title: Interactions between genotype and retrospective ADHD symptoms predict lifetime smoking risk in a sample of young adults.
abstract: Attention-deficit/hyperactivity disorder (ADHD) symptoms are associated with an increased risk of smoking, and genetic studies have identified similar candidate genes associated with both ADHD and smoking phenotypes. This paper addresses the question of whether ADHD symptoms interact with candidate gene variation to predict smoking risk. Participants were a subsample of individuals from the National Longitudinal Study of Adolescent Health (Add Health), a nationally representative sample of adolescents followed from 1995 to 2002. The sample analyzed included a subset from Add Health of 1,900 unrelated individuals with genotype data. Multiple logistic regression was used to examine relationships between self-reported ADHD symptoms, genotype, and lifetime history of regular smoking. Polymorphisms in the DRD2 gene and, among females, the MAOA gene interacted with retrospective reports of ADHD symptoms in contributing to risk for smoking. Trends were observed for interactions between the DRD4 gene and, among males, the MAOA gene and ADHD symptoms to predict smoking risk. No main effect for any of these polymorphisms was observed. We observed neither main effects nor interactions with CYP2A6, DAT, and SLC6A4 genes. These findings suggest that genotypes associated with catecholamine neurotransmission interact with ADHD symptoms to contribute to smoking risk.
authors.affiliation: Department of Psychiatry and Behavioral Sciences, Duke University Medical Cneter, Durham, NC 27708, USA. mccle011@mc.duke.edu
authors.forename: F Joseph
authors.initials: FJ
authors.lastname: McClernon
authors.forename: Bernard F
authors.initials: BF
authors.lastname: Fuemmeler
authors.forename: Scott H
authors.initials: SH
authors.lastname: Kollins
authors.forename: Melanie E
authors.initials: ME
authors.lastname: Kail
authors.forename: Allison E
authors.initials: AE
authors.lastname: Ashley-Koch
mesh_terms: D000293:Adolescent; D000328:Adult; D001189:Aryl Hydrocarbon Hydroxylases / Q000235:genetics; D001289:Attention Deficit Disorder with Hyperactivity / Q000453:epidemiology* / Q000235:genetics*; D015897:Comorbidity; D065637:Cytochrome P-450 CYP2A6; D007174:Disruptive, Impulse Control, and Conduct Disorders / Q000235:genetics; D050483:Dopamine Plasma Membrane Transport Proteins / Q000235:genetics; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D008137:Longitudinal Studies; D008297:Male; D006899:Mixed Function Oxygenases / Q000235:genetics; D011110:Polymorphism, Genetic; D017448:Receptors, Dopamine D2 / Q000235:genetics; D050637:Receptors, Dopamine D3 / Q000235:genetics; D050638:Receptors, Dopamine D4 / Q000235:genetics; D012189:Retrospective Studies; D012307:Risk Factors; D050486:Serotonin Plasma Membrane Transport Proteins / Q000235:genetics; D012907:Smoking / Q000453:epidemiology* / Q000235:genetics*
chemical_list: C493593:DRD3 protein, human; C493599:DRD4 protein, human; D050483:Dopamine Plasma Membrane Transport Proteins; D017448:Receptors, Dopamine D2; D050637:Receptors, Dopamine D3; C493230:SLC6A4 protein, human; D050486:Serotonin Plasma Membrane Transport Proteins; D050638:Receptors, Dopamine D4; D006899:Mixed Function Oxygenases; D001189:Aryl Hydrocarbon Hydroxylases; C585710:CYP2A6 protein, human; D065637:Cytochrome P-450 CYP2A6