Jonathan Daw1, Jason D Boardman2, Rachel Peterson3, Andrew Smolen4, Brett C Haberstick4, Marissa A Ehringer5, Susan T Ennett6, Vangie A Foshee6. 1. Department of Sociology, University of Alabama-Birmingham, United States. Electronic address: jddaw@uab.edu. 2. Department of Sociology, University of Colorado-Boulder, United States; Institute of Behavioral Science, University of Colorado-Boulder, United States; Institute for Behavioral Genetics, University of Colorado-Boulder, United States. 3. Department of Sociology, University of Colorado-Boulder, United States; Institute of Behavioral Science, University of Colorado-Boulder, United States. 4. Institute for Behavioral Genetics, University of Colorado-Boulder, United States. 5. Institute for Behavioral Genetics, University of Colorado-Boulder, United States; Department of Integrative Physiology and Institute for Behavioral Genetics, University of Colorado-Boulder, United States. 6. Department of Health Behavior, Gillings School of Global Public Health, University of North Carolina-Chapel Hill, United States.
Abstract
BACKGROUND: Previous cross-sectional research has shown that adolescents' cigarette use is interactively associated with that of their school peers and their 5HTTLPR genotype, such that the cigarette use of persons with more copies of the 5HTTLPR*S' allele is more dependent on school peers' cigarette use behaviors than their counterparts. This analysis seeks to extend this novel finding by examining whether the same conclusion can be reached when substituting neighborhood peers for school peers and examining the timing of the initiation of any and regular smoking in adolescence. METHODS: This analysis employs an independent sample with longitudinal measures of cigarette use among 6th through 8th graders clustered in 82 neighborhoods, of whom 1098 contributed genetic data. The proportion of respondents who had ever smoked cigarettes by the first wave was calculated for each census block group in the study. 5HTTLPR genotype was assayed using the method of Whisman et al. (2011). The timing of any or regular smoking initiation and over four years were modeled as dependent variables using Cox proportional hazard models. RESULTS: The interaction of neighborhood peer smoking behavior in the first wave and 5HTTLPR genotype statistically significantly predicted any smoking initiation (hazard ratio: 3.532; p-value=0.002) and regular smoking initiation (hazard ratio: 5.686; p-value=0.000), net of controls for sex, race/ethnicity, grade in the first wave of data, and parental educational attainment. These findings reach the same conclusions as previous cross-sectional research. CONCLUSIONS: These results differ in the model of gene-environment interaction that they support. The findings for any smoking initiation are consistent with the diathesis-stress model of gene-environment interaction; the findings for regular smoking initiation are consistent with the differential susceptibility model.
BACKGROUND: Previous cross-sectional research has shown that adolescents' cigarette use is interactively associated with that of their school peers and their 5HTTLPR genotype, such that the cigarette use of persons with more copies of the 5HTTLPR*S' allele is more dependent on school peers' cigarette use behaviors than their counterparts. This analysis seeks to extend this novel finding by examining whether the same conclusion can be reached when substituting neighborhood peers for school peers and examining the timing of the initiation of any and regular smoking in adolescence. METHODS: This analysis employs an independent sample with longitudinal measures of cigarette use among 6th through 8th graders clustered in 82 neighborhoods, of whom 1098 contributed genetic data. The proportion of respondents who had ever smoked cigarettes by the first wave was calculated for each census block group in the study. 5HTTLPR genotype was assayed using the method of Whisman et al. (2011). The timing of any or regular smoking initiation and over four years were modeled as dependent variables using Cox proportional hazard models. RESULTS: The interaction of neighborhood peer smoking behavior in the first wave and 5HTTLPR genotype statistically significantly predicted any smoking initiation (hazard ratio: 3.532; p-value=0.002) and regular smoking initiation (hazard ratio: 5.686; p-value=0.000), net of controls for sex, race/ethnicity, grade in the first wave of data, and parental educational attainment. These findings reach the same conclusions as previous cross-sectional research. CONCLUSIONS: These results differ in the model of gene-environment interaction that they support. The findings for any smoking initiation are consistent with the diathesis-stress model of gene-environment interaction; the findings for regular smoking initiation are consistent with the differential susceptibility model.
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