Initiation Of Regular Smoking Research Articles

Effect of smoking cessation medications on intracranial aneurysm risk: A Mendelian randomization study.

We aim to assess the association between smoking behavior and intracranial aneurysms (IAs) and the effect of smoking cessation medications on IAs at the genetic level. Causal effects of four phenotypes: 1) age at initiation of regular smoking, 2) cigarettes smoked per day, 3) smoking cessation, and 4) smoking initiation on IAs, were analyzed using two-sample inverse-variance weighted Mendelian randomization analyses. The effects of genes interacting with the smoking cessation medications were analyzed using cis-expression quantitative trait loci genetic instruments on IAs using summary statistics-based Mendelian randomization analyses. Colocalization analyses were then used to test whether the genes shared causal variants with IAs. The role of confounding phenotypes as potential causative mechanisms of IAs at these gene loci was tested. Cigarettes smoked per day (OR=2.89; 95% CI:1.85-4.51) and smoking initiation on IAs (OR=4.64; 95% CI: 2.64-8.15) were significantly associated with IA risk. However, age at initiation of regular smoking (OR=0.54; 95% CI: 0.10-2.8) and smoking cessation (OR=6.80; 95% CI: 0.01-4812) had no overall effect on IAs. Of 88 genes that interacted with smoking cessation medications, two had a causal effect on IA risk. Genetic variants affecting HYKK levels showed strong evidence of colocalization with IA risk. Higher HYKK levels in the blood were associated with a lower IA risk. Gene target analyses revealed that cigarettes/day could be a main mediator of HYKK's effect on IA risk. This study provides evidence supporting that smoking initiation on IAs and cigarettes/day may increase IA risk. Increased HYKK gene expression may reduce IA risk. This can be explained by the increased number of cigarettes consumed daily. HYKK could also reduce IA risk due to the positive effect of continuous abstinence and varenicline therapy on smoking cessation.

The impact of smoking and alcohol consumption on rosacea: a multivariable Mendelian randomization study.

Observational studies have shown that cigarette smoking is inversely associated with risk of rosacea, However, it remains uncertain whether this association is causal or it is a result of reverse causation, and whether this association is affected by drinking behaviors. This study utilized the summary-level data from the largest genome-wide association study (GWAS) for smoking, alcohol consumption, and rosacea. The objective was to investigate the effect of genetically predicted exposures to smoking and alcohol consumption on the risk of developing rosacea. Two-sample bidirectional Mendelian randomization (MR) was applied, accompanied by sensitive analyses to validate the robustness of findings. Furthermore, multivariable MR was conducted to evaluate the direct impact of smoking on rosacea. A decreased risk of rosacea was observed in individuals with genetically predicted lifetime smoking [odds ratio (OR)MR - IVW = 0.53; 95% confidence interval (CI), 0.318-0.897; P = 0.017], and number of cigarettes per day (ORMR - IVW = 0.55; 95% CI, 0.358-0.845; P = 0.006). However, no significant associations were found between initiation of regular smoking, smoking cessation, smoking initiation, alcohol consumption and rosacea. Reverse MR analysis did not show any associations between genetic liability toward rosacea and smoking or alcohol drinking. Importantly, the effect of lifetime smoking and the number of cigarettes per day on rosacea remained significant even after adjusting for alcohol consumption in multivariable MR analysis. Smoking was causally related to a lower risk of rosacea, while alcohol consumption does not appear to be associated with risk of rosacea.

Early-onset smoking theory of compulsivity development: a neurocognitive model for the development of compulsive tobacco smoking.

