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Toward a comprehensive developmental model of smoking initiation and nicotine dependence.

ABSTRACT: This study aims to identify predictors of smoking initiation and nicotine dependence (ND) to develop a comprehensive risk-factor model based on Kendler's development model for major depression.Data were drawn from the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC), Wave 2 (n=34,653). Risk factors were divided into five developmental tiers according to Kendler's model (childhood, early adolescence, late adolescence, adulthood, past-year). Hierarchical logistic regression models were built to predict the risk of smoking initiation and the risk of ND, given initiation. The continuation ratio (CR) was tested by ordinal logistic regression to examine whether the impact of the predictors was the same on smoking initiation or ND.The final models highlighted the importance of different tiers for each outcome. The CR identified substantial differences in the predictors of smoking initiation versus ND. Childhood tier appears to be more determinant for smoking initiation while the effect of more distal tiers (i.e. childhood and early adolescence) was tempered by more proximal ones (i.e. late adolescence, adulthood and past-year) in ND, with few sex differences.The differential effect of some predictors on each outcome shows the complexity of pathways from smoking initiation to ND. While some risk factors may be shared, others impact only at one stage or have even an inverse effect. An adaptation of Kendler's developmental model for major depression showed high predictive power for smoking initiation and ND.

SUBMITTER: Garcia-Rodriguez O

PROVIDER: S-EPMC4253146 | biostudies-literature | 2014 Nov

REPOSITORIES: biostudies-literature

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Toward a comprehensive developmental model of smoking initiation and nicotine dependence.

García-Rodríguez Olaya O Blanco Carlos C Wall Melanie M MM Wang Shuai S Jin Chelsea J CJ Kendler Kenneth S KS

Drug and alcohol dependence 20140916

<h4>Background</h4>This study aims to identify predictors of smoking initiation and nicotine dependence (ND) to develop a comprehensive risk-factor model based on Kendler's development model for major depression.<h4>Methods</h4>Data were drawn from the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC), Wave 2 (n=34,653). Risk factors were divided into five developmental tiers according to Kendler's model (childhood, early adolescence, late adolescence, adulthood, past-year ...[more]

PMID: 25262528

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Project description:Genome-wide hypothesis-free discovery methods have identified loci that are associated with heavy smoking in adulthood. Research is needed to understand developmental processes that link newly discovered genetic risks with adult heavy smoking.To test how genetic risks discovered in genome-wide association studies of adult smoking influence the developmental progression of smoking behavior from initiation through conversion to daily smoking, progression to heavy smoking, nicotine dependence, and struggles with cessation.A 38-year, prospective, longitudinal study of a representative birth cohort.The Dunedin Multidisciplinary Health and Development Study of New Zealand.The study included 1037 male and female participants.We assessed genetic risk with a multilocus genetic risk score. The genetic risk score was composed of single-nucleotide polymorphisms identified in 3 meta-analyses of genome-wide association studies of smoking quantity phenotypes.Smoking initiation, conversion to daily smoking, progression to heavy smoking, nicotine dependence (Fagerström Test of Nicotine Dependence), and cessation difficulties were evaluated at 8 assessments spanning the ages of 11 to 38 years.Genetic risk score was unrelated to smoking initiation. However, individuals at higher genetic risk were more likely to convert to daily smoking as teenagers, progressed more rapidly from smoking initiation to heavy smoking, persisted longer in smoking heavily, developed nicotine dependence more frequently, were more reliant on smoking to cope with stress, and were more likely to fail in their cessation attempts. Further analysis revealed that 2 adolescent developmental phenotypes-early conversion to daily smoking and rapid progression to heavy smoking-mediated associations between the genetic risk score and mature phenotypes of persistent heavy smoking, nicotine dependence, and cessation failure. The genetic risk score predicted smoking risk over and above family history.Initiatives that disrupt the developmental progression of smoking behavior among adolescents may mitigate genetic risks for developing adult smoking problems. Future genetic research may maximize discovery potential by focusing on smoking behavior soon after smoking initiation and by studying young smokers.

Project description:BackgroundNicotine dependence is a significant public health issue, and understanding the factors associated with nicotine dependence in this population is crucial for developing effective interventions. This study examined the association between family functioning and nicotine dependence levels of smoking fathers based on the McMaster model of family functioning (MMFF), providing evidence for future interventions.MethodsIn this study, we selected fathers of first- to fifth-grade students from 10 pilot elementary schools in Qingdao whose families smoked. We used the Fagerstrom test to assess nicotine dependence and the Family Assessment Device to evaluate family functioning. We performed univariate analysis to compare differences among those with different levels of nicotine dependence, and we used an ordinal logistic regression analysis to investigate the influences related to nicotine dependence.ResultsThis study included 874 smokers, with 78.5% having mild nicotine dependence, 11.7% having moderate dependence, and 9.84% having severe dependence. Univariate analysis showed that smokers with severe dependence had lower education levels, higher prevalence of chronic diseases, more frequent alcohol consumption, and poorer family functioning compared to those with mild to moderate dependence. Ordinal logistic regression analysis showed that poorer general functioning scores (OR = 1.087, 95% CI: 1.008-1.173, P = 0.030), poorer behavioral control (OR = 1.124, 95% CI: 1.026-1.232, P = 0.012), more quit attempts, frequent alcohol consumption, and longer smoking duration may be associated with a higher likelihood of developing severe nicotine dependence. The older age of starting smoking and higher education level may be associated with a lower likelihood of developing severe nicotine dependence. However, it is important to note that the cross-sectional nature of this study precludes the determination of causal relationships.ConclusionsThis study finds that heavy nicotine dependence in smoking fathers is associated with risky behaviors and demographics such as longer smoking duration and frequent alcohol consumption. Targeted smoking cessation interventions are crucial for this group, taking these specific factors into consideration. Family functioning, particularly general functioning and behavioral control, may also be linked to nicotine dependence, indicating the need for further research in this area.

