative affect at baseline, and weekly stressor counts and somatic symptoms. Data were analyzed using hierarchical linear modeling to conduct multilevel moderation analyses, with the dependent variable of weekly somatic symptoms, Level 1 within-subjects predictor variable of weekly stressors, and the Level 2 between-subjects moderator variables of baseline rumination and negative affect. Baseline depression was included as a control variable. As hypothesized, greater weekly stressors significantly predicted greater weekly somatic symptoms (β=.12, t = 4.44, p < .001). However, neither baseline rumination (β = 0.02, t = 0.75, p = .45) nor negative affect (β = 0.01, t = 0.19, p = .85) significantly moderated the relationship between stress and somatic symptoms while controlling for depression. The interaction effect between rumination and negative affect as a moderator was also not significant (β= 0.01, t = 0.25, p = .80). Rumination significantly moderated the relationship between stress and somatic symptoms when depression was not controlled for in the model (β= .04, t = 2.13, p = .03), while negative affect approached significance as a moderator when not controlling for depression (β = 0.04, t = 1.87, p = .06). Moderation effects were in the expected directions, with the effect of stress on somatic symptoms being stronger for individuals high in rumination or high in negative affect. This study uniquely contributed to the literature by examining the cognitive and affective vulnerabilities that impact stress’ effect on somatic symptoms. Clinical implications, limitations, and directions for future research are discussed.

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Copyright held by author.

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