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Aims: To investigate how strongly smoking dependence and smoking dependence motives are associated with depressive symptoms among daily smokers and if these associations are independent of measured confounders and shared familial factors. Design Cross‐sectional individual‐based and within‐pair analyses. Setting: Fourth wave of the population‐based Finnish Twin Cohort conducted in 2011. Participants: 918 daily smokers born 1945–1957 (48% men), mean age 59.5 years including 38 twin pairs discordant for depression. Measurements Depressive symptoms were assessed using the Center for Epidemiologic Studies Depression scale with a cut off value ≥20 for depression. Smoking dependence was assessed using the Fagerström Test for Cigarette Dependence (FTCD) and smoking dependence motives with three subscales from the multi‐dimensional Brief Wisconsin Inventory of Smoking Dependence Motives (WISDM): primary dependence motives (PDM), affective enhancement (AE), and Taste. Logistic regressions, using standardized scores of independent variables and adjusted for multiple confounders with correction for sampling as twin pairs, were used in the individual‐based analyses. Conditional logistic regression was used to control for shared familial factors in discordant twin pairs. Findings Prevalence of depression was 18% (n = 163: 61 [14%] in men, n = 102 [22%] in women). Higher smoking dependence measured by the FTCD (OR 1.45; 95% CI 1.20, 1.75), and dependence motives measured by the PDM (1.56; 1.30, 1.87) and the AE (1.54; 1.28, 1.85) were associated with higher odds of depression. The associations remained after adjusting for individual confounders, except for neuroticism, which attenuated all associations. FTCD, PDM, and AE showed associations with depression within depression‐discordant monozygotic pairs, suggesting an association independent of familial factors. Conclusions: Depression appears to be associated with smoking dependence and smoking dependence motives related to heavy, automatic use and use to regulate affective states. The associations appear to be confounded or mediated by neuroticism but are independent of shared familial influences. [ABSTRACT FROM AUTHOR]

Background and Aims: Previous twin research suggests relationship status can moderate underlying genetic liability towards alcohol misuse. This paper examined: (1) whether genome‐wide polygenic scores (GPS) for alcohol consumption are associated with alcohol misuse; (2) whether these GPS are moderated by romantic relationships (gene–environment interaction; G × E) and (3) whether G × E results are consistent across sex. Design: Linear mixed‐effects models were used to test associations between genome‐wide polygenic scores, relationship status and alcohol use/misuse. Setting: Finnish twins born between 1983 and 1987 identified through Finland's central population registry. Participants: An intensively studied subset of Finnish Twin Study (FinnTwin12) during the young adult phase (aged 20–26 years). The analytical sample includes those with complete interview and genetic data (n = 1201). Measurements Key measurements included involvement in a romantic partnership, drinking frequency, intoxication frequency and DSM‐IV alcohol dependence (AD) symptoms. Genome‐wide polygenic scores (GPS) were created from available summary statistics from a large genome‐wide association study (GWAS) of drinks per week. Results: GPS predicted drinking frequency [b = 0.109; 95% confidence interval (CI) = 0.050, 0.168], intoxication frequency (b = 0.111; 95% CI = 0.054, 0.168) and AD symptoms (b = 0.123; 95% CI = 0.064, 0.182). Having a romantic relationship negatively influenced the association between GPS and drinking frequency (b = −0.105; 95% CI = −0.211, −0.001), intoxication frequency (b = −0.118; 95% CI = −0.220, −0.016) and AD symptoms (b = −0.119; 95% CI = −0.229, −0.009). There was a three‐way interaction between sex, relationship status and GPS for intoxication frequency (b = 0.223; 95% CI = 0.013, 0.433), such that the reduced association between GPS and intoxication frequency for those in a relationship was only apparent in males. We found no evidence of three‐way interactions for drinking frequency or AD symptoms. Conclusions: Being in a romantic relationship reduced the association between genetic predisposition and drinking, high‐risk drinking and alcohol problems. However, for high‐risk drinking the protective effect was limited to males, mapping onto earlier findings suggesting that males benefit more from romantic partnerships. [ABSTRACT FROM AUTHOR]

Aims: To estimate birth cohort effects on alcohol consumption and abstinence in Finland and to test differences between birth cohorts in genetic and environmental sources of variation in Finnish adult alcohol use. Design The Older Finnish Twin Cohort longitudinal survey study 1975–2011. Setting: Finland. Participants: A total of 26 121 same‐sex twins aged 18–95 years (full twin pairs at baseline n = 11 608). Measurements Outcome variables were the quantity of alcohol consumption (g/month) and abstinence (drinking zero g/month). Predictor variables were 10‐year birth cohort categories and socio‐demographic covariates. In quantitative genetic models, two larger cohorts (born 1901–20 and 1945–57) were compared. Findings: Multi‐level models in both sexes indicated higher levels of alcohol consumption in more recent birth cohorts and lower levels in earlier cohorts, compared with twins born 1921–30 (all P < 0.003). Similarly, compared with twins born 1921–30, abstaining was more common in earlier and less common in more recent cohorts (all P < 0.05), with the exception of men born 1911–20. Birth cohort differences in the genetic and environmental variance components in alcohol consumption were found: heritability was 21% [95% confidence interval (CI) = 0–56%] in the earlier‐born cohort of women [mean age 62.8, standard deviation (SD) = 5.3] and 51% (95% CI = 36–56%) in a more recent cohort (mean age 60.2, SD = 3.7) at the age of 54–74. For men, heritability was 39% (95% CI = 27–45%) in both cohorts. In alcohol abstinence, environmental influences shared between co‐twins explained a large proportion of variation in the earlier‐born cohort (43%, 95% CI = 23–63%), whereas non‐shared environmental (54%, 95% CI = 39–72%) and additive genetic influences (40%, 95% CI = 13–61%) were more important among more recent cohorts of men and women. Conclusion: The contribution of genetic and environmental variability to variability in alcohol consumption in the Finnish population appears to vary by birth cohort. [ABSTRACT FROM AUTHOR]

