The dopamine receptor D4 gene (DRD4) moderates family environmental effects on ADHD

• Authors: Michelle M. Martel, University of New Orleans; Molly Nikolas, Michigan State University; Katherine Jernigan, Michigan State University; Karen Friderici, Michigan State University; Irwin Waldman, Emory University; Joel T. Nigg, Oregon Health and Science University
• Journal Title: Journal of Abnormal Child Psychology
• Volume: Volume 39, Number 1
• Publisher: Springer (part of Springer Nature): Springer Open Choice Hybrid Journals | 2011-01-01, Pages 1-10
• Type of Work: Article | Post-print: After Peer Review
• Publisher DOI: http://doi.org/10.1007/s10802-010-9439-5
• Subjects: Psychology, Developmental; Sociology, Individual and Family Studies; Biology, Genetics
• Keywords: Adolescent; Attention Deficit Disorder with Hyperactivity; Attention Deficit and Disruptive Behavior Disorders; Case-Control Studies; Child; Family Conflict; Female; Genotype; Homozygote; Humans; Male; Parenting; Polymorphism, Genetic; Promoter Regions, Genetic; Receptors, Dopamine D4; Surveys and Questionnaires; Tandem Repeat Sequences

Abstract

Attention-Deficit/Hyperactivity Disorder (ADHD) is a prime candidate for exploration of gene-by-environment interaction (i.e., G x E), particularly in relation to dopamine system genes, due to strong evidence that dopamine systems are dysregulated in the disorder. Using a G x E design, we examined whether the DRD4 promoter 120-bp tandem repeat polymorphism, previously associated with ADHD, moderated the effects of inconsistent parenting and marital conflict on ADHD or Oppositional-Defiant Disorder (ODD). Participants were 548 children with ADHD and non-ADHD comparison children and their parents. Homozygosity for the DRD4 promoter 120-bp tandem repeat insertion allele increased vulnerability for ADHD and ODD only in the presence of inconsistent parenting and appeared to increase susceptibility to the influence of increased child self-blame for marital conflict on ADHD inattention. DRD4 genotypes may interact with these proximal family environmental risk factors by increasing the individual's responsivity to environmental contingencies. © 2010 Springer Science+Business Media, LLC.