Date of Award
Doctor of Philosophy
Recent epidemiological data from the National Comorbidity Survey (NCS) estimate significant lifetime prevalence rates for anxiety and mood disorders, suggesting nearly one in three people would meet diagnostic criteria for an anxiety and/or mood disorder at some point during their lifetime (NCS, 2007). Comorbidity research has also revealed that people often suffer from these disorders concurrently (Rodriguez et al., 2004). Many have argued that anxiety and mood disorders frequently co-occur because they share similar etiological factors (Barlow, 1991; Clark & Watson, 1991; Watson, 2005). Additional empirical research has suggested that depressive and anxiety disorders share similar genetic diatheses and merely present differently because of variation in environmental stressors (Hettema, Neale, & Kendler, 2001; Rutter Moffit, & Caspi, 2006). As a result, an investigation of shared emotion regulation and affective processes across anxiety and mood disorders may reveal parallel etiological factors and areas for intervention. Research examining emotion and affective dysregulation indicates that mood and anxiety pathology may be characterized by similar emotional control and understanding deficits (Amstadter, 2008; Bradley, 2000; Sandin et al., 1996). Models of emotion dysregulation suggest that individuals suffering from anxiety pathology report decreased understanding of emotions, higher reactivity and sensitivity to emotions, and poor emotional management and mood repair skills (Mennin et al., 2005). Similarly, studies have observed parallel difficulties in those with depression (Liverant, Brown, Barlow, & Roemer, 2008; Rude and McCarthy, 2003). Additionally, research has indicated that efforts to reappraise or suppress emotions may affect the intensity and valence of emotional experiences (Gross & John, 2004). The current study builds off this research by incorporating elements of previous models of emotion dysregulation and anxiety and mood pathology in an effort to develop a comprehensive model of affective process that may underlie both anxious and depressive symptomatology. A total of 526 undergraduate students participated in the present investigation by completing a series of self-report instruments measuring affect and psychopathology. Response patterns were analyzed using AMOS 4.0 in order to examine the structural relationships between negative affectivity, positive affectivity, emotion reappraisal, emotion suppression, negative emotional reactivity, and poor understanding of emotions. Initial tests of a single model of emotion dysregulation suggested that the development of two separate models best represented subject responses. As a result, distinct models for suppression and reappraisal were tested concurrently. Tests of model invariance revealed similar structural qualities across gender, ethnicity, and levels of general distress for both models. Following modification, final fit indices suggested good fit for the reappraisal model (CFI = .99, TLI = .99, RMSEA = .057); however, the suppression model did not appear similarly representative of subject response behavior (CFI = .89, TLI = .85, RMSEA = .073). Findings of the current study suggest that the use of emotional reappraisal may be associated with increased positive affective and decreased negative affective states. Further, attempts to reappraise emotional experiences may influence the relationships poor understanding of emotions and fear of strong affect demonstrated with negative and positive affect. Data support previously articulated psychotherapy treatment strategies (Beck, 1979; Barlow & Cerny, 1988; Linehan, 1993; Hayes, 2004), but also indicate that current cognitive behavioral therapies may benefit from heightened attention to emotions and the incorporation of affective regulation skill building strategies. Future research directions, study strengths and limitations, and additional implications of present results are included.
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