In this study, we tested prospective associations between genetic risks and adolescent developmental and mature adult phenotypes of smoking behavior (Figure 1). We examined genetic risks in the Dunedin Study, a birth cohort (n=1,037) followed to age 38 years with >90% retention. We collected smoking behavior data at 8 assessments spanning ages 11-38 years. This allowed us to study the effects of genetic risk in the cohort as members initiated smoking during adolescence, converted to daily smoking and progressed to heavy smoking during the teenage and young adult years, and as they developed nicotine dependence and struggled with cessation in their 20s and 30s. We tested whether individuals at higher genetic risk progressed more rapidly from smoking initiation to heavy smoking, if they smoked more heavily as adults, if they were more nicotine dependent, and if they were more likely to fail in their cessation attempts. Finally, we tested the hypothesis that genetic risk accelerates the developmental progression from smoking initiation to heavy smoking, and this, in turn, increases the severity of adult smoking problems such as heavy, intractable smoking
