Significant Genotype �� ADHD Symptom interactions were also observed selleck chemicals llc for polymorphisms in the MAOA and DRD4 genes. This study was the first evidence of ADHD symptom by genotype interactions as predictors of any smoking outcome and suggested that putative smoking genotypes may interact with ADHD symptoms to increase risk for lifetime smoking. These interactions between genotype, ADHD, and lifetime risk for smoking, in combination with the previously identified link between initial reactions to cigarettes and risk for lifetime smoking, suggest that genetic factors may interact with ADHD symptoms to alter risk of nicotine dependence by influencing initial reactions to cigarettes.

Current Study This study used a large epidemiological sample of young adults (n = 1,900) and evaluated ADHD symptoms as a potential moderator of the relationship between candidate gene variation and initial reactions to cigarettes. Given previously identified relationships between lifetime smoking, ADHD, and monoamine neurotransmission (e.g., McClernon et al., 2008), we hypothesized that candidate genes associated with monoamine regulation would interact with ADHD symptoms to influence initial reactions to cigarettes. Methods Participants Data Source Participants were a subsample from the National Longitudinal Study of Adolescent Health (Add Health), a large nationally representative study of adolescent health behaviors (http://www.cpc.unc.edu/projects/addhealth). Details regarding the design and data collection have been described elsewhere (Harris et al., 2003; Resnick et al., 1997).

Study Sample The current study included the same sample (n = 1900) reported on in our previous paper (McClernon et al., 2008) and included respondents who (a) provided genetic data and (b) reported having smoked at least one cigarette in their lifetime. See Table 1 for demographic information on these individuals. Table 1. Demographics, Genotype, Attention Deficit Hyperactivity (ADHD) Symptoms, Conduct Disorder (CD) Symptoms, and Initial Reactions for Participants (n = 1,900) Genotyping DNA collection, extraction, and genotyping methods have been described previously (for further details, see www.cpc.unc.edu/projects/addhealth). Polymorphisms in the following six genes were genotyped: the rs28363170 of dopamine transporter (DAT) gene, a 44-bp ins/del polymorphism (5HTTLPR) in the promoter region of the AV-951 serotonin transporter (SLC6A4) gene, the rs1800497 of Taq1A polymorphism of the dopamine D2 receptor (DRD2) gene, a 48-bp VNTR polymorphism of the dopamine D4 receptor (DRD4) gene, a 30-bp VNTR in the promoter of the monoamine oxidase A (MAOA) gene, and the rs1801272 of the cytochrome P-450-A6 (CYP2A6) gene.