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1.
Nicotine Tob Res ; 2019 Jul 11.
Artigo em Inglês | MEDLINE | ID: mdl-31294817

RESUMO

INTRODUCTION: FTND (FagerstrÓ§m test for nicotine dependence) and TTFC (time to smoke first cigarette in the morning) are common measures of nicotine dependence (ND). However, genome-wide meta-analysis for these phenotypes has not been reported. METHODS: Genome-wide meta-analyses for FTND (N = 19,431) and TTFC (N = 18,567) phenotypes were conducted for adult smokers of European ancestry from 14 independent cohorts. RESULTS: We found that SORBS2 on 4q35 (p = 4.05 × 10-8), BG182718 on 11q22 (p = 1.02 × 10-8), and AA333164 on 14q21 (p = 4.11 × 10-9) were associated with TTFC phenotype. We attempted replication of leading candidates with independent samples (FTND, N = 7010 and TTFC, N = 10 061), however, due to limited power of the replication samples, the replication of these new loci did not reach significance. In gene-based analyses, COPB2 was found associated with FTND phenotype, and TFCP2L1, RELN, and INO80C were associated with TTFC phenotype. In pathway and network analyses, we found that the interconnected interactions among the endocytosis, regulation of actin cytoskeleton, axon guidance, MAPK signaling, and chemokine signaling pathways were involved in ND. CONCLUSIONS: Our analyses identified several promising candidates for both FTND and TTFC phenotypes, and further verification of these candidates was necessary. Candidates supported by both FTND and TTFC (CHRNA4, THSD7B, RBFOX1, and ZNF804A) were associated with addiction to alcohol, cocaine, and heroin, and were associated with autism and schizophrenia. We also identified novel pathways involved in cigarette smoking. The pathway interactions highlighted the importance of receptor recycling and internalization in ND. IMPLICATIONS: Understanding the genetic architecture of cigarette smoking and ND is critical to develop effective prevention and treatment. Our study identified novel candidates and biological pathways involved in FTND and TTFC phenotypes, and this will facilitate further investigation of these candidates and pathways.

2.
Nat Neurosci ; 22(7): 1196, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31168101

RESUMO

Several occurrences of the word 'schizophrenia' have been re-worded as 'liability to schizophrenia' or 'schizophrenia risk', including in the title, which should have been "GWAS of lifetime cannabis use reveals new risk loci, genetic overlap with psychiatric traits, and a causal effect of schizophrenia liability," as well as in Supplementary Figures 1-10 and Supplementary Tables 7-10, to more accurately reflect the findings of the work.

3.
Behav Genet ; 49(4): 349-365, 2019 07.
Artigo em Inglês | MEDLINE | ID: mdl-31111357

RESUMO

Studies testing the effect of single genetic variants on substance use have had modest success. This paper reviewed 39 studies using polygenic measures to test interaction with any type of environmental exposure (G×E) in alcohol, tobacco, and cannabis use. Studies using haplotype combinations, sum scores of candidate-gene risk alleles, and polygenic scores (PS) were included. Overall study quality was moderate, with lower ratings for the polygenic methods in the haplotype and candidate-gene score studies. Heterogeneity in investigated environmental exposures, genetic factors, and outcomes was substantial. Most studies (N = 30) reported at least one significant G×E interaction, but overall evidence was weak. The majority (N = 26) found results in line with differential susceptibility and diathesis-stress frameworks. Future studies should pay more attention to methodological and statistical rigor, and focus on replication efforts. Additional work is needed before firm conclusions can be drawn about the importance of G×E in the etiology of substance use.

