A Behavioural Genetic Model of the Mechanisms Underlying the Link Between Obesity and Dimensional Measures of Attention-Deficit/Hyperactivity Disorder (ADHD)

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dc.contributor.advisorDavis, Caroline A.
dc.creatorPatte, Karen Allison
dc.date.accessioned2015-12-16T19:30:37Z
dc.date.available2015-12-16T19:30:37Z
dc.date.copyright2015-08-05
dc.date.issued2015-12-16
dc.date.updated2015-12-16T19:30:37Z
dc.degree.disciplineKinesiology & Health Science
dc.degree.levelDoctoral
dc.degree.namePhD - Doctor of Philosophy
dc.description.abstractObjective: The purpose of this study was to investigate genetic and psycho-behavioural mechanisms contributing to the strong ADHD symptom-obesity association. Genetic variants associated with hypo-dopaminergic functioning have been implicated in ADHD, particularly the 7-repeat allele of a VNTR located on the DRD4 gene, likely due to the receptor’s predominance in the prefrontal cortex. Based on this evidence, some experts have suggested that a shared aetiology of a dysfunctional dopamine (DA) system is responsible for the link. However, this conflicts with accumulating evidence that it is actually an amplified DA signal that increases the risk for overeating and weight gain due to a stronger appetitive response to food cues. It seems plausible that individuals with ADHD symptoms who are predisposed overeat are those who also possess a high sensitivity to, and greater motivation to seek out, rewarding stimuli, as reflected by increased DA availability in the brain reward pathways. Accordingly, the current study tested the hypothesis that symptoms of ADHD, predicted by hypo-dopaminergic functioning in the prefrontal cortex, in combination with an enhanced appetitive drive, predict hedonic eating, and in turn, higher BMI. Methods: Functional markers of the DRD2 and DRD4 were genotyped to determine their contributions to ADHD symptoms and various indices of hedonic eating, respectively. The model was tested using Structural Equation Modeling procedures in a general population sample (n=421 adults) representing a broad range of body mass index (BMI) values. Results: Overall, the fit indices indicated that the proposed model was a good fit to the data. Controlling for education level, all parameter estimates were in the expected direction and statistically significant with the exception of the pathway from the DRD4 marker to ADHD symptoms. The indirect effect was significant, indicating that overeating mediated the association between ADHD symptoms and BMI. Conclusions: Results lend support to the hypothesis that overeating and an elevated DA signal in the ventral striatum – representative of a greater reward response – are responsible for the link between ADHD symptoms and obesity. The current study was the first to connect the most prominent and supported theories of ADHD with evidence-based models of hedonic eating.
dc.identifier.urihttp://hdl.handle.net/10315/30745
dc.language.isoen
dc.rightsAuthor owns copyright, except where explicitly noted. Please contact the author directly with licensing requests.
dc.subjectHealth sciences
dc.subjectPsychology
dc.subject.keywordsobesity
dc.subject.keywordsovereating
dc.subject.keywordsADHD
dc.subject.keywordsinattention
dc.subject.keywordsimpulsivity
dc.subject.keywordsdopamine
dc.subject.keywordsgenetics
dc.subject.keywordsdopamine D2 receptor gene
dc.subject.keywordshealth psychology
dc.subject.keywordsstructural equation modeling
dc.subject.keywordsattention-deficit/hyperactivity disorder
dc.subject.keywordshedonic eating
dc.subject.keywordsreward response
dc.subject.keywordsreward sensitivity
dc.subject.keywordsbinge eating
dc.subject.keywordsemotional eating
dc.subject.keywordsmediation model
dc.subject.keywordsdopamine d4 receptor gene
dc.subject.keywordsDRD4
dc.subject.keywordsDRD2
dc.subject.keywordsbody mass index
dc.subject.keywordsBMI
dc.subject.keywordsoverweight
dc.titleA Behavioural Genetic Model of the Mechanisms Underlying the Link Between Obesity and Dimensional Measures of Attention-Deficit/Hyperactivity Disorder (ADHD)
dc.typeElectronic Thesis or Dissertation

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