scholarly journals Genetic predispositions moderate the effectiveness of tobacco excise taxes

PLoS ONE ◽  
2021 ◽  
Vol 16 (11) ◽  
pp. e0259210
Author(s):  
Eric A. W. Slob ◽  
Cornelius A. Rietveld

Background Tobacco consumption is one of the leading causes of preventable death. In this study, we analyze whether someone’s genetic predisposition to smoking moderates the response to tobacco excise taxes. Methods We interact polygenic scores for smoking behavior with state-level tobacco excise taxes in longitudinal data (1992-2016) from the US Health and Retirement Study (N = 12,058). Results Someone’s genetic propensity to smoking moderates the effect of tobacco excise taxes on smoking behavior along the extensive margin (smoking vs. not smoking) and the intensive margin (the amount of tobacco consumed). In our analysis sample, we do not find a significant gene-environment interaction effect on smoking cessation. Conclusions When tobacco excise taxes are relatively high, those with a high genetic predisposition to smoking are less likely (i) to smoke, and (ii) to smoke heavily. While tobacco excise taxes have been effective in reducing smoking, the gene-environment interaction effects we observe in our sample suggest that policy makers could benefit from taking into account the moderating role of genes in the design of future tobacco control policies.

2019 ◽  
Vol 73 (5) ◽  
pp. 388-392 ◽  
Author(s):  
Jennifer Williams Robinette ◽  
Jason D Boardman ◽  
Eileen M Crimmins

BackgroundType 2 diabetes (T2D) is preventable, it is increasing in prevalence and it is a major risk factor for morbidity and mortality. Importantly, residents of neighbourhoods with high levels of disorder are more likely to develop T2D than those living in less disordered neighbourhoods and neighbourhood disorder may exacerbate genetic risk for T2D.MethodWe use genetic, self-reported neighbourhood, and health data from the Health and Retirement Study. We conducted weighted logistic regression analyses in which neighbourhood disorder, polygenic scores for T2D and their interaction predicted T2D.ResultsGreater perceptions of neighbourhood disorder (OR=1.11, p<0.001) and higher polygenic scores for T2D (OR=1.42, p<0.001) were each significantly and independently associated with an increased risk of T2D. Furthermore, living in a neighbourhood perceived as having high levels of disorder exacerbated genetic risk for T2D (OR=1.10, p=0.001). This significant gene×environment interaction was observed after adjusting for years of schooling, age, gender, levels of physical activity and obesity.ConclusionFindings in the present study suggested that minimising people’s exposure to vandalism, vacant buildings, trash and circumstances viewed by residents as unsafe may reduce the burden of this prevalent chronic health condition, particularly for subgroups of the population who carry genetic liability for T2D.


2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Yi Hou ◽  
Yong Gao ◽  
Yan Zhang ◽  
Si-Tong Lin ◽  
Yue Yu ◽  
...  

Abstract Background The association of diabetic nephropathy (DN) risk with single nucleotide polymorphisms (SNPs) within Engulfment and Cell Motility 1 (ELMO1) gene and gene–environment synergistic effect have not been extensively examined in, therefore, the purpose of this study is to explore the association between multiple SNPs in ELMO1 gene, and the relationship between gene–environment synergy effect and the risk of DN. Methods Genotyping for 4 SNPs was performed with polymerase chain reaction (PCR) and following restriction fragment length polymorphism (RFLP) methods. Hardy–Weinberg balance of the control group was tested by SNPstats (online software: http://bioinfo.iconologia.net/snpstats). The best combination of four SNPs of ELMO1 gene and environmental factors was screened by GMDR model. Logistic regression was used to calculating the OR values between different genotypes of ELMO1 gene and DN. Results The rs741301-G allele and the rs10255208-GG genotype were associated with an increased risk of DN risk, adjusted ORs (95% CI) were 1.75 (1.19–2.28) and 1.41 (1.06–1.92), respectively, both p-values were < 0.001. We also found that the others SNPs-rs1345365 and rs7782979 were not significantly associated with susceptibility to DN. GMDR model found a significant gene–alcohol drinking interaction combination (p = 0.0107), but no significant gene–hypertension interaction combinations. Alcohol drinkers with rs741301-AG/GG genotype also have the highest DN risk, compared to never drinkers with rs741301-AA genotype, OR (95% CI) 3.52 (1.93–4.98). Conclusions The rs741301-G allele and the rs10255208-GG genotype, gene–environment interaction between rs741301 and alcohol drinking were all associated with increased DN risk.


2001 ◽  
Vol 179 (2) ◽  
pp. 116-121 ◽  
Author(s):  
Judy Silberg ◽  
Michael Rutter ◽  
Michael Neale ◽  
Lindon Eaves

BackgroundThere is huge individual variation in people's response to negative life events.AimsTo test the hypothesis that genetic factors moderate susceptibility to the environmentally mediated risks associated with negative life events.MethodThe Virginia Twin Study of Adolescent Behavioral Development (VTSABD) was used to study the effects of independent life events (assessed from maternal interview) on depression/anxiety (assessed from child interview) in 184 same-gender female twin pairs, aged 14–17 years, measured on two occasions.ResultsThere was no genetic effect on the independent negative life events studied. A significant gene–environment interaction was found using structural equation modelling. There was no effect of independent life events on adolescents' depression in the absence of parental emotional disorder, but a significant effect in its presence.ConclusionsThere is an environmentally mediated effect of life events on depression/anxiety. Genetic factors play a significant role in individual differences in susceptibility to these environmentally mediated risks.