Project description:BackgroundWhile the heritability of cigarette smoking and nicotine dependence (ND) is well-documented, the contribution of specific genetic variants to specific phenotypes has not been closely examined. The objectives of this study were to test the associations between 321 tagging single-nucleotide polymorphisms (SNPs) that capture common genetic variation in 24 genes, and early smoking and ND phenotypes in novice adolescent smokers, and to assess if genetic predictors differ across these phenotypes.MethodsIn a prospective study of 1294 adolescents aged 12-13 years recruited from ten Montreal-area secondary schools, 544 participants who had smoked at least once during the 7-8 year follow-up provided DNA. 321 single-nucleotide polymorphisms (SNPs) in 24 candidate genes were tested for an association with number of cigarettes smoked in the past 3 months, and with five ND phenotypes (a modified version of the Fagerstrom Tolerance Questionnaire, the ICD-10 and three clusters of ND symptoms representing withdrawal symptoms, use of nicotine for self-medication, and a general ND/craving symptom indicator).ResultsThe pattern of SNP-gene associations differed across phenotypes. Sixteen SNPs in seven genes (ANKK1, CHRNA7, DDC, DRD2, COMT, OPRM1, SLC6A3 (also known as DAT1)) were associated with at least one phenotype with a p-value <0.01 using linear mixed models. After permutation and FDR adjustment, none of the associations remained statistically significant, although the p-values for the association between rs557748 in OPRM1 and the ND/craving and self-medication phenotypes were both 0.076.ConclusionsBecause the genetic predictors differ, specific cigarette smoking and ND phenotypes should be distinguished in genetic studies in adolescents. Fifteen of the 16 top-ranked SNPs identified in this study were from loci involved in dopaminergic pathways (ANKK1/DRD2, DDC, COMT, OPRM1, and SLC6A3).ImpactDopaminergic pathways may be salient during early smoking and the development of ND.

Project description:ImportanceMenthol may make cigarette smoke less aversive and could lead youth to smoke more frequently and become more dependent on nicotine.ObjectiveTo assess the association of menthol use with cigarette smoking frequency and nicotine dependence (ND) among youth cigarettes users.Design, setting, and participantsThis cohort study used a pooled sample of cohorts of US youth (aged 12-17 years at their baseline and follow-up interviews) in the Population Assessment of Tobacco and Health Study (September 2013 to November 2019). Household interviews were conducted using audio computer-assisted self-interviews. US youth who were past-30-day cigarette smokers at any of wave 2 through wave 5, completed the preceding survey (eg, wave 2 past-30-day cigarette smokers completed wave 1), and indicated whether they used menthol cigarettes were eligible. The association of menthol use with smoking frequency and ND was estimated using inverse probability of treatment weighting adjusted mean differences (aMDs), adjusted risk ratios (aRRs), and corresponding 95% CIs. Data were analyzed from December 2021 to March 2022.ExposuresMenthol use and transitions in use (switching to or from menthol cigarettes).Main outcomes and measuresMain outcomes were the number of days smoked in the past 30 days, the risk of frequent smoking (smoking ≥20 days in the past 30 days), and symptoms of ND.ResultsThere were a total of 1492 observations among 1096 US youth cigarette smokers, of whom 49.4% were female, 67.2% were non-Hispanic White, and 28.7% were aged 12 to 14 years at their baseline survey (all percentages are weighted). Among those who switched from not smoking to smoking (61% of the sample), menthol use was associated with smoking on 3.1 additional days (aMD; 95% CI, 1.9 to 4.2 days), 59% higher risk of being a frequent smoker (aRR, 1.59; 95% CI, 1.23 to 2.06), and 10% higher ND scores (aMD, 1.09; 95% CI, 1.02 to 1.17). Switching from smoking menthol to smoking nonmenthol (vs maintaining menthol use) was associated with smoking on 3.6 fewer days (aMD; 95% CI, -6.3 to -0.9 days) and 47% lower risk of being a frequent smoker (aRR, 0.68; 95% CI, 0.50 to 0.92).Conclusions and relevanceThese findings suggest that the addition of menthol to cigarettes is associated with increased smoking frequency and ND among US youth.

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Toward a comprehensive developmental model of smoking initiation and nicotine dependence.

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Toward a comprehensive developmental model of smoking initiation and nicotine dependence.

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