According to the literature, individuals who start tobacco smoking during adolescence are at greater risk of developing severe tobacco addiction and heavier smoking behavior in comparison with individuals who uptake tobacco smoking during subsequent developmental stages. As suggested by animal models, this may be related to the unique neuroadaptive and neurotoxic effects of nicotine on adolescents' fronto-striatal brain regions modulating cognitive control and impulsivity. Previous research has proposed that these neuroadaptive and neurotoxic effects may cause a heightened reward-oriented impulsive behavior that may foster smoking relapses during quit attempts. However, developments in the field of addiction neuroscience have proposed drug addiction to represent a type of compulsive behavior characterized by the persistent use of a particular drug despite evident adverse consequences. One brain region that has received increased attention in recent years and that has been proposed to play a central role in modulating such compulsive drug-seeking and using behavior is the insular cortex. Lesion studies have shown that structural damages in the insular cortex may disrupt smoking behavior, while neuroimaging studies reported lower gray matter volume in the anterior insular cortex of chronic smokers compared with non-smokers, in addition to correlations between gray matter volume in the anterior insular cortex and measures of compulsive cigarette smoking. Based on the findings of our recent study reporting on early-onset smokers (mean age at regular smoking initiation = 13.2 years) displaying lower gray matter and white matter volume in the anterior insular cortex compared to late-onset smokers (mean age at regular smoking initiation = 18.0 years), we propose that the anterior insular cortex may play a central role in mediating the association between smoking uptake during adolescence and smoking heaviness/tobacco addiction during adulthood.

Associations between genetic liabilities to smoking behavior and schizophrenia symptoms in patients with a psychotic disorder, their siblings and healthy controls

It is unknown how smoking behavior polygenic scores (PRS) relate to psychosis and psychotic symptoms. To elucidate this, genotype and phenotype data were collected from patients with schizophrenia, their unaffected siblings, and healthy controls in a six-year follow-up prospective cohort study. Associations between smoking behaviors, PRS and schizophrenia symptoms were explored using linear mixed-effect models. The mean number of cigarettes smoked per day were 18 for patients, 13 for siblings and 12 for controls. In the overall sample, PRSs-smoking initiation (i.e., ever smoking as a binary phenotype, PRS-SI) were positively associated with positive symptoms, negative symptoms, and depressive symptoms, whereas PRSs-AI (age at regular smoking initiation) were negatively associated with all symptom dimensions, with similar effect sizes. When considering groups separately, PRS were only associated with psychotic symptoms in siblings and controls. In conclusion, unaffected siblings show smoking behaviors at an intermediate level between patients and healthy controls. Additionally, PRS-SI and PRS-AI are associated with all symptom dimensions only in unaffected siblings and healthy controls, possibly owing to the dominant role of other (genetic) risk factors in patients. Future studies may examine mechanisms via which genetic risk for smoking affects mental health symptoms.

Causal Associations Between Tobacco, Alcohol Use and Risk of Infectious Diseases: A Mendelian Randomization Study.

The causal effects of smoking and alcohol use on the risk of infectious diseases are unclear, and it is hard investigate them in an observational study due to the potential confounding factors. The aim of this study was to use Mendelian randomization (MR) techniques to assess the causalities between smoking, alcohol use and risk of infectious diseases. Univariable and multivariable MR analyses were performed using genome-wide association data for the age of initiation of regular smoking (AgeSmk, N = 341,427), smoking initiation (SmkInit, N = 1,232,091), cigarettes per day (CigDay, N = 337,334), lifetime smoking (LifSmk, N = 462,690), drinks per week (DrnkWk, N = 941,280), sepsis (N = 486,484), pneumonia (N = 486,484), upper respiratory tract infection (URTI, N = 486,484) and urinary tract infection (UTI, N = 486,214) among individuals of European ancestry. Independent genetic variants that were significantly (P < 5 × 10-8) associated with each exposure were considered as instruments. The inverse-variance-weighted method was used in the primary analysis, which was followed by a series of sensitivity analyses. Genetically predicted SmkInit was associated with an increased risk of sepsis (OR 1.353, 95% CI 1.079-1.696, P = 0.009), pneumonia (OR 1.770, 95% CI 1.464-2.141, P = 3.8 × 10-9) and UTI (OR 1.445, 95% CI 1.184-1.764, P = 3 × 10-4). Moreover, genetically predicted CigDay was associated with a higher risk of sepsis (OR 1.403, 95% CI 1.037-1.898, P = 0.028) and pneumonia (OR 1.501, 95% CI 1.167-1.930, P = 0.00156). Furthermore, genetically predicted LifSmk was associated with an increased risk of sepsis (OR 2.200, 95% CI 1.583-3.057, P = 2.63 × 10-6), pneumonia (OR 3.462, 95% CI 2.798-4.285, P = 3.28 × 10-30), URTI (OR 2.523, 95% CI 1.315-4.841, P = 0.005) and UTI (OR 2.036, 95% CI 1.585-2.616, P = 3.0 × 10-8). However, there was no significant causal evidence for genetically predicted DrnkWk in sepsis, pneumonia, URTI or UTI. Multivariable MR analyses and sensitivity analyses showed that the above results for causal association estimations were robust. In this MR study, we demonstrated the causal association between tobacco smoking and risk of infectious diseases. However, no evidence was found to support causality between alcohol use and the risk of infectious diseases.