5.
Mol Psychiatry ; 2019 Jan 04.
Artigo em Inglês | MEDLINE | ID: mdl-30610198

RESUMO

Attention-deficit/hyperactivity disorder (ADHD) is a severely impairing neurodevelopmental disorder with a prevalence of 5% in children and adolescents and of 2.5% in adults. Comorbid conditions in ADHD play a key role in symptom progression, disorder course and outcome. ADHD is associated with a significantly increased risk for substance use, abuse and dependence. ADHD and cannabis use are partly determined by genetic factors; the heritability of ADHD is estimated at 70-80% and of cannabis use initiation at 40-48%. In this study, we used summary statistics from the largest available meta-analyses of genome-wide association studies (GWAS) of ADHD (n = 53,293) and lifetime cannabis use (n = 32,330) to gain insights into the genetic overlap and causal relationship of these two traits. We estimated their genetic correlation to be r2 = 0.29 (P = 1.63 × 10-5) and identified four new genome-wide significant loci in a cross-trait analysis: two in a single variant association analysis (rs145108385, P = 3.30 × 10-8 and rs4259397, P = 4.52 × 10-8) and two in a gene-based association analysis (WDPCP, P = 9.67 × 10-7 and ZNF251, P = 1.62 × 10-6). Using a two-sample Mendelian randomization approach we found support that ADHD is causal for lifetime cannabis use, with an odds ratio of 7.9 for cannabis use in individuals with ADHD in comparison to individuals without ADHD (95% CI (3.72, 15.51), P = 5.88 × 10-5). These results substantiate the temporal relationship between ADHD and future cannabis use and reinforce the need to consider substance misuse in the context of ADHD in clinical interventions.

8.
Nat Neurosci ; 21(9): 1161-1170, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30150663

RESUMO

Cannabis use is a heritable trait that has been associated with adverse mental health outcomes. In the largest genome-wide association study (GWAS) for lifetime cannabis use to date (N = 184,765), we identified eight genome-wide significant independent single nucleotide polymorphisms in six regions. All measured genetic variants combined explained 11% of the variance. Gene-based tests revealed 35 significant genes in 16 regions, and S-PrediXcan analyses showed that 21 genes had different expression levels for cannabis users versus nonusers. The strongest finding across the different analyses was CADM2, which has been associated with substance use and risk-taking. Significant genetic correlations were found with 14 of 25 tested substance use and mental health-related traits, including smoking, alcohol use, schizophrenia and risk-taking. Mendelian randomization analysis showed evidence for a causal positive influence of schizophrenia risk on cannabis use. Overall, our study provides new insights into the etiology of cannabis use and its relation with mental health.

9.
J Epidemiol Community Health ; 72(8): 708-710, 2018 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-29666151

RESUMO

BACKGROUND: Body mass index (BMI) is correlated negatively with subjective well-being and positively with depressive symptoms. Whether these associations reflect causal effects is unclear. METHODS: We examined bidirectional, causal effects between BMI and mental health with Mendelian randomisation using summary-level data from published genome-wide association studies (BMI: n=339 224; subjective well-being: n=204 966; depressive symptoms: n=161 460). Genetic variants robustly related to the exposure variable acted as instrumental variable to estimate causal effects. We combined estimates of individual genetic variants with inverse-variance weighted meta-analysis, weighted median regression and MR-Egger regression. RESULTS: There was evidence for a causal, increasing effect of BMI on depressive symptoms and suggestive evidence for a decreasing effect of BMI on subjective well-being. We found no evidence for causality in the other direction. CONCLUSION: This study provides support for a higher BMI causing poorer mental health. Further research should corroborate these findings and explore mechanisms underlying this potential causality.

10.
Drug Alcohol Depend ; 187: 296-299, 2018 06 01.
Artigo em Inglês | MEDLINE | ID: mdl-29702338

RESUMO

BACKGROUND: There is high comorbidity between antisocial behaviour (ASB) and substance use, and twin studies have shown that part of the covariation is due to overlapping genetic influences. Here we used measured genetic effects to estimate the genetic correlations of ASB with nicotine, alcohol, and cannabis use. METHODS: We meta-analysed data from two genome-wide association studies for ASB and used existing summary statistics from the largest genome-wide association studies into substance use (ever smoking, cigarettes smoked per day, weekly alcohol consumption, and lifetime cannabis use). We performed cross-trait LD-score regression to estimate genetic correlations between ASB and substance use phenotypes explained by all single nucleotide polymorphisms (SNPs). When significant, we tested whether the signs of the regression coefficients of SNPs from the ASB and substance use phenotypes were in the same direction across multiple p-value thresholds and examined enrichment in overlap of the strongest associated SNPs. RESULTS: We found nominally significant genetic correlations of ASB with lifetime cannabis use (rg = 0.69, p=.016) and cigarettes per day (rg = 0.59, p = 0.036) but not with weekly alcohol consumption or ever smoking. Sign-tests revealed consistent directions of effect of SNPs for ASB and cannabis use for all p-value thresholds except the most stringent one, whereas for ASB with cigarettes per day no consistent evidence was found. We found no evidence of enrichment in overlap of the most associated SNPs across these traits. CONCLUSION: Using measured genetic variants, we found preliminary support for a genetic correlation of ASB with lifetime cannabis use and cigarettes per day.


