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.

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Positive, but distal consequences of reducing alcohol use among at-risk users may have little impact on behavior due to temporal discounting (Mazur, 1987), in which delayed rewards are devalued relative to more proximal rewards, even if such distal rewards actually provide considerably more value. Delay discounting may be manipulated using a variety of means, one of which involves utilizing prospective thinking about future autobiographical events and is termed Episodic Future Thinking (Atance and ONeill, 2001). Episodic future thinking (EFT) has been demonstrated in previous studies to be effective in reducing delay discounting relative to a variety of control conditions (Benoit, Gilbert, and Burgess, 2011; Daniel, Stanton, and Epstein, 2013a, 2013b; Lin and Epstein, 2014; Peters and Büchel, 2010) and recently among substance-abusing populations (Snider, LaConte, and Bickel, 2016; Stein et al., 2016). The present study examined EFT in a novel sample of at-risk alcohol users. Participants were randomized to EFT, episodic past thinking (EPT), or a control condition in which non-autobiographical events were recalled (CET). Immediately following intervention, results demonstrated significantly less discounting in EFT and EPT, relative to CET. At follow-up, EFT demonstrated significantly less temporal discounting and alcohol use, when compared to both EPT and CET. No differences among conditions in alcohol demand or alcohol use intentions were observed. The present study contributes a number of novel findings to the literature, most notably that engaging in EFT predicts reductions in alcohol use prospectively and that reductions in delay discounting associated with EFT persist at least a week later, without any additional intervention. Such findings suggest that EFT manipulations influence the valuation of future rewards. Additionally, findings support EFT as a useful supplement to existing empirically-supported treatments or a component of novel substance use disorder treatments. / Ph. D.

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Pathological gambling is a maladaptive behaviour associated with diminished self-control over persistent compulsive gambling behaviour despite negative consequences. A significant revision to the clinical perspective of pathological gambling is underway, and the disorder will likely be recognized as a behavioural addiction in the fifth edition of Diagnostic and Statistical Manual of Mental Disorders. However, the neurobiological, cognitive and behavioural processes that drive a ‘behavioural addiction’ are unclear. A series of five studies were conducted to investigate cognitive mechanisms associated with neural and behavioural substrates of addictive processes in disordered gambling. Studies 1 through 3 investigated neurobiological correlates of addiction in individuals with pathological gambling as compared to individuals with cocaine dependence, and as compared to non-addicted healthy controls. Study 1 investigated brain activity associated with anticipatory and consummatory reward processing during slot-machine gambling. Study 2 investigated executive control processes by examining functional brain networks associated with loss-chasing behaviour. Study 3 employed voxel-based morphometry (VBM) to explore alterations in grey-matter volumes in individuals with addictive disorders. Studies 4 and 5 investigated the behavioural substrates of addiction in regular gamblers utilizing emerging and novel research techniques. Study 4 examined continuous hand motion trajectories to explore approach biases and implicit processing. Study 5 employed an adaptive testing methodology to explore the influence of gaming machine preferences on cognitive processes and gambling behaviour. Research identified neurobiological and behavioural substrates of gambling-related beliefs and biases that indicate significant contributions of cognitive mechanisms to the development and persistence of a behavioural addiction. Results suggest addictive disorders may share some common features of anticipatory reward processing and brain structure (Studies 1 and 3), while neural signals associated losing outcomes and decision-making during gambling may be specific to disordered gambling (Studies 1 and 2). Furthermore, cognitive distortions in regular gamblers may influence reinforcement and executive control processes (Study 4), and individual preferences for gaming speed may influence cognitions and behaviour during machine gambling. As additional psychological disorders are being considered for classification as behavioural addictions, and clinicians will be faced with the challenges of treating individuals with these non-substance-related addictive disorders, a better understanding of behavioural addictions, through the study of disordered gambling, will be essential under the new diagnostic framework.

To date, low rates of patient compliance have made it impractical to study whether regular exercise can contribute to positive outcomes in women with substance use disorders (SUD). One robust strategy for promoting and maintaining behavior change is contingency management (CM). CM has been used successfully to reinforce drug abstinence, treatment attendance, and other pro-social behaviors. CM delivers incentives (prizes) contingent upon target behaviors, though can be expensive. To reduce costs, CM is often delivered with an escalating variable-ratio schedule, first tested by Petry and colleagues (2005). As a Stage Ib behavioral therapies development project (Rounsaville et al., 2001), the primary aim of the present study was to test the use of behavioral incentives (BI) to promote regular physical activity in a residential SUD treatment setting with cocaine-dependent women. The target was physical activity, which was objectively defined at two levels: 30 minutes of treadmill walking at any pace and treadmill walking at moderate intensity. Specifically, a pilot RCT compared rates of physical activity over a six-week study period in a sample of N = 17 women with Cocaine Dependence. N = 10 were randomized to BI group and n = 7 were placed in the control (C) group. All participants completed baseline assessment, attended a 45-minute health and fitness education class, and were scheduled in exercise sessions three days/week. Those randomized to BI, however, were eligible three days/week, to receive incentives for meeting the target behavior(s). Follow-up assessment occurred at 3-weeks and 6-weeks post-randomization (midpoint and end of intervention), and 4-weeks post-discharge from the residential program. The primary outcome variables (percentage of sessions completed and total time spent in scheduled sessions) were used for effect size estimations, which were then used to perform power analyses so that sample size calculations could be estimated for the design of a Stage II RCT. A significant Group effect demonstrated that the BI group spent a significantly greater number of total minutes in scheduled exercise sessions than the C group. This dissertation provided benchmark data on the utility of BI for promoting physical activity for women with cocaine dependence. These promising findings support the use of BI procedures to promote exercise compliance, which will ultimately allow scientists to better develop SUD programs that directly utilize the mental and physical health benefits of physical activity.

