al., 2004a). Risk factors for smoking initiation in youth include peer and family smoking, family conflict, and exposure to tobacco industry promotional campaigns (Pierce et al., 1998; Choi et al., 2002). In contrast, physical activity has protective effects on youth smoking (Audrain-McGovern et al., 2003a). The importance of the social environment also is supported by evidence for the efficacy of some anti-tobacco media campaigns, smoke-free environment policies, and cigarette taxes (Holm, 1979; Chaloupka et al., 2002).

Once tobacco use has been initiated, smoking cessation can be difficult because of the development of an addiction to nicotine. There is abundant evidence from animal and human studies for an inherited susceptibility to the rewarding effects of nicotine and to nicotine addiction. In fact, data from twin studies indicate that as much as 70 percent of the variance in nicotine addiction is attributable to genetic factors (Sullivan and Kendler, 1999). Investigations of the specific genetic mechanisms that underlie nicotine addiction have focused on candidate genes in neurobiological pathways that play a role in nicotine’s reinforcing and addictive effects, including the dopamine, serotonin, and opioid pathways, as well as genetic variation in nicotine metabolic pathways and neuronal nicotinic receptors (Lerman and Berrettini, 2003). While several genetic associations have been reported in the literature, heterogeneity in ascertainment, population stratification, and limitations in phenotype definition have contributed to nonreplication (Lerman and Swan, 2002; Munafo and Flint, 2004; Redden et al., 2005). Given the importance of smoking persistence to health outcomes, efforts are increasing to elucidate the role of inherited genetic variation in response to pharmacotherapies for nicotine dependence (Lerman et al., 2005).

Clearly, tobacco use and nicotine addiction are complex traits arising from the interactions among social-environmental, psychological, and genetic factors (Swan et al., 2003). For example, evidence from twin studies suggests that the importance of genetic factors in cigarette smoking depends, in part, on family functioning (Kendler et al., 2004). Specifically, the heritability estimates for cigarette smoking were lower in families with reports of higher levels of family dysfunction. This finding highlights both the importance of gene-environment interactions in risk behaviors, as well as the potential for identifying and quantifying such interactions through careful research. Furthermore, the genetic effects on the progression to regular smoking among adolescents are greatest among those with higher levels of depressive symptoms (Audrain-McGovern et al., 2004a). Despite awareness of the importance of gene-environment interactions in tobacco use, few molecular genetic studies have incorporated social environmental effects, and few studies of social environment have considered whether such influences are moderated by genetic factors.



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