Genetic predisposition to smoking in relation to the risk of frailty in ageing

Frailty causes emerging global health burden due to its high prevalence and mortality. In this study, we used Mendelian randomization (MR) approach to examine the potential causal relationship between smoking and frailty in ageing. Using inverse-variance weighted (IVW) method, genetically predicted smoking initiation was associated with an increased risk of frailty in ageing (odd ratio (OR) 1.23, 95% confidence interval (CI) 1.19–1.27, P = 3.21 × 10–39). Similarly, per year increase in age of initiation of regular smoking was associated with a 25% decrease in the risk of frailty (95% CI 7–39%, P = 7.79 × 10–3, per year), while higher number of cigarettes per day was associated with a 12% increased risk (95% CI 4–20%, P = 1.76 × 10–3). Compared with former smokers, current smokers were associated with an increased risk of frailty (OR 1.12, 95% CI 1.02–1.22, P = 0.01). Lifetime smoking was associated with a 46% higher risk of frailty (95% CI 37–56%, P = 2.63 × 10–29). Sensitivity analysis using alternative MR methods yielded similar results. Our study indicates that genetic predisposition to smoking is associated with the risk of frailty in ageing. Further studies are warranted to examine the exact role of smoking in the development of frailty.

Smoking and coronary artery disease risk in patients with diabetes: A Mendelian randomization study.

Previous observational studies have shown an association between smoking and coronary artery disease (CAD) in patients with diabetes. Whether this association reflects causality remains unestablished. This study aimed to explore the causal effect of smoking on CAD in patients with diabetes. Genetic signatures for smoking were extracted from a large genome-wide association study (GWAS), consisted of up to 1.2 million participants. Four smoking phenotypes were included: smoking initiation, cigarettes per day, age at initiation of regular smoking, and smoking cessation. Genetic associations with CAD in patients with diabetes were extracted from another GWAS, which included 15,666 participants (3,968 CAD cases and 11,696 controls). The analyses were performed using the univariable and multivariable Mendelian randomization (MR) method. MR analysis revealed that smoking initiation was positively related to CAD risk in patients with diabetes (OR = 1.322, 95% CI = 1.114 - 1.568, P = 0.001), but this association was attenuated when adjusted for cardiovascular risk factors (OR = 1.212, 95% CI = 1.008 - 1.457, P = 0.041). Age at initiation of regular smoking was negatively related to CAD in patients with diabetes (OR = 0.214, 95% CI = 0.070 - 0.656, P = 0.007), but this association became insignificant when adjusted for cardiovascular risk factors. This study supported the effect of smoking initiation on the risk of CAD in patients with diabetes.

Chronic tobacco smoking, impaired reward-based decision-making, and role of insular cortex: A comparison between early-onset smokers and late-onset smokers.