Assuntos
Consumo de Bebidas Alcoólicas/genética , Transtorno da Personalidade Antissocial/genética , Abuso de Maconha/genética , Fumar/genética , Tabagismo/genética , Adolescente , Adulto , Consumo de Bebidas Alcoólicas/psicologia , Transtorno da Personalidade Antissocial/psicologia , Comorbidade , Feminino , Estudo de Associação Genômica Ampla , Humanos , Masculino , Abuso de Maconha/psicologia , Fenótipo , Polimorfismo de Nucleotídeo Único , Fumar/psicologia , Tabagismo/psicologia , Adulto Jovem
11.
Addiction ; 113(7): 1333-1338, 2018 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-29334416

RESUMO

BACKGROUND AND AIMS: Epidemiological studies consistently show co-occurrence of use of different addictive substances. Whether these associations are causal or due to overlapping underlying influences remains an important question in addiction research. Methodological advances have made it possible to use published genetic associations to infer causal relationships between phenotypes. In this exploratory study, we used Mendelian randomization (MR) to examine the causality of well-established associations between nicotine, alcohol, caffeine and cannabis use. METHODS: Two-sample MR was employed to estimate bidirectional causal effects between four addictive substances: nicotine (smoking initiation and cigarettes smoked per day), caffeine (cups of coffee per day), alcohol (units per week) and cannabis (initiation). Based on existing genome-wide association results we selected genetic variants associated with the exposure measure as an instrument to estimate causal effects. Where possible we applied sensitivity analyses (MR-Egger and weighted median) more robust to horizontal pleiotropy. RESULTS: Most MR tests did not reveal causal associations. There was some weak evidence for a causal positive effect of genetically instrumented alcohol use on smoking initiation and of cigarettes per day on caffeine use, but these were not supported by the sensitivity analyses. There was also some suggestive evidence for a positive effect of alcohol use on caffeine use (only with MR-Egger) and smoking initiation on cannabis initiation (only with weighted median). None of the suggestive causal associations survived corrections for multiple testing. CONCLUSIONS: Two-sample Mendelian randomization analyses found little evidence for causal relationships between nicotine, alcohol, caffeine and cannabis use.

12.
Eur Child Adolesc Psychiatry ; 27(9): 1123-1132, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-28638947

RESUMO

Conduct problems in children and adolescents can predict antisocial personality disorder and related problems, such as crime and conviction. We sought an explanation for such predictions by performing a genetic longitudinal analysis. We estimated the effects of genetic, shared environmental, and unique environmental factors on variation in conduct problems measured at childhood and adolescence and antisocial personality problems measured at adulthood and on the covariation across ages. We also tested whether these estimates differed by sex. Longitudinal data were collected in the Netherlands Twin Register over a period of 27 years. Age appropriate and comparable measures of conduct and antisocial personality problems, assessed with the Achenbach System of Empirically Based Assessment, were available for 9783 9-10-year-old, 6839 13-18-year-old, and 7909 19-65-year-old twin pairs, respectively; 5114 twins have two or more assessments. At all ages, men scored higher than women. There were no sex differences in the estimates of the genetic and environmental influences. During childhood, genetic and environmental factors shared by children in families explained 43 and 44% of the variance of conduct problems, with the remaining variance due to unique environment. During adolescence and adulthood, genetic and unique environmental factors equally explained the variation. Longitudinal correlations across age varied between 0.20 and 0.38 and were mainly due to stable genetic factors. We conclude that shared environment is mainly of importance during childhood, while genetic factors contribute to variation in conduct and antisocial personality problems at all ages, and also underlie its stability over age.


