Smoking as a Cause of Depression
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Adolescent smoking is a major public health problem, yet much remains to be learned about why some adolescents progress from smoking experimentation to regular smoking while others do not. Individual differences in genetic susceptibility may account, in part, for the variability in rates of adolescent smoking and progression. There is abundant evidence for the heritability of smoking initiation, age at smoking onset, and smoking persistence (1ЁC4). Heritable predisposition to smoking may be mediated, in part, by genetic variation in the dopamine pathway (5). Support for this hypothesis has emerged from studies linking smoking behavior with the more rare A1 and B1 alleles of the gene for the dopamine 2 receptor (DRD2) (6ЁC8) and the 10-repeat allele of the dopamine transporter gene (SLC6A3) (9, 10) in adults. However, these findings have not been replicated in all cases (11ЁC13). The 9-repeat allele of SLC6A3 has also been associated with a 22% reduction in dopamine transporter protein, resulting in less clearance and greater bioavailability of dopamine (14). Thus, it is possible that individuals who carry the other common allele of SLC6A3, the 10-repeat allele, may achieve greater reward from nicotineЎЇs effects on dopamine activity.
Although these genetic association studies have provided preliminary evidence for specific genetic effects on smoking practices, they have several limitations. For example, case-control designs have been criticized for not accounting for the potential biasing effects of ethnic admixture (i.e., cases and control subjects may have been drawn from populations with different ethnic ancestries) (5, 15). A second limitation of previous research has been small subject groups, which may have affected the ability to detect associations with genes having small effects (16). In addition, previous research has relied on general assessments of smoking status (e.g., smokers versus nonsmokers). Given the complex nature of smoking behavior and its etiology, it is critical that the phenotypes for genetic studies of smoking be well defined (17). Finally, there has been a lack of attention to adolescent populations in research evaluating genetic contributions to smoking behavior. The genes involved in smoking experimentation and acquisition of a habit during adolescence may be different from those that maintain a smoking habit or explain nicotine dependence in adulthood.
Another gap in our understanding relates to the interactions of genes with other factors that have been shown to increase adolescent vulnerability to smoking. For example, depression appears to be an important factor in adolescent smoking (18ЁC20). Evidence exists to suggest that there may be common influences, possibly genetic, on both depression and smoking (21, 22). Depression symptoms have also been shown to moderate the effects of dopaminergic genes on smoking practices (23). To generate new knowledge about the biobehavioral basis of adolescent smoking, the present study evaluated the Am J Psychiatry 161:7, July 2004 1225 AUDRAIN-McGOVERN, LERMAN, WILEYTO, ET AL.
Method
Study Group
The participants were 615 9th grade high school students of
European ancestry, each of whom was enrolled in one of five public
high schools in northern Virginia. These adolescents were participating
in a longitudinal cohort study of biobehavioral determinants
of adolescent health habits. Of these 615 adolescents,
293 (48%) were male and 322 (52%) were female.
This study group is a subset of a larger cohort that was drawn
from 2,393 students