IntroductionThe literature suggests that tobacco smoking may have a neurotoxic effect on the developing adolescent brain. Particularly, it may impair the decision-making process of early-onset smokers (<16 years), by rendering them more prone to impulsive and risky choices toward rewards, and therefore more prone to smoking relapses, in comparison to late-onset smokers (≥16 years). However, no study has ever investigated reward-based decision-making and structural brain differences between early-onset smokers and late-onset smokers.MethodsComputerized measures of reward-based decision-making [Cambridge Gambling Task (CGT); 5-trials adjusting delay discounting task (ADT-5)] were administered to 11 early-onset smokers (mean age at regular smoking initiation = 13.2 years), 17 late-onset smokers (mean age at regular smoking initiation = 18.0 years), and 24 non-smoker controls. Voxel-based morphometry (VBM) was utilized to investigate the gray matter (GM) and white matter (WM) volume differences in fronto-cortical and striatal brain regions between early-onset smokers, late-onset smokers, and non-smokers.ResultsEarly-onset smokers displayed a riskier decision-making behavior in comparison to non-smokers as assessed by the CGT (p < 0.01, Cohen’s f = 0.48). However, no significant differences (p > 0.05) in reward-based decision-making were detected between early-onset smokers and late-onset smokers. VBM results revealed early-onset smokers to present lower GM volume in the bilateral anterior insular cortex (AI) in comparison to late-onset smokers and lower WM volume in the right AI in comparison to late-onset smokers.ConclusionImpairments in reward-based decision-making may not be affected by tobacco smoking initiation during early adolescence. Instead, lower GM and WM volume in the AI of early-onset smokers may underline a vulnerability to develop compulsive tobacco seeking and smoking behavior during adulthood.

Using multivariate endophenotypes to identify psychophysiological mechanisms associated with polygenic scores for substance use, schizophrenia, and education attainment.

Background.To better characterize brain-based mechanisms of polygenic liability for psychopathology and psychological traits, we extended our previous report (Liu et al. Psychophysiological endophenotypes to characterize mechanisms of known schizophrenia genetic loci. Psychological Medicine, 2017), focused solely on schizophrenia, to test the association between multivariate psychophysiological candidate endophenotypes (including novel measures of θ/δ oscillatory activity) and a range of polygenic scores (PGSs), namely alcohol/cannabis/nicotine use, an updated schizophrenia PGS (containing 52 more genome-wide significant loci than the PGS used in our previous report) and educational attainment.Method.A large community-based twin/family sample (N = 4893) was genome-wide genotyped and imputed. PGSs were constructed for alcohol use, regular smoking initiation, lifetime cannabis use, schizophrenia, and educational attainment. Eleven endophenotypes were assessed: visual oddball task event-related electroencephalogram (EEG) measures (target-related parietal P3 amplitude, frontal θ, and parietal δ energy/inter-trial phase clustering), band-limited resting-state EEG power, antisaccade error rate. Principal component analysis exploited covariation among endophenotypes to extract a smaller number of meaningful dimensions/components for statistical analysis.Results.Endophenotypes were heritable. PGSs showed expected intercorrelations (e.g. schizophrenia PGS correlated positively with alcohol/nicotine/cannabis PGSs). Schizophrenia PGS was negatively associated with an event-related P3/δ component [β = −0.032, nonparametric bootstrap 95% confidence interval (CI) −0.059 to −0.003]. A prefrontal control component (event-related θ/antisaccade errors) was negatively associated with alcohol (β = −0.034, 95% CI −0.063 to −0.006) and regular smoking PGSs (β = −0.032, 95% CI −0.061 to −0.005) and positively associated with educational attainment PGS (β = 0.031, 95% CI 0.003–0.058).Conclusions.Evidence suggests that multivariate endophenotypes of decision-making (P3/δ) and cognitive/attentional control (θ/antisaccade error) relate to alcohol/nicotine, schizophrenia, and educational attainment PGSs and represent promising targets for future research.