Healthcare big data are a growing source of real-world data with which to identify and validate medications with repurposing potential. Previously, we developed a claims-based workflow to evaluate medications with potential to treat stimulant use disorders. In order to test the workflow, the framework was applied in the context of opioid use disorders (OUDs), for which there are medications with known efficacy. Using the Truven Marketscan Commercial Claims Database, a nested case-control analysis was conducted to determine the association between OUD medications (buprenorphine, naltrexone) and remission. Cases were defined as enrollees with a remission diagnosis and matched (1:4) to controls (individuals without remission) using incidence density sampling, with age group, sex, region, and index year as additional matching variables. After adjusting for behavioral health visits, polysubstance use disorders, and psychiatric disorders using conditional logistic regression, the odds of OUD medication exposure were 3.8 (99% confidence interval: 3.0 – 4.9) times higher in cases than controls. Evaluation of angiotensin converting enzyme inhibitors (e.g. lisinopril) as a negative control revealed no significant association between the medication and remission. This work demonstrates the feasibility of using administrative health claims data to evaluate the effectiveness of medications to treat substance use disorders.

After reviewing currently available diagnostic assessment instruments for substance use disorders this paper describes the format and structure of the Munich-Composite International Diagnostic Interview (M-CIDI) substance disorder section. In addition, the test-retest reliability of diagnoses and criteria for nicotine, alcohol, illegal and prescription drugs, is reported. Findings obtained in community sample of adolescents and young adults indicate that the substance section is acceptable for almost all types of respondents, efficient in terms of time and ease of administration as well as reliable in terms of consistency of findings over time. The test-retest reliability over a period of an average of 1 month, as examined by two independent interviewers indicates good-to-excellent kappa values for all substance disorders assessed, with significant kappa values ranging between 0.55 for drug abuse and 0.83 for alcohol abuse. There was also fairly consistently high agreement for the assessment of single DSM-IV diagnostic criteria for abuse and dependence as well as the M-CIDI quantity-frequency and time-related questions. To conclude, although – unlike previous studies – this study was conducted in a community sample and not in patients and used considerably longer time intervals of more than a month between investigations, our M-CIDI reliability findings are at least as high as those from previous studies.

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abstract: The present study utilized longitudinal data from a high-risk community sample (n=254, 52.8% female, 47.2% children of alcoholics, 74% non-Hispanic Caucasian) to test questions concerning the effects of genetic risk, parental knowledge, and peer substance use on emerging adult substance use disorders (SUDs). Specifically, this study examined whether parental knowledge and peer substance use mediated the effects of parent alcohol use disorder (AUD) and genetic risk for behavioral undercontrol on SUD. The current study also examined whether genetic risk moderated effects of parental knowledge and peer substance use on risk for SUD. Finally, this study examined these questions over and above a genetic "control" which explained a large proportion of variance in the outcome, thereby providing a stricter test of environmental influences. Analyses were performed in a path analysis framework. To test these research questions, the current study employed two polygenic risk scores. The first, a theory-based score, was formed using single-nucleotide polymorphisms (SNPs) from receptor systems implicated in the amplification of positive effects in the presence of new/exciting stimuli and/or pleasure derived from using substances. The second, an empirically-based score, was formed using a data-driven approach that explained a large amount of variance in SUDs. Together, these scores allowed the present study to test explanations for the relations among parent AUD, parental knowledge, peer substance use, and SUDs. Results of the current study found that having parents with less knowledge or an AUD conferred greater risk for SUDs, but only for those at higher genetic risk for behavioral undercontrol. The current study replicated research findings suggesting that peer substance use mediated the effect of parental AUD on SUD. However, it adds to this literature by suggesting that some mechanism other than increased behavioral undercontrol explains relations among parental AUD, peer substance use, and emerging adult SUD. Taken together, these findings indicate that children of parents with AUDs comprise a particularly risky group, although likelihood of SUD within this group is not uniform. These findings also suggest that some of the most important environmental risk factors for SUDs exert effects that vary across level of genetic propensity. / Dissertation/Thesis / Doctoral Dissertation Psychology 2015