While these genetic association findings (Furberg, et al., 2010; Thorgeirsson, et al., 2010) are clearly important in understanding the genetic and neurological etiology of nicotine use and addiction, they were obtained in a large heterogeneous sample of adults from multiple studies. We hypothesize that the relative impact of genetic risk is moderated by development, such that children and adolescents are driven to smoke less by nicotine-specific genetic risk, but more by impulsivity/disinhibitory processes. As individuals who experiment with substances age and mature, we expect nicotine-specific processes to become more and more important in addiction. Indeed, (Thorgeirsson, et al., 2010) found evidence of this, if only because they did not find considerable overlap between SNPs associated with cigarettes smoked per day and SNPs associated with smoking initiation. In the present study we test the association of the aggregate effect of SNPs identified in (Thorgeirsson, et al., 2010) with CPD at ages 14, 17, 20, and 24, providing a direct assessment of the extent to which the relationship is moderated by age.