Genetically determined tobacco and alcohol use and risk of atrial fibrillation

BackgroundThe causality between the use of alcohol and cigarettes and atrial fibrillation (AF) remains controversial. We conducted a Mendelian randomization (MR) study to evaluate the association of genetic variants related to tobacco and alcohol use with AF.MethodsSingle nucleotide polymorphisms (SNPs) related to smoking initiation (N = 374), age at initiation of regular smoking (N = 10), cigarettes per day (N = 55), and smoking cessation (N = 24) were derived from a genome-wide association studies (GWAS) of tobacco use (N = 1.2 million individuals). SNPs related to heavy alcohol use (N = 6) were derived from a GWAS of UK biobank (N = 125,249 individuals). The genetically matching instrumented variables were obtained from the GWAS of AF (N = 588,190 individuals). The estimates between tobacco and alcohol use and AF were combined by inverse-variance weighted (IVW), simple median, weighted median, MR-robust adjusted profile score method, MR-PRESSO, and multivariable MR.ResultsA total of 65,446 AF patients and 522,744 referents were included. In the IVW analysis, the odds ratio per one-unit increase of smoking initiation was 1.11 (95% CI, 1.06–1.16; P = 3.35 × 10−6) for AF. Genetically predicted age at initiation of regular smoking, cigarettes per day and smoking cessation were not associated with AF. The IVW estimate showed that heavy alcohol consumption increased AF risk (OR, 1.11; 95% CI, 1.04–1.18; P = 0.001). The results were consistent in complementary analyses and multivariable MR.ConclusionOur MR study indicated that regular smoking was associated with increased risk of AF, no matter the age at initiation of regular smoking, or the number of cigarettes smoked per day. Genetically predicted heavy alcohol consumption increased the risk of AF.

Smoking and heart failure: a Mendelian randomization and mediation analysis.

AimsWe performed a Mendelian randomization (MR) study to elucidate the associations of ever smoking, lifelong smoking duration, and smoking cessation with heart failure (HF) risk.Methods and resultsWe extracted genetic variants associated with smoking initiation, age at initiation of regular smoking, cigarettes per day, and smoking cessation from the genome‐wide association study and Sequencing Consortium of Alcohol and Nicotine use (1.2 million individuals), as well as a composite lifetime smoking index from the UK Biobank (462 690 individuals). The associations between smoking phenotypes and HF were explored in the Heart Failure Molecular Epidemiology for Therapeutic Targets Consortium (47 309 cases; 930 014 controls) employing inverse variance‐weighted meta‐analysis and multivariable MR. The mediation effects of coronary artery disease and atrial fibrillation on smoking–HF risk were explored using mediation analysis. The odds ratios (ORs) for HF were 1.28 [95% confidence interval (CI), 1.22–1.36; P = 1.5 × 10−18] for ever regular smokers compared with never smokers and 1.25 (95% CI, 1.09–1.44; P = 1.6 × 10−3) for current smokers vs. former smokers. Genetic liability to smoking more cigarettes per day (OR, 1.37; 95% CI, 1.20–1.58; P = 6.4 × 10−6) and a higher composite lifetime smoking index (OR, 1.49; 95% CI, 1.31–1.70; P = 2.5 × 10−9) were associated with a higher risk of HF. The results were robust and consistent in all sensitivity analyses and multivariable MR after adjusting for HF risk factors, and their associations were independent of coronary artery disease and atrial fibrillation.ConclusionsGenetic liability to ever smoking and a higher lifetime smoking burden are associated with a higher risk of HF.

Smoking prevalence, nicotine dependence, and intention to quit among cigarettes smokers

