The interactive effect of neighborhood peer cigarette use and 5HTTLPR genotype on individual cigarette use

Jonathan Kyle Daw, Jason D. Boardman, Rachel Peterson, Andrew Smolen, Brett C. Haberstick, Marissa A. Ehringer, Susan T. Ennett, Vangie A. Foshee

Research output: Contribution to journalArticle

7 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)1804-1810
Number of pages7
JournalAddictive Behaviors
Volume39
Issue number12
DOIs
StatePublished - Jan 1 2014

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Tobacco Products
Smoking
Genotype
Hazards
Gene-Environment Interaction
Genes
Disease Susceptibility
Censuses
Proportional Hazards Models
Research
Alleles

All Science Journal Classification (ASJC) codes

  • Medicine (miscellaneous)
  • Clinical Psychology
  • Toxicology
  • Psychiatry and Mental health

Cite this

Daw, J. K., Boardman, J. D., Peterson, R., Smolen, A., Haberstick, B. C., Ehringer, M. A., ... Foshee, V. A. (2014). The interactive effect of neighborhood peer cigarette use and 5HTTLPR genotype on individual cigarette use. Addictive Behaviors, 39(12), 1804-1810. https://doi.org/10.1016/j.addbeh.2014.07.014
Daw, Jonathan Kyle ; Boardman, Jason D. ; Peterson, Rachel ; Smolen, Andrew ; Haberstick, Brett C. ; Ehringer, Marissa A. ; Ennett, Susan T. ; Foshee, Vangie A. / The interactive effect of neighborhood peer cigarette use and 5HTTLPR genotype on individual cigarette use. In: Addictive Behaviors. 2014 ; Vol. 39, No. 12. pp. 1804-1810.
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Daw, JK, Boardman, JD, Peterson, R, Smolen, A, Haberstick, BC, Ehringer, MA, Ennett, ST & Foshee, VA 2014, 'The interactive effect of neighborhood peer cigarette use and 5HTTLPR genotype on individual cigarette use', Addictive Behaviors, vol. 39, no. 12, pp. 1804-1810. https://doi.org/10.1016/j.addbeh.2014.07.014

The interactive effect of neighborhood peer cigarette use and 5HTTLPR genotype on individual cigarette use. / Daw, Jonathan Kyle; Boardman, Jason D.; Peterson, Rachel; Smolen, Andrew; Haberstick, Brett C.; Ehringer, Marissa A.; Ennett, Susan T.; Foshee, Vangie A.

In: Addictive Behaviors, Vol. 39, No. 12, 01.01.2014, p. 1804-1810.

Research output: Contribution to journalArticle

TY - JOUR

T1 - The interactive effect of neighborhood peer cigarette use and 5HTTLPR genotype on individual cigarette use

AU - Daw, Jonathan Kyle

AU - Boardman, Jason D.

AU - Peterson, Rachel

AU - Smolen, Andrew

AU - Haberstick, Brett C.

AU - Ehringer, Marissa A.

AU - Ennett, Susan T.

AU - Foshee, Vangie A.

PY - 2014/1/1

Y1 - 2014/1/1

N2 - 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.

AB - 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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