title: A preliminary analysis of interactions between genotype, retrospective ADHD symptoms, and initial reactions to smoking in a sample of young adults.
abstract: BACKGROUND
  Initial reactions to cigarettes predict later regular smoking. Symptoms of attention deficit hyperactivity disorder (ADHD) have also been shown to increase smoking risk and may moderate the relationship between genotype and smoking. We conducted an exploratory study to assess whether ADHD symptoms interact with genetic variation to predict self-reported initial reactions to smoking.
  
  
  METHODS
  Participants were a subsample of 1,900 unrelated individuals with genotype data drawn from the National Longitudinal Study of Adolescent Health (Add Health), a nationally representative sample of adolescents followed from 1995 to 2002. Linear regression was used to examine relationships among self-reported ADHD symptoms, genotype, and self-reported initial reactions to cigarettes (index scores reflecting pleasant and unpleasant reactions).
  
  
  RESULTS
  Polymorphisms in the DRD2 gene, SLC6A4 gene, and among males, the MAOA gene interacted with retrospective reports of ADHD symptoms in predicting pleasant initial reaction to cigarettes. Polymorphisms in the CYP2A6 gene and, among females, the MAOA gene interacted with retrospective reports of ADHD symptoms in predicting unpleasant initial reaction to cigarettes. No main effect for any of these polymorphisms was observed nor were any interactions with DRD4 and DAT genes.
  
  
  CONCLUSIONS
  These findings suggest that genotypes associated with monoamine neurotransmission interact with ADHD symptoms to influence initial reactions to cigarette smoking. Given that an initial pleasant reaction to cigarettes increases risk for lifetime smoking, these results add to a growing body of literature that suggests that ADHD symptoms increase risk for smoking and should be accounted for in genetic studies of smoking.
authors.affiliation: Department of Psychiatry and Human Behavior, Warren Alpert School of Medicine, Brown University, 1 Hoppin Street, Providence, RI 02903, USA. cinnamon_bidwell@brown.edu
authors.forename: L Cinnamon
authors.initials: LC
authors.lastname: Bidwell
authors.forename: Melanie E
authors.initials: ME
authors.lastname: Garrett
authors.forename: F Joseph
authors.initials: FJ
authors.lastname: McClernon
authors.forename: Bernard F
authors.initials: BF
authors.lastname: Fuemmeler
authors.forename: Redford B
authors.initials: RB
authors.lastname: Williams
authors.forename: Allison E
authors.initials: AE
authors.lastname: Ashley-Koch
authors.forename: Scott H
authors.initials: SH
authors.lastname: Kollins
mesh_terms: D001189:Aryl Hydrocarbon Hydroxylases / Q000235:genetics; D001289:Attention Deficit Disorder with Hyperactivity / Q000453:epidemiology / Q000235:genetics* / Q000473:pathology*; D065637:Cytochrome P-450 CYP2A6; D005106:Exploratory Behavior; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D016014:Linear Models; D008137:Longitudinal Studies; D008297:Male; D008995:Monoamine Oxidase / Q000235:genetics; D011110:Polymorphism, Genetic; D017448:Receptors, Dopamine D2 / Q000235:genetics; D050638:Receptors, Dopamine D4 / Q000235:genetics; D012189:Retrospective Studies; D012307:Risk Factors; D057566:Self Report; D050486:Serotonin Plasma Membrane Transport Proteins / Q000235:genetics; D012907:Smoking / Q000453:epidemiology / Q000235:genetics*; D009435:Synaptic Transmission; D055815:Young Adult
chemical_list: C493599:DRD4 protein, human; D017448:Receptors, Dopamine D2; C493230:SLC6A4 protein, human; D050486:Serotonin Plasma Membrane Transport Proteins; D050638:Receptors, Dopamine D4; D001189:Aryl Hydrocarbon Hydroxylases; C585710:CYP2A6 protein, human; D065637:Cytochrome P-450 CYP2A6; D008995:Monoamine Oxidase