Abstract Introduction Tobacco consumption remains a challenging issue to the global and public health that requires close monitoring of the spread of this epidemic and its impact. This study aims to assess the national prevalence and determinates of cigarette smoking and nicotine dependence in Saudi Arabia. Methods A cross-sectional national survey of a sample of 5148 of Saudi residents' ages 18 years or older was conducted through web-based-computer assisted telephone interviews. The two main measurements were current cigarette smoking status and nicotine dependence assessed using the Fagerstrom Test for Nicotine Dependence. Data was weighted by age, gender, and region to account for the different probabilities of selection. Descriptive and logistic regression analyses were used to assess cigarette smoking and nicotine dependence determinants. Results The national prevalence of cigarette smoking was 16.18% (95% CI:14.59-17.77) with 14.12% (95% CI:12.64-15.59) current daily smoking prevalence. Almost 72% of smokers started smoking before the age of 22 and 27% of smokers were highly dependent on nicotine. Having a smoker parent (AOR=1.84[95%CI:1.31-2.58], P &amp;lt; 0.001) or a smoker close friend (AOR=6.49[95%CI:3.89-10.81], P &amp;lt; 0.001) were significantly associated with being a smoker. Higher nicotine dependence level was significantly associated with early onset of regular smoking (ages&amp;lt;18) (AOR=2.71 [95%CI:1.38-5.34],P&amp;lt;0.001) and lower attempting to quit (AOR=0.51[95% CI:0.32-0.83],P&amp;lt;0.01). Conclusions Cigarettes smoking and nicotine dependence are prevalent in Saudi Arabia. The study found the majority of smokers started regular smoking before the age of 22 and the early onset of smoking was associated with a higher nicotine dependence level. Restrict access to tobacco products to those below the age of 22 will help reduce smoking prevalence and lifetime addiction to nicotine. Key messages Majority of smokers initiated smoking by the age of 21 and early regular smoking initiation was associated with higher nicotine dependence. Strategies to prevent initiation before the age of 21 will help prevent addiction to nicotine.

Comparing the potential causal influence of two indicators of early alcohol use on later alcohol use disorder symptoms.

Age of first drink (AFD) has repeatedly been found to be associated with alcohol use disorder (AUD); however, some studies suggest this is a noncausal effect that may be due to childhood risk factors or familial influences. In contrast to indicators of any early alcohol use, such as AFD, indicators of a pattern of repeated drinking may be more likely to be causally associated with later problematic alcohol use. The current study examined AFD and age of onset of regular drinking (ARD; defined as drinking at least once a month for 6 or more months) as quasicausal predictors of lifetime AUD symptoms. Participants were 3,005 adult Australian twins who reported having been regular drinkers in their lifetime. Semistructured interviews were conducted to assess AFD, ARD, AUD, externalizing symptomatology, and other substance use. Personality traits were assessed via questionnaire. Unadjusted and adjusted multilevel discordant twin models were conducted using data from 1,041 complete twin pairs; adjusted models included socioeconomic status, personality, conduct disorder, and early initiation of regular smoking and marijuana use as covariates. Results from fully adjusted models controlling for familial confounds provided evidence for a causal influence of ARD on AUD symptoms, whereby twins with an earlier age of regular drinking than their cotwin had more lifetime AUD symptoms. However, AFD did not significantly predict AUD symptoms after adjusting for confounds. These results suggest that early regular drinking may serve as a causal risk factor for future problems, while early initiation of any alcohol use may indicate genetic liability. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Investigating the genetic and causal relationship between initiation or use of alcohol, caffeine, cannabis and nicotine

BackgroundCaffeine, alcohol, nicotine and cannabis are commonly used psychoactive substances. While the use of these substances has been previously shown to be genetically correlated, causality between these substance use traits remains unclear. We aimed to revisit the genetic relationships among different measures of SU using genome-wide association study (GWAS) summary statistics from the UK Biobank, International Cannabis Consortium, and GWAS & Sequencing Consortium of Alcohol and Nicotine use. MethodsWe obtained GWAS summary statistics from the aforementioned consortia for ten substance use traits including various measures of alcohol consumption, caffeine consumption, cannabis initiation and smoking behaviours. We then conducted SNP-heritability (h2) estimation for individual SU traits, followed by genetic correlation analyses and two-sample Mendelian randomisation (MR) studies between substance use trait pairs. ResultsSNP h2 of the ten traits ranged from 0.03 to 0.11. After multiple testing correction, 29 of the 45 trait pairs showed evidence of being genetically correlated. MR analyses revealed that most SU traits were not causally associated with each other. However, we found evidence for an MR association between regular smoking initiation and caffeine consumption 40.17 mg; 95 % CI: [24.01, 56.33] increase in caffeine intake per doubling of odds in smoking initiation). Our findings were robust against horizontal pleiotropy, SNP-outliers, and the direction of causality was consistent in all MR analyses. ConclusionsMost of the substance traits were genetically correlated but there is little evidence to establish causality apart from the relationship between smoking initiation and caffeine consumption.