Aims To determine (1) the prospective associations of conduct problems during early adolescence with tobacco, alcohol and cannabis use in young adulthood and (2) to what extent these associations are due to overlapping genetic versus environmental influences. Design A prospective twin study using biometric twin modelling. Setting Finland. Participants A total of 1847 Finnish twins (943 males and 904 females) were interviewed in early adolescence, 73% of whom ( n = 1353, 640 males and 713 females) were retained in young adulthood. Measurements Symptom counts of conduct disorder (CD) criteria were obtained from a semi-structured clinical interview in early adolescence [age 14-15 years, mean = 14.2, standard deviation (SD) = 0.15]. Frequency of alcohol, tobacco and cannabis use was obtained from a semi-structured clinical interview in young adulthood (age 19.9-26.6 years, mean = 22.4, SD = 0.7). Findings We found modest to moderate phenotypical correlations ( r = 0.16-0.35) between early adolescent CD symptoms and substance use in young adulthood. In males, the phenotypical correlations of CD symptoms with all three substance use variables are explained largely by overlapping genetic influences. In females, overlapping shared environmental influences predominantly explain the phenotypical correlation between CD symptoms and tobacco and cannabis use. Conclusions Conduct disorder symptoms in early adolescence appear to moderately predict substance use in early adulthood. In males, genetic influences seem to be most important in explaining the relationship between conduct disorder symptoms and substance use whereas in females, shared environmental influences seem to be most important. [ABSTRACT FROM AUTHOR]

Aims To determine if associations of alcohol consumption with all-cause mortality replicate in discordant monozygotic twin comparisons that control for familial and genetic confounds. Design A 30-year prospective follow-up. Setting Population-based older Finnish twin cohort. Participants Same-sex twins, aged 24-60 years at the end of 1981, without overt comorbidities, completed questionnaires in 1975 and 1981 with response rates of 89 and 84%. A total of 15 607 twins were available for mortality follow-up from the date of returned 1981 questionnaires to 31 December 2011; 14 787 twins with complete information were analysed. Measurements Self-reported monthly alcohol consumption, heavy drinking occasions (HDO) and alcohol-induced blackouts. Adjustments for age, gender, marital and smoking status, physical activity, obesity, education and social class. Findings Among twins as individuals, high levels of monthly alcohol consumption (≥ 259 g/month) associated with earlier mortality [hazard ratio (HR) = 1.63, 95% confidence interval (CI) = 1.47-1.81]. That association was replicated in comparisons of all informatively drinking-discordant twin pairs (HR = 1.91, 95% CI = 1.49-2.45) and within discordant monozygotic (MZ) twin pairs (HR = 2.24, 95% CI = 1.31-3.85), with comparable effect size. Smaller samples of MZ twins discordant for HDO and blackouts limited power; a significant association with mortality was found for multiple blackouts (HR = 2.82, 95% CI = 1.30-6.08), but not for HDO. Conclusions The associations of high levels of monthly alcohol consumption and alcohol-induced blackouts with increased all-cause mortality among Finnish twins cannot be explained by familial or genetic confounds; the explanation appears to be causal. [ABSTRACT FROM AUTHOR]

Previous studies have found inverse associations between intelligence quotient (IQ) and cigarette smoking, but the causal pathways linking IQ with smoking status and nicotine dependence (ND) are not well understood. The aim of this study was to explore the associations between IQ and ND using a genetically informative twin design to detect whether any association is because of shared genetic or environmental factors. A population-based twin cohort with IQ measured in adolescence and ND later in life, analysed by classical twin modeling based on linear structural equations. Swedish national registry data. A total of 5040 male twins born 1951-84. IQ was measured at military conscription at a mean age of 18 years. ND was self-reported at the ages of 22-57 years using the Fagerström Test for ND scale (FTND). Both cigarette smoking and Swedish snus use were analysed. Both IQ and ND showed moderate heritability (0.58 and 0.39, respectively). The heritability of ND was similar for cigarette smoking and snus use. The phenotypic correlation between IQ and ND was weak: −0.11 (−0.16, −0.06) for total ND. Bivariate analysis revealed that this correlation was mainly because of genetic factors, but still the genetic correlation between IQ and ND from cigarette smoking was only −0.24. Nicotine dependence, as measured by the Fagerström Test for Nicotine Dependence, shows moderate heritability in both smokers and snus users but is only weakly associated with intelligence quotient; common genetic factors underlying nicotine dependence and intelligence quotient probably account for little of the observed association between smoking and intelligence quotient. [ABSTRACT FROM AUTHOR]