Assuntos
Transtorno da Personalidade Antissocial/genética , Transtorno da Conduta/genética , Doenças em Gêmeos/genética , Exposição Ambiental/efeitos adversos , Adolescente , Adulto , Idoso , Transtorno da Personalidade Antissocial/patologia , Criança , Transtorno da Conduta/patologia , Doenças em Gêmeos/patologia , Feminino , Humanos , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Adulto Jovem
13.
Nicotine Tob Res ; 20(7): 836-842, 2018 Jun 07.
Artigo em Inglês | MEDLINE | ID: mdl-28575460

RESUMO

Introduction: Classical twin studies show that smoking is heritable. To determine if shared family environment plays a role in addition to genetic factors, and if they interact (G×E), we use a children-of-twins design. In a second sample, we measure genetic influence with polygenic risk scores (PRS) and environmental influence with a question on exposure to smoking during childhood. Methods: Data on smoking initiation were available for 723 children of 712 twins from the Netherlands Twin Register (64.9% female, median birth year 1985). Children were grouped in ascending order of risk, based on smoking status and zygosity of their twin-parent and his/her co-twin: never smoking twin-parent with a never smoking co-twin; never smoking twin-parent with a smoking dizygotic co-twin; never smoking twin-parent with a smoking monozygotic co-twin; and smoking twin-parent with a smoking or never smoking co-twin. For 4072 participants from the Netherlands Twin Register (67.3% female, median birth year 1973), PRS for smoking were computed and smoking initiation, smoking heaviness, and exposure to smoking during childhood were available. Results: Patterns of smoking initiation in the four group children-of-twins design suggested shared familial influences in addition to genetic factors. PRS for ever smoking were associated with smoking initiation in all individuals. PRS for smoking heaviness were associated with smoking heaviness in individuals exposed to smoking during childhood, but not in non-exposed individuals. Conclusions: Shared family environment influences smoking, over and above genetic factors. Genetic risk of smoking heaviness was only important for individuals exposed to smoking during childhood, versus those not exposed (G×E). Implications: This study adds to the very few existing children-of-twins (CoT) studies on smoking and combines a CoT design with a second research design that utilizes polygenic risk scores and data on exposure to smoking during childhood. The results show that shared family environment affects smoking behavior over and above genetic factors. There was also evidence for gene-environment interaction (G×E) such that genetic risk of heavy versus light smoking was only important for individuals who were also exposed to (second-hand) smoking during childhood. Together, these findings give additional incentive to recommending parents not to expose their children to cigarette smoking.

14.
Drug Alcohol Depend ; 183: 7-12, 2018 02 01.
Artigo em Inglês | MEDLINE | ID: mdl-29220643

RESUMO

BACKGROUND: Genetic and environmental factors contribute about equally to alcohol-related phenotypes in adulthood. In the present study, we examined whether more stress at home or low satisfaction with life might be associated with heavier drinking or more alcohol-related problems in individuals with a high genetic susceptibility to alcohol use. METHODS: Information on polygenic scores and drinking behavior was available in 6705 adults (65% female; 18-83 years) registered with the Netherlands Twin Register. Polygenic risk scores (PRSs) were constructed for all subjects based on the summary statistics of a large genome-wide association meta-analysis on alcohol consumption (grams per day). Outcome measures were quantity of alcohol consumption and alcohol-related problems assessed with the Alcohol Use Disorders Identification Test (AUDIT). Stress at home and life satisfaction were moderating variables whose significance was tested by Generalized Estimating Equation analyses taking familial relatedness, age and sex into account. RESULTS: PRSs for alcohol were significantly associated with quantity of alcohol consumption and alcohol-related problems in the past year (R2=0.11% and 0.10% respectively). Participants who reported to have experienced more stress in the past year and lower life satisfaction, scored higher on alcohol-related problems (R2=0.27% and 0.29 respectively), but not on alcohol consumption. Stress and life satisfaction did not moderate the association between PRSs and the alcohol outcome measures. CONCLUSIONS: There were significant main effects of polygenic scores and of stress and life satisfaction on drinking behavior, but there was no support for PRS-by-stress or PRS-by-life satisfaction interactions on alcohol consumption and alcohol-related problems.


