scholarly journals Polymorphisms in HTR2A and DRD4 Predispose to Smoking and Smoking Quantity

PLoS ONE ◽  
2017 ◽  
Vol 12 (1) ◽  
pp. e0170019 ◽  
Author(s):  
Gloria Pérez-Rubio ◽  
Alejandra Ramírez-Venegas ◽  
Valeri Noé Díaz ◽  
Leonor García Gómez ◽  
Karina Elvira Fabián ◽  
...  
Keyword(s):  
Smoking Quantity

Tobacco Smoking and Motivation to Quit in Psychiatric Patients

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
I. Ganhão ◽  
E. Gonçalves ◽  
A. Paixão ◽  
M. Trigo
Keyword(s):  
Quality Of Life ◽  
Risk Factors ◽  
Patient Population ◽  
Psychiatric Patients ◽  
Major Health ◽  
Smoking Restrictions ◽  
Motivation To Quit ◽  
Smoking Quantity ◽  
Heavy Smokers

Introduction:Smoking is a major health risk in the population in general with significantly increased morbility/mortality with severe consequences on the quality of life and tremendous economic burden on society. It is well known that psychiatric patients have an even higher prevalence of smoking, of heavy smokers and of other risk factors that contribute to the same illnesses.Non-smoking campaigns/smoking restrictions have flourished and it appears that more people are quitting or seriously contemplating the idea. When once, many non-smokers tolerated smokers, today the stigma associated with smoking is undeniable. Psychiatric patients, already greatly stigmatized, risk even becoming more so. Furthermore, smoking cessation programs and interventions frequently are not available, exclude many psychiatric patients and/or are ill-adapted to the special needs in this patient population.Aim:To establish the prevalence of smoking, quantity of tobacco smoked, other factors of dependence by psychiatric diagnosis in a portuguese psychiatric hospital.Establish the motivation of these patients to seek help by professionals and motivation to quit.Methods:Application of questionnaires including Fagerstrom's Modified Questionnaire to patients under care by one team of a Psychaitric hospital in Lisbon, Portugal (CHPL - Sector A).Discussion and conclusions:The study is under way therefore, there are no valid conclusions yet.Certainly it will be possible to confirm high levels of smoking tobacco in this patient population. Hopefully, we may also conclude that there is the desire to change smoking habits making cessation programs a needed and welcomed intervention in psychiatric settings.

scholarly journals Developmental Changes in Genetic and Shared Environmental Contributions to Smoking Initiation and Subsequent Smoking Quantity in Adolescence and Young Adulthood

2015 ◽  
Vol 18 (5) ◽  
pp. 497-506 ◽  
Author(s):  
Cristina B. Bares ◽  
Kenneth S. Kendler ◽  
Hermine H. Maes
Keyword(s):  
Cigarette Smoking ◽  
Young Adulthood ◽  
Environmental Influences ◽  
Smoking Initiation ◽  
Developmental Changes ◽  
Adolescent And Young Adult ◽  
Shared Environment ◽  
Adult Health ◽  
Cigarette Use ◽  
Smoking Quantity

Background: Few studies examining the genetic architecture of cigarette smoking have focused on adolescents or examined developmental changes in additive genetic, shared environment, and unique environmental influences on liability to initiate cigarette smoking and quantity of cigarettes smoked. The aim of this study was to add to the literature on liability to initiate and use cigarettes during adolescence using a nationally representative sample. Method: Data for this study came from adolescent and young adult twin pairs (aged 14–33 years) from the National Longitudinal Study of Adolescent to Adult Health. We ran a series of developmental causal–contingent–common pathway models to examine whether additive genetic, shared, and unique environmental influences on liability to the initiation of cigarette use are shared with those on smoking quantity, and whether their contributions change across development. Results: We found evidence for a developmental shift in genetic and shared environmental contributions to cigarette use. Early in adolescence, genetic and environmental influences work independently on liability to cigarette smoking initiation and quantity of cigarettes smoked, but liability to these behaviors becomes correlated as individuals age into young adulthood. Conclusions: These findings provide insight into the causal processes underlying the liability to smoke cigarettes. With age, there is greater overlap in the genetic and environmental factors that influence the initiation of cigarette smoking and quantity of cigarettes smoked.

scholarly journals Mediation Role of C-Reactive Protein on the Association between Smoking Quantity and Type 2 Diabetes in Current Chinese Smokers

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Dan Feng ◽  
Tao Liu ◽  
Hui Wang ◽  
Emma Karp ◽  
Wenhua Ling ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Binary Logistic Regression ◽  
Positive Association ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Smoking Quantity ◽  
Develop Type ◽  
Who 1999 Criteria

