Assessing the amplification of distress: factor analytic, experimental, and genetic evaluation of distress intolerance
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Abstract
Distress intolerance (DI)--the perceived inability to tolerate distressing somatic and affective states--is associated with a range of psychological disorders. Across these disorders, DI is hypothesized to amplify distress and motivate maladaptive avoidance behavior, and studies have identified links between DI and behaviors such as substance use, self-injury, and binge eating. Accordingly, DI is a particularly important pathological factor that can be targeted for intervention across disorders or co-occurring conditions. However, despite the clear importance of DI to psychopathology research and clinical intervention, its ongoing study has been hampered by limitations in its measurement. Specifically, there is a clear need for the establishment of empirically validated measurement strategies to facilitate consistency across studies and to advance a broader understanding of this construct. The current series of studies was designed to address these assessment issues. Appropriate to the transdiagnostic nature of DI, these studies included several diagnostic groups: unselected, healthy, emotional disordered patients, and substance-dependent patients. In the first study, shared variance among self-report measures of DI was examined in a large sample using a factor analysis. In the second and third studies, a novel DI scale was examined relative to current measures across several methodological approaches including group comparison, laboratory manipulation, and candidate gene testing. Results were as follows. First, DI was a heterogeneous construct that varied based on the domain of distress. Second, a new self-report measure derived from analysis of existing measures performed well relative to both alternative self-report and behavioral indices of DI. Third, the use of a domain-general measure of DI was an acceptable proxy for DI across domains. Fourth, substance-dependent samples exhibited great DI relative to those with emotional disorders and no Axis I disorder, and profiles of intolerance across domains of distress were characteristic of select diagnostic groups. Fifth, the serotonin transporter gene was not associated with DI as hypothesized. This series of studies helps clarify the nature of DI and offers a new measure to the field that may better capture the core DI construct. Clinical and research implications of these findings are discussed.
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Thesis (Ph.D.)--Boston University
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PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.