2020 ◽  
Author(s):  
Benjamin Domingue ◽  
Sam Trejo ◽  
Emma Armstrong-Carter ◽  
Elliot M. Tucker-Drob

Interest in the study of gene-environment interaction has recently grown due to the sudden availability of molecular genetic data—in particular, polygenic scores—in many long-running cohort studies. Identifying and estimating statistical interactions comes with several analytic and inferential challenges; these challenges are heightened when used to integrate observational genomic and social science data. We articulate some of these key challenges, provide new perspectives on the study of gene-environment interactions, and finally offer some practical guidance for conducting research in this area. Given the sudden availability of well-powered polygenic scores, we anticipate a substantial increase in research testing for interaction between such scores and environments. The issues we discuss, if not properly addressed, may impact the enduring scientific value of gene-environment interaction studies.


2020 ◽  
pp. 1-12
Author(s):  
Xiaoya Zhang ◽  
Jay Belsky

Abstract Some Gene × Environment interaction (G×E) research has focused upon single candidate genes, whereas other related work has targeted multiple genes (e.g., polygenic scores). Each approach has informed efforts to identify individuals who are either especially vulnerable to the negative effects of contextual adversity (diathesis stress) or especially susceptible to both positive and negative contextual conditions (differential susceptibility). A critical step in all such molecular G×E research is the selection of genetic variants thought to moderate environmental influences, a subject that has not received a great deal of attention in critiques of G×E research (beyond the observation of small effects of individual genes). Here we conceptually distinguish three phases of G×E work based on the selection of genes presumed to moderate environmental effects and the theoretical basis of such decisions: (a) single candidate genes, (b) composited (multiple) candidate genes, and (c) GWAS-derived polygenic scores. This illustrative, not exhaustive, review makes it clear that implicit or explicit theoretical assumptions inform gene selection in ways that have not been clearly articulated or fully appreciated.


2009 ◽  
Vol 36 (11) ◽  
pp. 1113-1124 ◽  
Author(s):  
Michael G. Vaughn ◽  
Matt DeLisi ◽  
Kevin M. Beaver ◽  
John Paul Wright

The study of serious, violent, and chronic offenders is a primary research area in criminology; however, its genetic underpinnings are relatively unknown. Based on genetically sensitive data from the National Longitudinal Study of Adolescent Health (Add Health), this study empirically explored the genetic antecedents of chronic and dangerous criminal behavior. Controlling for age, gender, cognitive ability, and self-control, the models yielded some significant effects for the genetic polymorphisms dopamine transporter (DAT1) and serotonin transporter (5HTT), and these effects were conditioned by the delinquent peer network within which adolescents were situated—thereby suggesting a significant Gene × Environment interaction.


2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
A. Rodriguez

The intrauterine environment is likely to play a key role in the etiology of psychopathology because the brain is particularly sensitive during the entire gestation as it undergoes the most rapid period of development. Neurodevelopmental deficits, such as attention problems, are a manifestation of these brain disturbances, which can in the end be linked to disorders, the most common being Attention Deficit Hyperactivity Disorder (ADHD). Animal models provide strong evidence in support for programming. Human studies present added complexity as genetic predisposition in mothers can increase the risk of e.g. pregnancy smoking or distress, thus, the effect may be carried entirely or in part by genetic transmission. However, neither genes nor environment operate in isolation, but rather in a complex interplay. Although ADHD has been the focus of intense research, little is known about the gene-environment interaction because such studies require very large sample sizes to be sufficiently statistically powered, thus necessitating multi-site collaborations. This presentation covers methodological difficulties associated with gene-environment studies and some of the ways in which our team has tackled these challenges. Data is presented on common maternal lifestyle factors during pregnancy and their relation to mental health problems in children, particularly ADHD, in a backdrop of genetic predisposition.


2020 ◽  
Author(s):  
Eric A.W. Slob ◽  
Cornelius A. Rietveld

AbstractTobacco consumption is one of the leading causes of preventable death. While some public policies have been effective in reducing the smoking prevalence in the United States, high tobacco excise taxes do not appear to deter all individuals from starting smoking nor to affect the smoking intensity of all those who do smoke. Here, we analyse whether someone’s genetic predisposition to smoking may explain why individuals smoke despite high tobacco excise taxes. For this purpose, we interact polygenic risk scores for smoking behaviour with state-level excise tax rates on tobacco. Our analyses exploiting longitudinal data (1992-2016) from the US Health and Retirement Study show that someone’s genetic propensity to smoking moderates the effect of tobacco excise taxes on smoking behaviour along the extensive margin (smoking vs. not smoking) and the intensive margin (the amount of tobacco consumed). That is, when tobacco excise taxes are relatively low, those with a high genetic predisposition to smoking are more likely (i) to smoke, and (ii) to smoke a relatively high number of cigarettes per day. In our sample, we do not find a significant interaction effect on smoking cessation.


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