Objective. Previous studies have indicated that cigarette smokers are more likely to develop type 2 diabetes and that both smoking and type 2 diabetes are associated with C-reactive protein (CRP). This study examined whether CRP mediates the association between smoking quantity and type 2 diabetes.Methods. Nine hundred and eighty-four current Chinese smokers were selected from a community-based chronic disease survey conducted in Guangzhou and Zhuhai. Type 2 diabetes was defined according to the WHO 1999 criteria. CRP was measured with flow cytometry. Binary logistic regression was performed to assess the mediation.Results. A positive association was observed between smoking quantity and type 2 diabetes (P<0.05). After controlling for potential confounders, daily cigarette consumption was significantly associated with higher CRP levels. Current smokers with type 2 diabetes had higher CRP levels than smokers without type 2 diabetes. The association between the smoking quantity and type 2 diabetes was mediated by CRP, which accounted for 50.77% of the association.Conclusions. This study provides further evidence that smoking quantity is positively associated with type 2 diabetes and suggests that the association between smoking and type 2 diabetes might be mediated by CRP.

scholarly journals Ethnic-Specific Genetic Association of Variants in the Corticotropin-Releasing Hormone Receptor 1 Gene with Nicotine Dependence

2015 ◽  
Vol 2015 ◽  
pp. 1-7
Author(s):  
Xiujun Tang ◽  
Shumin Zhan ◽  
Liping Yang ◽  
Wenyan Cui ◽  
Jennie Z. Ma ◽  
...  
Keyword(s):  
Association Analysis ◽  
Hormone Receptor ◽  
Multiple Testing ◽  
Nucleotide Polymorphisms ◽  
Corticotropin Releasing Hormone ◽  
Single Nucleotide ◽  
Releasing Hormone ◽  
Smoking Quantity ◽  
Smoking Addiction ◽  
Smoking Index

Twin and family studies indicate that smoking addiction is highly influenced by genetic factors. Variants in the corticotropin-releasing hormone receptor 1 (CRHR1) gene have been associated with alcoholism and depression. In this study, we tested five single nucleotide polymorphisms (SNPs) inCRHR1for their association with ND, which was assessed by smoking quantity (SQ), the Heaviness of Smoking Index (HSI), and the Fagerström test for ND (FTND) in 2,037 subjects from 602 families of either European American (EA) or African American (AA) ancestry. Association analysis of the five SNPs revealed a significant association of rs171440 with SQ in the AA sample and with SQ and FTND in the pooled AA and EA samples. Haplotype-based association analysis indicated significant association of haplotypes C-C (56.9%) and T-C (38.9%), formed by SNPs rs171440 and rs1396862, with SQ in the AA sample, C-C-G (47.6%) with SQ, and T-C-G (42.3%), formed by SNPs rs171440, rs1396862, and rs878886, with SQ and FTND in the pooled AA and EA samples. However, none of these associations remained significant after correction for multiple testing. Together, our results provide suggestive evidence for the involvement ofCRHR1in ND, which warrants further investigation using larger independent samples.

scholarly journals Little Evidence of Modified Genetic Effect of rs16969968 on Heavy Smoking Based on Age of Onset of Smoking

2020 ◽  
Author(s):  
Christine Adjangba ◽  
Richard Border ◽  
Pamela N Romero Villela ◽  
Marissa A Ehringer ◽  
Luke M Evans
Keyword(s):  
Interaction Effect ◽  
Complex Traits ◽  
Age Of Onset ◽  
Genetic Effect ◽  
Potential Interaction ◽  
Effect Sizes ◽  
Heavy Smoking ◽  
Genome Wide ◽  
Increased Risk ◽  
Smoking Quantity

Abstract Introduction Tobacco smoking is the leading cause of preventable death globally. Smoking quantity, measured in cigarettes per day (CPD), is influenced both by the age of onset of regular smoking (AOS) and by genetic factors, including a strong effect of the non-synonymous single nucleotide polymorphism rs16969968. A previous study by Hartz et al. reported an interaction between these two factors, whereby rs16969968 risk allele carriers who started smoking earlier showed increased risk for heavy smoking compared to those who started later. This finding has yet to be replicated in a large, independent sample. Methods We performed a preregistered, direct replication attempt of the rs16969968×AOS interaction on smoking quantity in 128,383 unrelated individuals from the UK Biobank, meta-analyzed across ancestry groups. We fit statistical association models mirroring the original publication as well as formal interaction tests on multiple phenotypic and analytical scales. Results We replicated the main effects of rs16969968 and AOS on CPD but failed to replicate the interaction using previous methods. Nominal significance of the rs16969968×AOS interaction term depended strongly on the scale of analysis and the particular phenotype, as did associations stratified by early/late AOS. No interaction tests passed genome-wide correction (α=5e-8), and all estimated interaction effect sizes were much smaller in magnitude than previous estimates. Conclusions We failed to replicate the strong rs16969968×AOS interaction effect previously reported. If such gene-moderator interactions influence complex traits, they likely depend on scale of measurement, and current biobanks lack the power to detect significant genome-wide associations given the minute effect sizes expected. Implications We failed to replicate the strong rs16969968×AOS interaction effect on smoking quantity previously reported. If such gene-moderator interactions influence complex traits, current biobanks lack the power to detect significant genome-wide associations given the minute effect sizes expected. Furthermore, many potential interaction effects are likely to depend on the scale of measurement employed.

