title: Does 5HTTLPR Genotype Moderate the Association of Family Environment With Child Attention-Deficit Hyperactivity Disorder Symptomatology?
abstract: Problematic family dynamics are common among youth with attention-deficit hyperactivity disorder (ADHD). Multiple mechanisms, including diathesis-stress (vulnerability) and differential susceptibility Gene × Environment interaction effects (G × E), have been proposed to account for this association. G × E effects for ADHD were examined via interactions between a genetic marker hypothesized to influence sensitivity to the environment (the promoter polymorphism of the serotonin transporter gene -5HTTLPR) and family conflict and cohesion in predicting ADHD symptoms. There were 498 youth ages 6-17 years (251 ADHD, 213 non-ADHD) and their parents who completed a multistage, multi-informant assessment (including parent and youth reports on the Family Environment Scale), and saliva sample collection for genotyping. Linear regression analyses examined interactions between 5HTTLPR genotype and the Family Environment Scale scales of conflict and cohesion reported by parent and child. Criteria laid out by Roisman et al. ( 2012 ) were applied to evaluate diathesis stress versus differential susceptibility G × E mechanisms. Results demonstrated interactions between 5HTTLPR genotype and both conflict and cohesion in predicting inattention but not hyperactivity-impulsivity. Both interactions were highly consistent with differential susceptibility models of G × E effects. 5HTTLPR genotype appeared to moderate the relationship between family conflict/cohesion and inattentive symptoms. Interactions highlight the role of 5HTTLPR genotype as a potential marker of environmental sensitivity and provide support for differential susceptibility models of G × E effects for ADHD.
authors.affiliation: a Department of Psychology , University of Iowa.
authors.forename: Alexis L
authors.initials: AL
authors.lastname: Elmore
authors.affiliation: b Department of Psychiatry , Oregon Health and Science University.
authors.forename: Joel T
authors.initials: JT
authors.lastname: Nigg
authors.affiliation: c Department of Microbiology and Molecular Genetics , Michigan State University.
authors.forename: Karen H
authors.initials: KH
authors.lastname: Friderici
authors.affiliation: c Department of Microbiology and Molecular Genetics , Michigan State University.
authors.forename: Katherine
authors.initials: K
authors.lastname: Jernigan
authors.affiliation: a Department of Psychology , University of Iowa.
authors.forename: Molly A
authors.initials: MA
authors.lastname: Nikolas
mesh_terms: D000293:Adolescent; D000328:Adult; D001288:Attention / Q000502:physiology; D001289:Attention Deficit Disorder with Hyperactivity / Q000235:genetics* / Q000523:psychology; D002648:Child; D054541:Family Conflict; D005195:Family Relations; D005260:Female; D059647:Gene-Environment Interaction; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D010290:Parents / Q000523:psychology; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic / Q000235:genetics*; D012463:Saliva; D050486:Serotonin Plasma Membrane Transport Proteins / Q000235:genetics*; D012931:Social Environment
chemical_list: C493230:SLC6A4 protein, human; D050486:Serotonin Plasma Membrane Transport Proteins