Comorbid substance use disorders (SUDs) are highly prevalent in bipolar disorder (BD), with up to 60% of individuals with BD developing an SUD at some point in their lifetime. In addition, research suggests that individuals with this comorbid presentation (BD+SUD) typically have worse outcomes -- including increased mortality, morbidity, and functional impairment -- than individuals with BD alone. Given the increased illness burden associated with BD+SUD, I conducted a systematic review evaluating existing psychosocial treatments for individuals with these comorbidities. Results from this review indicated that no existing psychosocial treatments for these comorbid conditions effectively target both the substance use and mood domain of symptoms. An alternative path to treatment development is to identify mechanisms that underlie BD+SUD that can subsequently be targeted in treatment. Accordingly, I evaluated impairments in risk avoidance (a tendency to engage in a persistent pattern of problematic behaviors despite negative outcomes resulting from such behaviors) as a potential mechanism underlying negative illness outcomes in BD+SUD. Participants with BD (n = 45) or BD+SUD (n = 31) in a relatively euthymic mood state completed clinical risk behavior assessments, laboratory-based risk avoidance assessments, and neurocognitive assessments in a single study session. I hypothesized that the BD+SUD group would exhibit increased clinical risk behaviors, increased impairments on laboratory-based measures of risk avoidance, and increased deficits on neurocognitive assessments relative to the bipolar disorder alone group. Contrary to my hypotheses, results indicated a lack of notable between-group differences in clinical risk behaviors, laboratory-based risk avoidance assessments, and neurocognitive assessments, with the exception of self-reported executive dysfunction which was elevated among individuals with BD+SUD. Collapsing across group, I found that increased discounting of delayed rewards, older age, and an earlier age of (hypo)mania onset predicted increased clinical risk behaviors. These findings underscore the potential importance of delay discounting as a mechanistic target for reducing clinical risk behaviors among individuals with BD both with and without comorbid SUDs. I also discuss the neurocognitive correlates of delay discounting and interventions for addressing delay discounting as potential new directions for treating the disability associated with BD.
| Identifer | oai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/45523 |
| Date | 26 January 2023 |
| Creators | Gold, Alexandra K. |
| Contributors | Otto, Michael W. |
| Source Sets | Boston University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis/Dissertation |
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