scholarly journals The Impact of Cigarette Excise Tax Increases on Regular Drinking Behavior: Evidence from China

2020 ◽  
Vol 17 (9) ◽  
pp. 3327
Author(s):  
Zili Zhang ◽  
Rong Zheng
Keyword(s):  
Alcohol Consumption ◽  
Drinking Behavior ◽  
Daily Smoking ◽  
Excise Tax ◽  
Excise Taxes ◽  
Smoking Quantity ◽  
Negative Effect ◽  
The Impact ◽  
The Relationship ◽  
Regular Alcohol Consumption

(1) Background: Many studies have shown that increasing taxation on cigarettes does play a role in tobacco control, but few studies have focused on whether increasing cigarette excise taxes significantly affects alcohol consumption. In this article, we aim to examine the effects of China’s 2015 increase in the cigarette excise tax on residents’ regular drinking behavior. (2) Methods: Using survey data from China Family Panel Studies (CFPS), we performed a panel logit regression analysis to model the relationship between the cigarette excise tax and regular drinking behavior. The Propensity Score Matching with Difference-in-Differences (PSM-DID) approach was adopted to determine the extent to which the cigarette excise tax affected residents’ drinking behavior. To test whether the cigarette excise tax could change regular drinking behavior by decreasing daily smoking quantity, we used an interaction term model. (3) Results: China’s 2015 increase in the cigarette excise tax had a significant negative effect on the probability of regular alcohol consumption among smokers, and the cigarette excise tax worked by reducing the average daily smoking of smokers. We also found that the regular drinking behavior of male smokers was more deeply affected by the increased cigarette excise tax than females. (4) Conclusions: Our research results not only give a deeper understanding of the impact of the cigarette excise tax, but also provide an important reference with which to guide future decisions concerning excise taxes imposed on cigarettes.

scholarly journals Predictors of reduced smoking quantity among recovering alcohol dependent men in a smoking cessation trial

2018 ◽  
Vol 84 ◽  
pp. 263-270 ◽  
Author(s):  
Matthew J. Worley ◽  
Melodie Isgro ◽  
Jaimee L. Heffner ◽  
Soo Yong Lee ◽  
Belinda E. Daniel ◽  
...  
Keyword(s):  
Smoking Cessation ◽  
Smoking Quantity ◽  
Alcohol Dependent

scholarly journals Gene–Environment Interactions Between Depressive Symptoms and Smoking Quantity

2016 ◽  
Vol 19 (4) ◽  
pp. 322-329 ◽  
Author(s):  
Kaisu Keskitalo-Vuokko ◽  
Tellervo Korhonen ◽  
Jaakko Kaprio
Keyword(s):  
Depressive Symptoms ◽  
Population Based ◽  
Depression Score ◽  
Genetic Effects ◽  
Phenotypic Correlation ◽  
Environmental Correlations ◽  
Gene By Environment Interactions ◽  
Smoking Quantity ◽  
Genetic And Environmental Factors ◽  
Shared Genetic

We investigated genetic and environmental correlations and gene by environment interactions (GxE) between depressive symptoms measured by the Beck Depression Inventory (BDI) and quantity smoked measured by number of cigarettes smoked per day (CPD) using quantitative genetic modeling. The population-based sample consisted of 12,063 twin individuals from the Finnish Twin Cohort Study. Bivariate Cholesky decomposition revealed that the phenotypic correlation (r = 0.09) between BDI and CPD was explained by shared genetic (rg = 0.18) and environmental (re = 0.08) factors. GxE models incorporating moderator effects were built by using CPD as trait and BDI as moderator and vice versa. The importance of the genetic variance component increased with increasing moderator value in both models. Thus, the influence of genetic effects on variance of smoking quantity was enhanced in individuals with elevated depression score and vice versa; the genetic effects on depression variance were potentiated among heavy smokers. In conclusion, shared genetic and environmental factors as well as GxE underlie the association of smoking with depression.

Influences on cigarette smoking quantity: Selection, stress, or culture?

1993 ◽  
Vol 24 (2) ◽  
pp. 125-126
Author(s):  
S. Serxner ◽  
R. Catalano ◽  
D. Dooley ◽  
S. Mishra
Keyword(s):  
Cigarette Smoking ◽  
Smoking Quantity
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