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 and nicotine dependence. This model has relevance to public-health interventions that might delay the developmental progression to heavy smoking. To put the magnitudes of genetic risk effects in context and to determine whether molecular genetic measurements provided novel information about risk, we conducted an additional analysis comparing molecular genetic information to family history information. These analyses asked how large molecular genetic effects were relative to family history effects and whether molecular genetic effects were independent of family history effects in predicting risk.