Assuntos
Consumo de Bebidas Alcoólicas/genética , Alcoolismo/genética , Herança Multifatorial/genética , Satisfação Pessoal , Estresse Psicológico/psicologia , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Alcoolismo/complicações , Feminino , Interação Gene-Ambiente , Estudo de Associação Genômica Ampla , Humanos , Masculino , Pessoa de Meia-Idade , Países Baixos , Fenótipo , Fatores de Risco , Estresse Psicológico/complicações , Adulto Jovem
15.
Appetite ; 120: 565-570, 2018 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-29017907

RESUMO

A large proportion of adolescents eats too many energy-dense snacks, which is detrimental for their current and future health. To understand how to promote healthy dietary behaviors in adolescents, we need to identify factors that affect their snacking. While previous cross-sectional work has shown mother-child similarities in eating behavior, longitudinal studies are lacking. Hence, the first aim of this study was to examine whether maternal snacking predicted changes in adolescents' snacking over time. A second aim was to examine whether adolescents' television viewing magnified the strength of this longitudinal association. Television viewing may increase the motivation to eat the snacks consumed by mothers later on, for example through food advertisement exposure and mindless eating. To address both aims, 2051 adolescents (Mage baseline = 13.81; 51.5% boys) were asked to report on their snacking and television viewing three times, with intervals of one year. Moreover, a subsample of mothers of adolescents (N = 1080) reported on their snacking at baseline as well. The results indicate that maternal snacking indeed predicts adolescents' snacking over time and that this effect is more pronounced among adolescents who watch a great amount of television. These findings attest to the importance of mothers in forming adolescents' snacking, not only concurrently but also prospectively. Additionally, this study highlights the relevance of assessing other home environmental factors that may influence maternal effects on their children's snacking.


Assuntos
Comportamento Alimentar , Relações Mãe-Filho , Lanches , Televisão , Adolescente , Criança , Dieta , Feminino , Comportamentos Relacionados com a Saúde , Humanos , Estudos Longitudinais , Masculino , Mães , Fatores Socioeconômicos
17.
Eur J Epidemiol ; 33(3): 323-334, 2018 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-29260431

RESUMO

Alternative tobacco products are increasing in popularity. An important question is whether their use is associated with or even leads to conventional smoking, but large-scale (European) studies are scarce. In two cohorts of Dutch adolescents (Cohort I n = 6819, mean age = 13.8 SD = 1.1, 48.2% female; Cohort II n = 2758, mean age = 17.3 SD = 1.8, 61.3% female), we investigated use of electronic (e)-cigarettes with nicotine, e-cigarettes without nicotine and waterpipe. Generalized estimating equation modelling was conducted with ever conventional smoking as the dependent variable (0 = no, 1 = yes) and ever alternative tobacco use as the independent variable, correcting for clustering within schools, age, sex and education in both cohorts. In a subsample (n = 2100), the association between alternative tobacco use at baseline and conventional smoking 6 months later was tested, taking into account smoking propensity (based on personality, susceptibility to peer pressure and smoking intentions). Ever use prevalence was 13.7% for e-cigarettes with nicotine, 29.4% for e-cigarettes without nicotine and 22.1% for waterpipe in Cohort I and 12.3, 27.6 and 45.3% respectively in Cohort II. Ever smokers had tried alternative tobacco products more often than never smokers. Among never-smoking adolescents at baseline, alternative tobacco use predicted ever smoking 6 months later (e-cigarettes with nicotine OR 11.90 95% CI 3.36-42.11; e-cigarettes without nicotine OR 5.36 95% CI 2.73-10.52; waterpipe OR 5.36 95% CI 2.78-10.31). This association was strongest for adolescents with a low baseline risk of smoking. Experimenting with alternative tobacco products is common among Dutch youth. Alternative tobacco use predicts (future) smoking, especially among adolescents with a low smoking propensity.

