Cognitive impairments and changes in the structure and function of related brain regions, namely the prefrontal cortex and striatum, have long been implicated in drug addiction. However, it is unknown whether these abnormalities predate substance abuse, potentially serving as risk factors for dependence, or if they are the consequence of protracted use. To address this question, endophenotype research using stimulant-dependent individuals’ biological siblings has been used to investigate traits implicated in the pathology of addiction. Impairments present in both groups suggest an underlying risk-state for dependence, while additional abnormalities present only in stimulant-dependent individuals reflect potential effects of the drugs themselves. Contrastingly, there are also individuals who use stimulant drugs in a controlled manner without developing dependence. These ‘recreational users’ may lack the underlying traits that comprise a greater risk for dependence, or they might maintain additional protective factors against the development of addiction. Experiments in the first half of this dissertation used functional magnetic resonance imaging to investigate neurocognitive similarities and differences between dependent stimulant users, their non-dependent siblings, recreational users of cocaine, and unrelated healthy control volunteers. In Chapter 2, performance on a colour-word Stroop task was impaired in both stimulant-dependent individuals and their siblings, suggesting an endophenotype of cognitive inefficiency. However, neural activity significantly differed between the groups, indicating additional changes specific to the use of stimulant drugs. In Chapter 3, dependent users showed significant attentional bias to salient stimuli on a cocaine-word Stroop task, with a concurrent increase in prefrontal activation. Conversely, recreational users showed resilience in the face of cocaine cues and a decrease in arousal. Finally, Chapter 4 explored differences in reward sensitivity to both generic and drug-specific reinforcers, comparing the effects of personal and family history of stimulant exposure on a monetary incentive delay task. It is also under debate whether the neurocognitive differences seen in stimulant-dependent individuals are unique to substance abuse, or if parallel changes in behaviour and neurobiology are present in similar addiction-spectrum disorders, such as binge eating leading to obesity. In Chapter 5, stimulant-dependent and obese individuals with binge-eating behaviours showed differences in their substance-specific and general reward responsivity on a novel reward-valuation task. However, in Chapter 6 a similar decline in orbitofrontal cortex grey matter volume in relation to both years of stimulant use and body mass index was identified, implicating an overlap in this area between both conditions. These findings are integrated in Chapter 7, discussing the neurocognitive risk and protective factors that underlie an individual’s vulnerability for addiction, not only to stimulant drugs, but also potentially for other addictive behaviours.

The current dissertation is comprised of two studies that examined the relationship between group dynamics, attachment anxiety, and post-treatment outcomes in a sample of women (N = 102) with binge eating disorder (BED) who received Group Psychodynamic Interpersonal Psychotherapy. The first study explored the relationship between the development of group cohesion, the individuals’ level of attachment anxiety, and frequency of binge eating, symptoms of depression, and self-esteem at post-treatment. The second study explored the relationship between the interpersonal learning, individuals’ level of attachment anxiety, and outcomes. Interpersonal learning was conceptualized as the convergence between multiple perspectives of group cohesion: one’s own and the group’s perception of one’s cohesion to the group. Parallel measures of individual self-rated cohesion (CQ-I) and mean group-rated cohesion (CQ-G) were developed based on the original Cohesion Questionnaire (CQ; Piper et al., 1983) for this study. Participants were assigned to homogeneous groups composed of either high or low attachment anxiety to assess the impact of pre-treatment attachment anxiety. Findings indicated significant growth in cohesion over time, and a significant convergence in multiple ratings of cohesion. These processes did not differ significantly based on level of attachment anxiety. Growth in cohesion was related to greater reductions in binge eating for those high in attachment anxiety, while the convergence in ratings of cohesion (i.e., interpersonal learning) was related to improvements in self-esteem for individuals in both attachment anxiety conditions. The findings support the importance of group interventions for BED that are sensitive to individuals’ attachment anxiety, and that emphasize cohesiveness, and interpersonal learning to improve outcomes.

