Hyperactivity/attention problems (HAP) and conduct problems (CP) are common and impairing disruptive behaviors in childhood and adolescence. Previous research has established that HAP and CP are highly comorbid, and that outcomes are worse for youth exhibiting both symptom clusters relative to youth with only one disruptive behavior type. Despite ample evidence that HAP and CP share common etiological factors and maladaptive outcomes, the nature of their developmental association remains unclear. This dissertation clarifies three important characteristics of comorbid HAP and CP development, in two replicate, longitudinal, population samples of youth. First, I test the theory that within-person variation in HAP relates to subsequent within-person in variation CP, but not vice versa. Second, I apply growth mixture modeling to identify comorbid HAP-CP developmental trajectories, as well as their uniquely associated risk factors. Finally, I attempt to replicate a well-known candidate gene by environment interaction as a predictor of CP. Altogether, these analyses expand the literature on the etiologies of HAP, CP, and their cross-construct relations.
","abstract_html":"<p>Hyperactivity/attention problems (HAP) and conduct problems (CP) are common and impairing disruptive behaviors in childhood and adolescence. Previous research has established that HAP and CP are highly comorbid, and that outcomes are worse for youth exhibiting both symptom clusters relative to youth with only one disruptive behavior type. Despite ample evidence that HAP and CP share common etiological factors and maladaptive outcomes, the nature of their developmental association remains unclear. This dissertation clarifies three important characteristics of comorbid HAP and CP development, in two replicate, longitudinal, population samples of youth. First, I test the theory that within-person variation in HAP relates to subsequent within-person in variation CP, but not vice versa. Second, I apply growth mixture modeling to identify comorbid HAP-CP developmental trajectories, as well as their uniquely associated risk factors. Finally, I attempt to replicate a well-known candidate gene by environment interaction as a predictor of CP. Altogether, these analyses expand the literature on the etiologies of HAP, CP, and their cross-construct relations.</p>","abstract_has_math":false,"creators":["Arnett, Anne Bernard"],"institution":null,"degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":null,"degree_department":null,"school":null,"contributors":["Bruce F. Pennington, Ph.D."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2016,"date_issued":"2016-01-01T08:00:00Z","date_published":"2016-01-01T08:00:00Z","updated_at":"2026-07-24T02:03:19Z","subjects":["ADHD","Attention deficit hyperactivity disorder","Attention","Child","Conduct disorder","Developmental psychology","Hyperactivity","Clinical Psychology","Psychology"],"languages":["en"],"rights":["Copyright is held by the author. User is responsible for all copyright compliance.
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"],"dc:subject":["ADHD","Attention deficit hyperactivity disorder","Attention","Child","Conduct disorder","Developmental psychology","Hyperactivity","Clinical Psychology","Psychology"],"dc:title":["Biopsychosocial Models of the Development of Childhood Disruptive Behaviors"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Ph.D."]},"updated_at":"2026-07-24T02:03:19Z"}