Association between polygenic risk for tobacco or alcohol consumption and liability to licit and illicit substance use in young Australian adults

BackgroundCo-morbid substance use is very common. Despite a historical focus using genetic epidemiology to investigate comorbid substance use and misuse, few studies have examined substance-substance associations using polygenic risk score (PRS) methods. MethodsUsing summary statistics from the largest substance use GWAS to date (258,797- 632,802 subjects), GWAS and Sequencing Consortium of Alcohol and Nicotine use (GSCAN), we constructed PRSs for smoking initiation (PRS-SI), age of initiation of regular smoking (PRS-AI), cigarettes per day (PRS-CPD), smoking cessation (PRS-SC), and drinks per week (PRS-DPW). We then estimated the fixed effect of individual PRSs on 22 lifetime substance use and substance use disorder phenotypes collected in an independent sample of 2463 young Australian adults using genetic restricted maximal likelihood (GREML) in Genome-wide Complex Trait Analysis (GCTA), separately in females, males and both sexes together. ResultsAfter accounting for multiple testing, PRS-SI significantly explained variation in the risk of cocaine (0.67%), amphetamine (1.54%), hallucinogens (0.72%), ecstasy (1.66%) and cannabis initiation (0.97%), as well as DSM-5 alcohol use disorder (0.72%). PRS-DPW explained 0.75%, 0.59% and 0.90% of the variation of cocaine, amphetamine and ecstasy initiation respectively. None of the 22 phenotypes including emergent classes of substance use were significantly predicted by PRS-AI, PRS-CPD, and PRS-SC. ConclusionsTo our knowledge, this is the first study to report significant genetic overlap between the polygenic risks for smoking initiation and alcohol consumption and the risk of initiating major classes of illicit substances. PRSs constructed from large discovery GWASs allows the detection of novel genetic associations.

Adolescence and Later Life Disease Burden: Quantifying the Contribution of Adolescent Tobacco Initiation From Longitudinal Cohorts

PurposeAdolescence is a time of initiation of behaviors leading to noncommunicable diseases (NCDs). We use tobacco to illustrate a novel method for assessing the contribution of adolescence to later burden. MethodsData on initiation of regular smoking during adolescence (10–19 years) and current adult smoking were obtained from the 1958 British Birth Cohort, the U.S. National Longitudinal Study of Adolescent Health (Add Health), the Pelotas 1982 Birth Cohort, and the Victorian Adolescent Health Cohort Study. We estimated an “adolescent attributable fraction” (AAF) by calculating the proportion of persisting adult daily smoking initiated < age 20 years. We used findings to estimate AAFs for >155 countries using contemporary surveillance data. ResultsIn the 1958 British Birth Cohort, 81.6% of daily smokers at age 50 years initiated < age 20 years, with a risk ratio of 6.1 for adult smoking related to adolescent initiation. The adjusted AAF was 69.1. Proportions of smokers initiating <20 years, risk ratio, and AAFs were 83.3%, 7.0%, and 70.4% for Add Health; 75.5%, 3.7%, and 50.2% in Victorian Adolescent Health Cohort Study; and 70.9%, 5.8%, and 56.9% in Pelotas males and 89.9%, 6.4%, and 75.9% in females. Initiation <16 years resulted in the highest AAFs. Estimated AAFs globally ranged from 35% in China to 76% in Argentina. ConclusionsThe contribution of adolescent smoking initiation to adult smoking burden is high, suggesting a need to formulate and implement effective actions to reduce smoking initiation in adolescents. Similar trends in other NCD risks suggest that adolescents will be central to future efforts to control NCDs.

Determinants of regular smoking onset in South Africa using duration analysis

ObjectivesSouth Africa has achieved significant success with its tobacco control policy. Between 1994 and 2012, the real price of cigarettes increased by 229%, while regular smoking prevalence decreased from about...

