General and Specific Predictors of Nicotine and Alcohol Dependence in Early Adulthood: Genetic and Environmental Influences

Samek, Diana R.; Keyes, Margaret A.; Hicks, Brian M.; Bailey, Joanne; Iacono, William G.

doi:10.15288/jsad.2014.75.623

Cited by 14 publications

(15 citation statements)

References 47 publications

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“…We have now replicated this basic phenotypic model in several data sets (Bailey et al 2014; Samek et al 2014) and at different developmental stages (Epstein et al 2013). We have shown consistent evidence linking the general adolescent family environment (e.g., low parent-child conflict, high management) to the general externalizing latent factor in later adulthood – with a moderate effect size (i.e., the poorer the general family environment in adolescence, the greater the likelihood for externalizing problems in adulthood).…”

Section: Conceptual Model Guiding Our On-going Collaborationmentioning

confidence: 86%

“…There was limited attrition over time (range 90% to 94% retention). The total eligible SIBS sample size is 1,226 participants from 613 eligible families (56% adoptive, 55% female; 53% European ancestry, 39% Asian ancestry, 1% African ancestry, 7% mixed or other ancestry; see McGue et al 2007; Samek et al 2014 for more detail).…”

Section: Methodsmentioning

confidence: 99%

“…We have shown consistent evidence linking the general adolescent family environment (e.g., low parent-child conflict, high management) to the general externalizing latent factor in later adulthood – with a moderate effect size (i.e., the poorer the general family environment in adolescence, the greater the likelihood for externalizing problems in adulthood). There has been less consistent evidence linking the unique adolescent family smoking and drinking environments to unique variance in adult nicotine dependence and alcohol use disorder (Bailey et al 2014; Samek et al 2014), thus one effort is now focused on evaluating more complex patterns of gene-environment interplay relevant to the general pathway rather than substance-specific pathways. In addition, we are developing potential measures of general and drug-specific genetic influence for inclusion in this model.…”

Section: Conceptual Model Guiding Our On-going Collaborationmentioning

confidence: 99%

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A Test-Replicate Approach to Candidate Gene Research on Addiction and Externalizing Disorders: A Collaboration Across Five Longitudinal Studies

et al. 2016

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This study presents results from a collaboration across five longitudinal studies seeking to test and replicate models of gene-environment interplay in the development of substance use and externalizing disorders (SUDs, EXT). We describe an overview of our conceptual models, plan for gene-environment interplay analyses, and present main effects results evaluating six candidate genes potentially relevant to SUDs and EXT (MAOA, 5-HTTLPR, COMT, DRD2, DAT1, and DRD4). All samples included rich longitudinal and phenotypic measurements from childhood/adolescence (ages 5–13) through early adulthood (ages 25–33); sample sizes ranged from 3,487 in the test sample, to ~600–1000 in the replication samples. Phenotypes included lifetime symptom counts of SUDs (nicotine, alcohol and cannabis), adult antisocial behavior, and an aggregate externalizing disorder composite. Covariates included the first 10 ancestral principal components computed using all autosomal markers in subjects across the data sets, and age at the most recent assessment. Sex, ancestry, and exposure effects were thoroughly evaluated. After correcting for multiple testing, only one significant main effect was found in the test sample, but it was not replicated. Implications for subsequent gene-environment interplay analyses are discussed.

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Section: Conceptual Model Guiding Our On-going Collaborationmentioning

confidence: 86%

Section: Methodsmentioning

confidence: 99%

Section: Conceptual Model Guiding Our On-going Collaborationmentioning

confidence: 99%

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A Test-Replicate Approach to Candidate Gene Research on Addiction and Externalizing Disorders: A Collaboration Across Five Longitudinal Studies

et al. 2016

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“…There has been extensive research into individual differences in alcohol and tobacco use, and the genetic component of these behaviours is well established. Heritability estimates range from 10 to 60% for alcohol use [1][2][3], with alcohol use disorders tending to have higher estimates than for levels of consumption [3,4]. Similarly, smoking behaviours have a genetic component with the heritability estimates of nicotine dependence higher (60-70%) than tobacco use (ever vs never) (40-50%) [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

