Cigarette use is one of the most potent public health risk factors for disease and represents a potentially modifiable form of drug abuse. However, despite substantial efforts to reduce the use of cigarettes in youth, initiation of smoking in adolescence and progression to more regular use in the transition to adulthood continues at unacceptable levels. Both genetic and environmental factors have been shown to exert substantial effects on the likelihood to initiate smoking in adolescence and progress to higher levels of smoking intensity in early adulthood. This proposal focuses on an integrated model that positions sibling contagion for smoking at the interface of social and genetic risk for smoking. Exposure to sibling smoking represents a robust risk factor for smoking initiation that typically exceeds the effects of parent smoking and contributes independent of peer smoking, and prior work suggests that such sibling contagion reflects shared environmental effects driven by level of sibling connectedness. In this proposal, we seek to expand this work to conduct novel longitudinal analyses of sibling contagion for smoking spanning adolescence and emerging adulthood in a genetically-informative sample participating in the National Longitudinal Study of Adolescent Health (Add Health). We propose to provide new data on the relative contributions of genes and environment on sibling connectedness in early adulthood and to test the extent to which there are unique shared environmental effects during this developmental period along with continuity of effects from adolescence. A series of models are provided to examine the evidence for sibling contagion via level of connectedness on smoking in early adulthood, with emphasis on detection of unique proximal environmental effects in early adulthood as well as continuity of effects from adolescence. New evidence for gene-environment interaction (or moderation of heritability attributable to sibling connectedness) is hypothesized. The theme of gene- environment interaction is carried forward to incorporate candidate gene markers as proxies for genetic risk for smoking in early adulthood. This work will provide a much better understanding of the developmental continuities and discontinuities in the socializing effect of sibling contagion on smoking behavior in early adulthood and bridge links with genetic risk, a likely source of influence on smoking. The execution of the aims will yield novel targets for family-based intervention and prevention efforts during the transition from adolescence to early adulthood, the typical period of progression to levels of smoking that severely compromise health. In particular, as we learn more about the ways in which siblings can encourage each other's forays into risky and health compromising behaviors and provide social reinforcement that interacts with genetic propensity, we can start to devise intervention and prevention strategies that capitalize on the influence siblings have with each other to promote resistance to and desistance from smoking. 7. Project Narrative Relevance: Siblings represent one of the most influential interpersonal relationship through the lifespan and sibling smoking is a strong predictor of both smoking initiation and progression to regular smoking. This proposal attempts to understand both environmental and genetic pathways by which siblings influence each other's progression of smoking during adolescence and early adulthood, given that siblings share common environmental experiences as well as common genes. Successful completion of our study aims will yield novel targets for family-based intervention and prevention programs that may harness the strong emotional connection between siblings to promote resistance to smoke and successful quit attempts for those who have already started smoking. ? ? ?
| Rende, Richard; Slomkowski, Cheryl (2009) Incorporating the family as a critical context in genetic studies of children: implications for understanding pathways to risky behavior and substance use. J Pediatr Psychol 34:606-16 |
