Graduation Year

2015

Document Type

Dissertation

Degree

Ph.D.

Degree Name

Doctor of Philosophy (Ph.D.)

Degree Granting Department

Community and Family Health

Major Professor

Rita R. DeBate, Ph.D.

Co-Major Professor

Bruce L. Levin, Ph.D.

Committee Member

Julie Baldwin, Ph.D.

Committee Member

Eun Sook Kim, Ph.D.

Abstract

Evidence suggests comorbidity of ADHD and eating disorders (EDs) among females. Capitalizing on the comorbidity of ADHD and EDs and subsequent obesity could lead to improved prevention and treatment of all three conditions. However, additional information regarding the comorbidity is necessary to develop such interventions, as little is known about how or why this co-occurrence exists. A comprehensive model of the underlying mechanisms associated with comorbid ADHD and EDs is needed to improve understanding of the development of the comorbidity. Moreover, while there are gender differences within each disorder, literature is limited regarding to the comorbidity among males, leading to a call for further investigation.

Based on the literature, this study investigated three hypotheses of the underlying mechanisms of the ADHD/ED comorbidity, including: 1) ADHD and EDs are the expression of a common genetic or neurobiological dysfunction that manifests itself as binge eating and ADHD, 2) psychosocial factors common to both EDs and ADHD mediate the association between the two conditions, and 3) a third underlying mental health condition mediates the relationship between the two conditions. Underlying factors proposed within these three hypotheses include dopamine, serotonin, and monoamine oxidase A genes, family support, social support, neuroticism, conscientiousness, cognitive control, working memory, major depression, anxiety disorder, alcohol use and substance use disorders, and childhood abuse.

In order to simultaneously investigate the three hypotheses, this study utilized secondary data analysis from 6,289 females and 5,248 males as part of the National Longitudinal Study of Adolescent Health. This data was used to test a model constructed via a combination of five theories, specifically, the Biopsychosocial Model, the Life Course Approach, the Risk Regulator Framework, the Research Domain Criteria Matrix, and the Person-Environment Transaction Theory.

Findings of this study suggest that cognitive control, family support, and additional comorbid mental health illnesses such as depression, anxiety, and substance abuse disorder all mediate the relationship between ADHD and EDs. However, rather than leading to the comorbidity, ADHD led to other mental health issues which were then subsequently correlated to EDs; suggesting a comorbidity between these additional disorders and EDs with ADHD being a possible predictor of that comorbidity. In regards to genetics, the factors investigated in this study were not found to be directly associated with the comorbidity. Rather, these factors were connected to the psychosocial and psychiatric mediators, suggesting an indirect relationship between genetics and the comorbidity. With regards to males, differences were found between males with the comorbidity, ADHD alone, EDs alone, and neither disorder in regards to education attainment, BMI and obesity, delinquent behavior, and sexual behaviors were all observed. However, very few of the proposed underlying mechanisms among females were significantly associated with the comorbidity among males.

Results provide initial support for continued research on the underlying mechanisms of the ADHD/ ED comorbidity. This research has potential implications in many areas including primary and secondary prevention of EDs, improved treatment plans, prevention of psychostimulant medication abuse, and prevention and treatment of obesity. Next steps include the use of advanced statistical techniques in order to explore multiple combinations of underlying factors to the comorbidity and direct interactions between factors, including gene x environment interactions. Additional study replications are also needed with the incorporation of additional genetic components.

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