18.
Appetite ; 123: 191-200, 2018 04 01.
Artigo em Inglês | MEDLINE | ID: mdl-29277519

RESUMO

Although parents often report positive intentions to promote and create a healthy food environment for their children (e.g., setting limits to snacks offered), they also experience difficulties in translating these intentions into actual behaviors. In this position paper, we argue that automatic processes explain an important part of the gap between parents' intentions and their actual food parenting behaviors. We provide a conceptual framework in which we hypothesize that automatic effects on food parenting occur through two key interrelated constructs: habits (key outcome construct) and volitional regulation behaviors (key mediating construct). Moreover, we discuss potentially important impulse-focused techniques that may directly change habits (e.g., nudging; inhibitory control training) or indirectly through volitional regulation behaviors (e.g., implementation intentions; mental contrasting). We make use of the literature on the role of intention-behavior discordance in general health behaviors and discuss implications for food parenting practices. Our framework provides a dual process view towards food parenting and may help to explain when and why parents are likely to engage in (un)healthy food parenting behaviors. In addition, this framework may hopefully stimulate research on (combinations of old and) new techniques to promote good food parenting behaviors.


Assuntos
Comportamento Infantil/psicologia , Dieta/psicologia , Comportamentos Relacionados com a Saúde , Intenção , Poder Familiar/psicologia , Criança , Humanos , Metanálise como Assunto , Relações Pais-Filho , Pais/psicologia , Autonomia Pessoal , Lanches
19.
Behav Genet ; 48(1): 1-11, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-29043520

RESUMO

For the participants in the Netherlands Twin Register (NTR) we constructed the extended pedigrees which specify all relations among nuclear and larger twin families in the register. A total of 253,015 subjects from 58,645 families were linked to each other, to the degree that we had information on the relations among participants. We describe the algorithm that was applied to construct the pedigrees. For > 30,000 adolescent and adult NTR participants data were available on harmonized neuroticism scores. We analyzed these data in the Mendel software package (Lange et al., Bioinformatics 29(12):1568-1570, 2013) to estimate the contributions of additive and non-additive genetic factors. In contrast to much of the earlier work based on twin data rather than on extended pedigrees, we could also estimate the contribution of shared household effects in the presence of non-additive genetic factors. The estimated broad-sense heritability of neuroticism was 47%, with almost equal contributions of additive and non-additive (dominance) genetic factors. A shared household effect explained 13% and unique environmental factors explained the remaining 40% of the variance in neuroticism.


Assuntos
Doenças em Gêmeos/genética , Neuroticismo/fisiologia , Gêmeos/genética , Família/psicologia , Feminino , Humanos , Masculino , Modelos Genéticos , Países Baixos/epidemiologia , Linhagem , Sistema de Registros , Meio Social , Gêmeos Dizigóticos/genética , Gêmeos Monozigóticos/genética
20.
Nicotine Tob Res ; 2017 Dec 08.
Artigo em Inglês | MEDLINE | ID: mdl-29228387

RESUMO

Introduction: The common genetic variant (rs1051730) in the 15q24 nicotinic acetylcholine receptor gene cluster CHRNA5-CHRNA3-CHRNB4 was associated with smoking quantity and has been reported to be associated also with reduced ability to quit smoking in pregnant women but results were inconsistent in non pregnant women. The aim of this study was to explore the association between rs1051730 and smoking cessation during pregnancy in a sample of Dutch women. Methods: Data on smoking during pregnancy were available from 1,337 women who ever smoked registered at the Netherlands Twin Register (NTR). Logistic regression was used to assess evidence for association of rs1051730 genotype on smoking during pregnancy. In a subsample of 561 women we investigated the influence of partner's smoking. Educational attainment and year of birth were used as covariates in both analyses. Results: There was evidence for a significant association between having 1 or more T allele's of the rs1051730 polymorphism and the likelihood of smoking during pregnancy (P = 0.03, odds ratio = 1.28, 95% confidence interval: 1.02, 1.61). However, this association attenuated when adjusting for birth cohort and educational attainment (P = 0.37, odds ratio = 1.12, 95% confidence interval: 0.87, 1.43). In the subsample, Smoking spouse was highly associated with smoking during pregnancy, even when educational attainment and birth cohort were included in the model. Conclusions: Our results did not support a strong association between this genetic variant and smoking during pregnancy. However, a strong association was observed with smoking behavior of the partner, regardless of the genotype of the women. Implications: The present study emphasizes the importance of social influences like spousal smoking on smoking behavior of pregnant women. Further research is needed to address the role of rs1051730 genetic variant in influencing smoking cessation and the interaction with important environmental factors like smoking behavior of the partner.

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