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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]

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]

Background Coffee is a highly popular drink associated with the pathogenesis of several diseases and the use of tobacco and alcohol. Considering the worldwide consumption, coffee has a substantial effect on individual wellbeing and public health. The role of genetic factors contributing to interindividual differences and their stability in coffee use is not well known. Aims We analysed the heritability of coffee consumption and its stability in a large population-based sample of Finnish twins. Design In 1975 and 1981 a postal questionnaire on coffee consumption was sent to all Finnish same-sex twin pairs born before 1958. Responses were obtained from 10 716 complete twin pairs in 1975 (3409 monozygotic and 7307 dizygotic), of whom 8124 also responded in 1981. The data were analysed using classical twin modelling based on linear structural equations. Findings Additive genetic and unique environmental factors affected coffee drinking, whereas shared environmental factors did not show any effect. Heritability of coffee consumption, adjusted for age and sex, was estimated as 0.56 in 1975 and 0.45 in 1981. Coffee consumption showed a moderate correlation between these two time-points ( r = 0.58 in men and 0.55 in women). Genetic factors affecting coffee consumption were stable: additive genetic correlations were 0.84 in men and 0.83 in women, whereas unique environmental correlations were moderate (0.45 and 0.36). Additive genetic factors had the highest contribution in young adults. Conclusions Coffee consumption is affected by both additive genetic and unique environmental factors, each of which plays an almost equally important role. The long-term stability of coffee consumption is affected mainly by a stable set of additive genetic factors. [ABSTRACT FROM AUTHOR]

Aims To control for familial confounds, we studied the association between adolescent physical activity and later smoking in twin siblings discordant for their baseline physical activity. Design and measurements In this prospective population-based twin study, we asked whether persistent physical activity/inactivity in adolescence (assessed at 16, 17 and 18.5 years) predicted questionnaire-reported daily smoking at ages 22–27. Twins who, on the three baseline questionnaires, consistently reported frequent leisure physical activity (more than three times weekly) were classified as persistent exercisers, those who exercised less than three times monthly were called persistently inactive, others were occasional exercisers. Setting Finland. Participants A total of 4240 individuals, including 1870 twin pairs. Findings In analyses of individual twins, compared to persistent activity, persistent physical inactivity predicted increased risk of daily smoking (age- and sex-adjusted odds ratio 5.53, 95% confidence interval 3.88–7.88, P < 0.001). The risk remained elevated even after excluding all those who had smoked 50 cigarettes or more life-time at baseline and adjusted for educational level in adolescence. In within-pair analyses compared to the active members of discordant twin pairs, the physically inactive co-twins had increased risk of future daily smoking (sex-adjusted odds ratio 3.39, 95% confidence interval 1.56–7.39, P = 0.002). Conclusions Persistent physical inactivity in adolescence relates to adult smoking, even after familial factors are taken into account. [ABSTRACT FROM AUTHOR]

In this article the author comments on the study "Interplay of genetic risk factors and parent monitoring in risk for nicotine dependence." The author mentions that the study focuses on the gene-environment interaction in nicotine addiction. He notes that the study advances the knowledge about smoking behavior because it links a specific gene variant known to relate disease risk. He points out that it also discusses the effects of parent monitoring on adolescent smoking and alcohol use.

The article comments on the study conducted by M. Agrawal and M. Lynskey related to genetic epidemiology of cannabis use, abuse and dependence. The study explored the relationships between the use of cannabis together with tobacco and alcohol. It reflects that the study has various limitations in terms of addiction provenance and its genetic effects. The genetic epidemiology of cannabis has also been compared with alcoholism in terms of impacts on environmental and gene-environment interactions.

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]

To examine how adolescents’ inattentive behaviour, together with parental smoking patterns, predicts smoking initiation by age 14. A prospective, longitudinal study: baseline at ages 11–12, follow-up at age 14. A population-based sample of Finnish twins, born 1983–1987, with parents and classroom teachers as additional informants. Two groups were formed, allocating the co-twins of each family into separate groups: the study sample and a replication sample. Twin individuals ( n = 4552), aged 11–12 at baseline and 14 (average 14.04 years) at follow-up. At baseline, inattentiveness was assessed with the Multidimensional Peer Nomination Inventory (MPNI, Teacher Form) and parental smoking with individual questionnaires completed by each twins’ parents; at the age 14 follow-up, adolescent smoking was assessed with a self-report questionnaire. At age 14, 57% reported never having smoked, 34% had experimented with cigarettes and 9% were current smokers. Inattentiveness and parental smoking additively predicted both experimental and current smoking in adolescence. The effects were independent of each other. The risk related to inattentiveness itself is high, but in combination with the effects of parental smoking, the probability of current smoking can rise as high as 38%, compared with 5% without these two risk factors. For prevention purposes, parental commitment to non-smoking should be emphasized. [ABSTRACT FROM AUTHOR]