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Research suggests binge eating (BE) is equally prevalent across racial/ethnic groups. However, the majority of data concerning the assessment and treatment of BE come from clinical trials or specialty clinics where racial/ethnic minorities are underrepresented. Data regarding symptoms and treatment are needed from urban clinical settings where minorities are more likely to seek treatment. The current study assessed racial/ethnic group differences in BE prevalence, clinical and cognitive symptoms, and treatment retention in an ethnically-diverse weight loss treatment-seeking sample. Participants included 127 Hispanic, 204 African-American and 99 Caucasian adults who completed self-report measures of BE frequency, distress, eating-related cognitive symptoms including shape and weight concerns and dietary restraint, depression, stress, and treatment barriers. Data concerning number of treatment sessions attended and body mass index (BMI) were collected at 6-month follow up. The first study developed and validated the Dimensional Assessment of Loss of Control Eating (DALC) scale. The 2-factor DALC demonstrated good internal consistency and convergent, construct and incremental validity. The DALC contributed to variance in eating pathology and depression beyond existing BE measures. The second study examined racial/ethnic differences in BE prevalence, eating-related cognitive symptoms, and BMI. As hypothesized, no racial/ethnic differences in BE frequency were found and the rate of recurrent BE was 20% to 30%; participants with recurrent BE had higher BMIs, levels of depression, and global eating pathology than individuals without; African-American participants with BE had higher BMIs than other racial/ethnic groups, controlling for demographic variables. The hypotheses that Hispanic participants have higher weight and shape concerns, and that African-Americans have higher levels of restraint, were not supported. The third study examined the hypothesis that ethnicity is associated with obesity treatment retention and outcome. African-American participants had lower retention rates than Hispanics and Caucasians combined, and had lower levels of obesity-based stigma, which accounted for their lower retention rates. African-Americans lost less weight than Caucasians but this difference disappeared after accounting for age and income. The findings suggest high BE rates among racial/ethnic minorities at a common entry point for health services utilization. Stigma and African-American ethnicity should be considered when developing retention interventions.

This study investigated the extent biological, cultural, and psychological factors predispose individuals to eating disorders and compared the prevalence between (N = 103) male and female students (18-27 years of age) from Mississippi State University (MSU). Data was collected from the Eating Disorder Screen for Primary Care (ESP), a media consumption questionnaire, the Contour Drawing Rating Scale (CDRS), the Diet History Questionnaire III (DHQ III), the Eating Attitudes Test-26 (EAT-26), and the Rosenberg Self Esteem Scale. Age of onset was collected if participants identified as having an eating disorder. Data was analyzed using the Mann-Whitey U test and Pearson correlations to determine biological, cultural, and psychological susceptibility. This study determined that there are significant biological, cultural, and psychological predispositions that should be considered when diagnosing and treating individuals with eating disorders. Findings from MSU students were compared to current evidence and provides a basis for the development of future studies.

Diagnostic practices utilized in studies of participants with Anorexia Nervosa, Bulimia Nervosa, and Binge-Eating Disorder were investigated. A reliable coding system was used by two reviewers to analyze the diagnostic documentation practices in articles from the top-thirty most cited articles for each diagnostic category. Interrater agreements were all above .95. Results showed that many important diagnostic practices and criteria are either not being employed or not being documented. Uniform reporting procedures are necessary to help readers know how each article’s sampling procedure and subject pool differs from other samples used in the literature. Researchers reported the most details about sample characteristics with the recently proposed Binge-Eating Disorder category. Discussion focuses on identifying the specific diagnostic and sampling procedures deserving better documentation in the eating disorder literatures.

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Executive functioning (EF) problems may serve as vulnerability or maintenance factors for Binge-Eating Disorder (BED). However, it is unclear if EF problems observed in BED are related to overweight status or BED status. The current study extends this literature by examining EF in overweight-BED (n=32), normal-weight BED (n=23), overweight healthy controls (n=48), and normal-weight healthy controls (n=48). Participants were administered an EF battery which utilized tests from the National Institutes of Health (NIH) toolkit and Delis-Kaplan Executive Function System (D-KEFS). After controlling for years of education and minority status, overweight individuals with and without BED performed more poorly than normal-weight individuals with and without BED on a task of cognitive flexibility (p < 0.01) requiring generativity and speed and on psychomotor performance tasks (p < 0.01). Normal-weight and overweight BED performed worse on working memory tasks compared to normal-weight healthy controls (p = 0.04). Unexpectedly, normal-weight BED individuals out-performed all other groups on an inhibitory control task (ps < 0.01). No significant differences were found between the four groups on tasks of planning. Our findings support a link between poorer working memory performance and BED status. Additionally, overweight status is associated with poorer psychomotor performance and cognitive inflexibility. Replication of the finding that normal-weight BED is associated with enhanced inhibitory control is needed. / Psychology