Abstract
Comorbid substance use disorders are highly prevalent in bipolar disorder, and research suggests that individuals with the comorbid presentation typically have worse outcomes than individuals with bipolar disorder without this comorbidity. However, psychosocial treatments for the comorbid presentation have not demonstrated effectiveness for both mood and substance use symptom domains, suggesting novel treatments are needed. An alternative path to treatment development is to identify mechanisms that underlie comorbid bipolar disorder and substance use disorders that can subsequently be targeted in treatment. We evaluated neurocognitive markers for impairments in risk avoidance (the tendency to engage in a persistent pattern of problematic behaviors despite negative outcomes resulting from such behaviors) as potential mechanistic variables underlying negative illness outcomes in the comorbid population. Participants with bipolar disorder (n = 45) or comorbid bipolar disorder and substance use disorders (n = 31) in a relatively euthymic mood state completed clinical risk behavior assessments, task-based risk avoidance assessments, and neurocognitive assessments. Results indicated a lack of notable between-group differences in the clinical risk composite score, task-based risk avoidance assessments, and neurocognitive assessments, with the exception of self-reported executive dysfunction which was elevated among the comorbid sample. Collapsing across group, we found that increased discounting of delayed rewards, older age, and an earlier age of (hypo)mania onset predicted an increased clinical risk composite score. These findings underscore the potential importance of delay discounting as a novel mechanistic target for reducing clinical risk behaviors among individuals with bipolar disorder both with and without comorbid substance use disorders.