Background and aims: Research on adolescent predictors of later alcohol misuse is typically conducted on samples of singletons, and associations may be confounded by between‐family differences. To address potential confounding, we applied a co‐twin comparison design to evaluate whether differences between co‐twins in a wide array of adolescent risk factors predicted differences in young adult alcohol misuse. Design Longitudinal study in which associations between characteristics of the sample as adolescents were used to predict young adult alcohol misuse in individual‐level analyses and co‐twin comparisons. Setting: Finland. Participants: A total of 3402 individuals (1435 complete twin pairs; 36% monozygotic; 57% female) from the FinnTwin12 study. Measurements The young adult alcohol misuse outcome was a composite score of alcohol use and intoxication frequency. Adolescent predictors included factor scores representing academic performance, substance use, externalizing problems, internalizing problems, peer environment, physical health and relationship with parents; and single measures tapping alcohol expectancies, life events and pubertal development. Findings In individual‐level analyses, individuals with higher adolescent substance use, externalizing problems, time with friends, peer deviance, sports involvement, sleeping difficulties, parental discipline, positive alcohol expectancies and difficulty of life events reported higher alcohol misuse in young adulthood (Ps < 0.019, R2 = 0.0003–0.0310%). Conversely, those with higher adolescent internalizing problems, parent–child relationship quality and time with parents reported lower alcohol misuse (Ps < 0021, R2 = 0.0018–0.0093%). The associations with adolescent substance use and alcohol expectancies remained significant in co‐twin comparisons (Ps < 0.049, R2 = 0.0019–0.0314%). Further, academic performance emerged as a significant predictor, such that individuals with higher grades compared with their co‐twin reported higher young adult alcohol misuse (Ps < 0.029, R2 = 0.0449–0.0533%). Conclusions: Adolescent substance use, positive alcohol expectancies and higher academic performance appear to be robust predictors of later alcohol misuse. [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 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]

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]

Aims To investigate whether substance use disorders (SUDs) are associated with verbal intellectual ability, psychomotor processing speed, verbal and visual working memory, executive function and verbal learning in young adults, and to study the associations of SUD characteristics with cognitive performance. Participants A population-based sample ( n = 466) of young Finnish adults aged 21–35 years. Measurements Diagnostic assessment was based on all available information from a structured psychiatric interview (SCID-I) and in- and out-patient medical records. Established neuropsychological tests were used in the cognitive assessment. Confounding factors included in the analyses were comorbid psychiatric disorders and risk factors for SUDs, representing behavioural and affective factors, parental factors, early initiation of substance use and education-related factors. Findings Adjusted for age and gender, life-time DSM-IV SUD was associated with poorer verbal intellectual ability, as measured with the Wechsler Adult Intelligence Scale–Revised (WAIS-R) vocabulary subtest, and slower psychomotor processing, as measured with the WAIS-R digit symbol subtest. Poorer verbal intellectual ability was accounted for by parental and own low basic education, whereas the association with slower psychomotor processing remained after adjustment for SUD risk factors. Poorer verbal intellectual ability was related to substance abuse rather than dependence. Other SUD characteristics were not associated with cognition. Conclusions Poorer verbal intellectual ability and less efficient psychomotor processing are associated with life-time alcohol and other substance use disorders in young adulthood. Poorer verbal intellectual ability seems to be related to parental and own low basic education, whereas slower psychomotor processing is associated with SUD independently of risk factors. [ABSTRACT FROM AUTHOR]

Aims To explore the developmental relationships between early-onset depressive disorders and later use of addictive substances. Design, setting and participants A sample of 1545 adolescent twins was drawn from a prospective, longitudinal study of Finnish adolescent twins with baseline assessments at age 14 years and follow-up at age 17.5 years. Measurements At baseline, DSM-IV diagnoses were assessed with a professionally administered adolescent version of Semi-Structured Assessment for Genetics of Alcoholism (C-SSAGA-A). At follow-up, substance use outcomes were assessed via self-reported questionnaire. Findings Early-onset depressive disorders predicted daily smoking [odds ratio (OR) 2.29, 95% confidence interval (CI) 1.49–3.50, P < 0.001], smokeless tobacco use (OR = 2.00, 95% CI 1.32–3.04, P = 0.001), frequent illicit drug use (OR = 4.71, 95% CI 1.95–11.37, P = 0.001), frequent alcohol use (OR = 2.02, 95% CI 1.04–3.92, P = 0.037) and recurrent intoxication (OR = 1.83, 95% CI 1.18–2.85, P = 0.007) 3 years later. ORs remained significant after adjustment for comorbidity and exclusion of baseline users. In within-family analysis of depression-discordant co-twins (analyses that control for shared genetic and familial background factors), early-onset depressive disorders at age 14 predicted significantly frequent use of smokeless tobacco and alcohol at age 17.5. Conclusions Our results suggest important predictive associations between early-onset depressive disorders and addictive substance use, and these associations appear to be independent of shared familial influences. [ABSTRACT FROM AUTHOR]