Associations Between Cigarette Print Advertising and Smoking Initiation Among African Americans.

The objective of this study was to examine changes in the annual number of cigarette advertisements in magazines with a predominantly African-American audience following the broadcast ban on tobacco, and whether fluctuations in cigarette print advertising targeting African Americans during the late-1970s until the mid-1980s were associated with declines in smoking initiation. We tabulated the annual number of cigarette advertisements from magazines with large African-American readerships (Ebony, Essence, and Jet) from 1960 to 1990. Advertisements were coded depending on whether they featured African-American models. We calculated the incidence rate of regular smoking initiation from 1975 to 1990 for African-American 14-25years old using data from the 1992-1993, 1995-1996, 1998-1999, and 2001-2002 Tobacco Use Supplements of the Current Population Survey. We examined whether trends in smoking initiation coincided with trends in cigarette advertising practices among African Americans. The annual aggregated number of printed cigarette advertisements in Ebony, Essence, and Jet magazines increased at least five-fold starting in 1971, following the broadcast ban on cigarette advertising. A decrease in the percentage of ads by Brown & Williamson that showed African-American models was positively correlated (r=0.30) with declines in the incidence rate of smoking initiation among African Americans from the late-1970s to the mid-1980s. The tobacco industry adapted quickly following the broadcast ban on cigarettes by increasing print advertising in African-American magazines. However, changes in print advertising practices by were associated with declines in smoking initiation among African Americans from the late-1970s to mid-1980s.

Socioeconomic Disparities in Age of Initiation and Ever Tobacco Smoking: Findings from Romania

Smoking initiation is considered the fundamental behaviour that determines the future health burden of tobacco smoking in a society. The aim of the study was to evaluate the socio-demographic factors associated with initiation of regular smoking among adults. The data source was the 2011 Global Adult Tobacco Survey Romania (GATS), which is a cross-sectional, nationally representative study. Multivariate logistic regression model was applied for relevant analysis. Among males, the regular smoking initiation rate was significantly higher compared to females (52.4% vs. 18.5%; p<0.001). Mean age of smoking initiation was lower in men compared to women (18.4±4.8 vs. 21.5±6.8; p<0.001). Age in men, awareness of environmental tobacco smoke consequences and place of living for women as well as educational attainment and employment status in both genders were associated with ever regular smoking. Moreover, cohabitation with a smoker was associated with greater odds for initiating smoking among both genders. GATS revealed a significant but diverse role of socioeconomic factors in initiation of regular smoking among adult Romanians.

The association between peer, parental influence and tobacco product features and earlier age of onset of regular smoking among adults in 27 European countries.

Factors that influence smoking initiation and age of smoking onset are important considerations in tobacco control. We evaluated European Union (EU)-wide differences in the age of onset of regular smoking, and the potential role of peer, parental and tobacco product design features on the earlier onset of regular smoking among adults <40 years old in 27 EU countries. We analysed data from 4442 current and former smokers aged 15-39 years, collected for the Eurobarometer 77.1 survey (2012). Respondents reported their age at regular smoking onset and factors that influenced their decision to start smoking, including peer influence, parental influence and features of tobacco products. Multi-variable logistic regression, adjusted for age; geographic region; education; difficulty to pay bills; and gender, was used to assess the role of the various pro-tobacco influences on early onset of regular smoking (i.e. <18 years). Among ever smokers, the mean age of onset of regular smoking was 16.6 years, ranging from 15.8 to 18.8 years in member countries. 68.1% responded that they started smoking regularly when they were <18 years old. Ever smokers who reported they were influenced by peers (OR = 1.70; 95%CI 1.30-2.20) or parents (OR = 1.60; 95%CI 1.21-2.12) were more likely to have started smoking regularly <18 years old. No significant association between design and marketing features of tobacco products and an early initiation of regular smoking was observed (OR = 1.04; 95%CI 0.83-1.31). We identified major differences in smoking initiation patterns among EU countries, which may warrant different approaches in the prevention of tobacco use.