Why Have Tobacco Control Policies Stalled? Using Genetic Moderation to Examine Policy Impacts

Sanjay Gandhi Medical Institute, India
PLoS ONE (Impact Factor: 3.23). 12/2012; 7(12):e50576. DOI: 10.1371/journal.pone.0050576
Source: PubMed


Research has shown that tobacco control policies have helped produce the dramatic decline in use over the decades following the 1964 surgeon general's report. However, prevalence rates have stagnated during the past two decades in the US, even with large tobacco taxes and expansions of clean air laws. The observed differences in tobacco control policy effectiveness and why policies do not help all smokers are largely unexplained.
The aim of this study was to determine the importance of genetics in explaining response to tobacco taxation policy by testing the potential of gene-policy interaction in determining adult tobacco use.
A moderated regression analysis framework was used to test interactive effects between genotype and tobacco policy in predicting tobacco use. Cross sectional data of US adults from the National Health and Nutrition Examination Survey (NHANES) linked with genotype and geocodes were used to identify tobacco use phenotypes, state-level taxation rates, and variation in the nicotinic acetylcholine receptor (CHRNA6) genotype. Tobacco use phenotypes included current use, number of cigarettes smoked per day, and blood serum cotinine measurements.
Variation in the nicotinic acetylcholine receptor was found to moderate the influence of tobacco taxation on multiple measures of tobacco use. Individuals with the protective G/G polymorphism (51% of the sample) responded to taxation while others had no response. The estimated differences in response by genotype were C/C genotype: b = -0.016 se  = 0.018; G/C genotype: b = 0.014 se  = 0.017; G/G genotype: b = -0.071 se 0.029.
This study provides novel evidence of "gene-policy" interaction and suggests a genetic mechanism for the large differences in response to tobacco policies. The inability for these policies to reduce use for individuals with specific genotypes suggests alternative methods may be needed to further reduce use.

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Available from: Jason Fletcher, Aug 22, 2015
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    • "A primary challenge is that polygenic influences will be correlated among family members ; any genetic predisposition to social attainment will be shared between parents and children. Thus a child's genetic and social inheritances will be correlated (e.g., Boardman, Domingue, & Fletcher, 2012). Attempts to quantify genetic effects must therefore account for social differences between children. "
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    ABSTRACT: Recent studies have begun to uncover the genetic architecture of educational attainment. We build on this work using genome-wide data from siblings in the National Longitudinal Study of Adolescent to Adult Health (Add Health). We measure the genetic predisposition of siblings to educational attainment using polygenic scores. We then test how polygenic scores are related to social environments and educational outcomes. In Add Health, genetic predisposition to educational attainment is patterned across the social environment. Participants with higher polygenic scores were more likely to grow up in socially advantaged families. Even so, the previously published genetic associations appear to be causal. Among pairs of siblings, the sibling with the higher polygenic score typically went on to complete more years of schooling as compared to their lower-scored co-sibling. We found subtle differences between sibling fixed-effect estimates of the genetic effect versus those based on unrelated individuals.
    Preview · Article · Aug 2015
    • "In the same article, he also outlines research designs best suited to blending public policy research to capture important genetic and environment interactions. In another article, Fletcher (2012) links genotypes and geocodes with the National Health and Nutrition Examination Survey (NHANES) to use genetic data to explain heterogeneous response to tobacco taxation, and highlighting the limitations of traditional sin taxes in moderating tobacco use. Such studies are likely to proliferate as policy researchers learn how to use information from the over 300 million biospecimens stored in U.S. biobanks that are publically and privately owned (Maschke, 2008). "

    No preview · Article · Jan 2008 · Journal of Policy Analysis and Management
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    ABSTRACT: Background: Smoking behaviour is a major public health problem worldwide. Several sources have confirmed the implication of genomic factors in smoking behaviour. These factors interact both with environmental factors and interventions to develop a certain behaviour. Objectives: Describing the environmental and genomic factors as well as the interventions influencing smoking cessation (SC) and developing a working model incorporating the different factors influencing SC were our main objectives. Methods: Two systematic reviews were conducted using articles in English from the Cochrane library, PubMed and HuGENet from January 2000 to September 2012: (1) a systematic review of systematic reviews and meta-analyses and (2) a systematic review of original research for genomic factors. The proposed working model was developed by making use of previous models of SC and applying an iterative process of discussion and re-examination by the authors. Results: We confirmed the importance of the 4 main factors influencing SC: (1) environmental factors, (2) genomic factors, (3) gene-environment interactions, and (4) evidence-based interventions. The model demonstrates the complex network of factors influencing SC. Conclusion: The working model of SC proposed a global view of factors influencing SC, warranting future research in this area. Future testing of the model will consolidate the understanding of the different factors affecting SC and will help to improve interventions in this field.
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