“…It is clear from heritability studies that a significant proportion of the phenotypic variance in individual differences comes from environmental, or other unmeasured sources, and measurement error. Childhood trauma, parental substance dependence, parental divorce and stressful life events have all been cited as environmental risk factors [4,7,8]. Environmental influences on substance use are typically found to be more pronounced in adolescence and are associated with first use [8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Genetic and shared couple environmental contributions to smoking and alcohol use in the UK population

et al. 2019

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Alcohol use and smoking are leading causes of death and disability worldwide. Both genetic and environmental factors have been shown to influence individual differences in the use of these substances. In the present study we tested whether genetic factors, modelled alongside common family environment, explained phenotypic variance in alcohol use and smoking behaviour in the Generation Scotland (GS) family sample of up to 19,377 individuals. SNP and pedigree-associated effects combined explained between 18 and 41% of the variance in substance use. Shared couple effects explained a significant amount of variance across all substance use traits, particularly alcohol intake, for which 38% of the phenotypic variance was explained. We tested whether the within-couple substance use associations were due to assortative mating by testing the association between partner polygenic risk scores in 34,987 couple pairs from the UK Biobank (UKB). No significant association between partner polygenic risk scores were observed. Associations between an individual's alcohol PRS (b = 0.05, S.E. = 0.006, p < 2 × 10 −16) and smoking status PRS (b = 0.05, S.E. = 0.005, p < 2 × 10 −16) were found with their partner's phenotype. In support of this, G carriers of a functional ADH1B polymorphism (rs1229984), known to be associated with greater alcohol intake, were found to consume less alcohol if they had a partner who carried an A allele at this SNP. Together these results show that the shared couple environment contributes significantly to patterns of substance use. It is unclear whether this is due to shared environmental factors, assortative mating, or indirect genetic effects. Future studies would benefit from longitudinal data and larger sample sizes to assess this further.

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The Developmental Unfolding of Sibling Influences on Alcohol Use over Time

Samek

Goodman

Riley

et al. 2017

J Youth Adolescence

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Research has long demonstrated that siblings are similar in their alcohol use, however much of this work relies on cross-sectional samples or samples of adolescents alone and/or exclusive focus on older siblings' impact on younger siblings. Using a three time-point design from early adolescence to early adulthood (M ages = 14.9, 18.3, and 22.4 years, respectively; 55% female; 54% European ancestry, 38% Asian ancestry), we evaluated the prospective older and younger sibling influences on alcohol use across time (N = 613 sibling pairs; 35% sisters, 26% brothers, 39% mixed-gender; average age difference = 2.34 years; 34% full-biological siblings, 46% genetically-unrelated adopted siblings, 20% pairs where one child was the biological offspring of parents and the other was adopted). The results from both the traditional and random-intercept cross-lagged panel analyses showed that older siblings' alcohol use predicted younger siblings' alcohol use across each developmental transition and across a variety of sibling contexts (e.g., gender composition, age difference, genetic relatedness). On the other hand, younger siblings' alcohol use only predicted older siblings' alcohol use when siblings were close in age (1.5 years or less) and under conditions of high sibling companionship. These results add to a body of literature illustrating how both older and younger siblings are important socializing agents of adolescent and early adult alcohol use. Assessing or co-treating siblings for alcohol problems may be an important add-on to existing adolescent and early adult alcohol prevention and intervention programs.

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General and Specific Predictors of Nicotine and Alcohol Dependence in Early Adulthood: Genetic and Environmental Influences

Cited by 14 publications

References 47 publications

A Test-Replicate Approach to Candidate Gene Research on Addiction and Externalizing Disorders: A Collaboration Across Five Longitudinal Studies

A Test-Replicate Approach to Candidate Gene Research on Addiction and Externalizing Disorders: A Collaboration Across Five Longitudinal Studies

Genetic and shared couple environmental contributions to smoking and alcohol use in the UK population

The Developmental Unfolding of Sibling Influences on Alcohol Use over Time

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