Erik G Willcutt1. 1. University of Colorado Boulder, Professor of Psychology and Neuroscience, Director, Eunice Kennedy Shriver NICHD Colorado Learning Disabilities Research Center, Director of Clinical Training, Faculty Fellow, Institute for Behavior Genetics, Faculty, Center for Neuroscience, Department of Psychology and Neuroscience, 345 UCB, University of Colorado Boulder, Boulder, CO 80309.
Abstract
PURPOSE OF REVIEW: This review provides an overview of studies that used behavioral genetic methods to understand the genetic and environmental influences that lead to comorbidity, the co-occurrence of two or more developmental disorders in the same individual. RECENT FINDINGS: Comorbidity is primarily explained by shared genetic influences for most pairs of disorders that have been studied, including attention deficit hyperactivity disorder (ADHD) and learning disabilities, conduct disorder and ADHD, anxiety and depression, and anxiety and autism spectrum disorder (ASD). Molecular genetic studies indicate that the etiologies of developmental disorders are highly multifactorial, with dozens or even hundreds of genes acting in combination with environmental risk factors to lead to each individual disorder and the extensive comorbidity between disorders. Due to this complexity, current state-of-the-art studies are now combining molecular genetic data from multiple large samples to begin to achieve adequate statistical power to identify the specific genetic polymorphisms that lead to comorbidity. SUMMARY: An extensive literature demonstrates the pervasiveness and potential importance of comorbidity between developmental disorders, and results of family, twin, and molecular genetic studies indicate that these comorbidities may be largely explained by shared genetic influences. Additional studies are ongoing to identify the specific genetic polymorphisms that increase risk for each developmental disorder and comorbidity between disorders.
PURPOSE OF REVIEW: This review provides an overview of studies that used behavioral genetic methods to understand the genetic and environmental influences that lead to comorbidity, the co-occurrence of two or more developmental disorders in the same individual. RECENT FINDINGS: Comorbidity is primarily explained by shared genetic influences for most pairs of disorders that have been studied, including attention deficit hyperactivity disorder (ADHD) and learning disabilities, conduct disorder and ADHD, anxiety and depression, and anxiety and autism spectrum disorder (ASD). Molecular genetic studies indicate that the etiologies of developmental disorders are highly multifactorial, with dozens or even hundreds of genes acting in combination with environmental risk factors to lead to each individual disorder and the extensive comorbidity between disorders. Due to this complexity, current state-of-the-art studies are now combining molecular genetic data from multiple large samples to begin to achieve adequate statistical power to identify the specific genetic polymorphisms that lead to comorbidity. SUMMARY: An extensive literature demonstrates the pervasiveness and potential importance of comorbidity between developmental disorders, and results of family, twin, and molecular genetic studies indicate that these comorbidities may be largely explained by shared genetic influences. Additional studies are ongoing to identify the specific genetic polymorphisms that increase risk for each developmental disorder and comorbidity between disorders.
Authors: Erik G Willcutt; Bruce F Pennington; Laramie Duncan; Shelley D Smith; Janice M Keenan; Sally Wadsworth; John C Defries; Richard K Olson Journal: J Dev Behav Pediatr Date: 2010-09 Impact factor: 2.225
Authors: K G Wigg; Y Feng; J Crosbie; R Tannock; J L Kennedy; A Ickowicz; M Malone; R Schachar; C L Barr Journal: Genes Brain Behav Date: 2008-11 Impact factor: 3.449
Authors: Melanie C Friedman; Nomita Chhabildas; Nisha Budhiraja; Erik G Willcutt; Bruce F Pennington Journal: Am J Med Genet B Neuropsychiatr Genet Date: 2003-07-01 Impact factor: 3.568
Authors: S J Docherty; O S P Davis; Y Kovas; E L Meaburn; P S Dale; S A Petrill; L C Schalkwyk; R Plomin Journal: Genes Brain Behav Date: 2009-11-10 Impact factor: 3.449