Smoking and depression : twin cohort studies among adolescents and adults

It is understood that cigarette smoking is associated with depressive symptoms, and depression can also be associated with quitting smoking. Longitudinal twin studies provide genetically informative data and a better understanding of such complex relationships; however, the causal nature of this relationship is still poorly understood. Longitudinal data helps to confirm the direction of the association between smoking status and depressive symptoms. It is crucial to account for confounding by measured covariates and by underlying shared genetic and environmental factors affecting smoking behaviour and depression. The genetically informative data allows us to control for possible mechanisms underlying the associations and strengthens causal inference. This thesis aimed to study the complex relationships between depressive symptoms and various aspects of cigarette smoking behaviour. Further, by using data from twins who grew up together this thesis sought to control for shared genetic and environmental factors underlying the association. All sub-studies utilised population-based Finnish Twin Cohort data collected at the University of Helsinki. The FinnTwin12 cohort data were used for study I (N=4,152) and study II (N=2,954), where adolescents and young adults were studied at the ages of 14, 17, and 22 years. Study III utilised the Older Twin Cohort data, where participants at the baseline (in 1990) were linked with antidepressant prescription data from the Finnish Social Insurance Institution (in 1995–2004) (N=10,652). Study IV also utilised Older Twin Cohort data where daily smokers in 1990 were followed-up for their smoking status in 2011 (N=1,438). The General Behaviour Inventory (GBI) and the Beck Depression Inventory (BDI) were used to measuring self-reported depressive symptoms. Participants self-reported their smoking behaviour in the questionnaire surveys. Cigarette smoking at age 14 was associated with subsequent depressive symptoms at age 17. Regular smokers and those consuming a higher number of cigarettes had higher depression scores at the age of 17. Further, there existed a reciprocal association between cigarette smoking and depressive symptoms when studied among twins from adolescence (age 17) to young adulthood (age 22). Daily smoking at the age of 17 predicted higher depression scores at the age of 22, and depressive symptoms in adolescence were associated with an increased risk of cigarette smoking in young adulthood. However, the associations were not independent of shared familial factors. Among older twins, daily smokers at baseline had an elevated likelihood of having antidepressant prescriptions in follow-up, even after controlling for essential confounders and familial factors. Furthermore, daily smokers reporting depressive symptoms at baseline had a lower likelihood of smoking cessation during a 20-year follow-up period. A higher number of cigarettes smoked at baseline, and familial factors partly explained the observed association between depressive symptoms and smoking cessation. These studies concluded that there is a reciprocal relationship between cigarette smoking and depressive symptoms among the young population. Later in life, daily smoking predicts a higher likelihood of anti-depressant prescriptions, and depressive symptoms predict a lower likelihood of smoking cessation. Shared familial factors (genetic and environmental) and measured confounders (for example, alcohol use) partly explain the observed associations between smoking behaviour and depression. Thus, findings from genetically informative twin data bring us a step closer to the causal inference and provide additional evidence for scientific use. In a public health setting, the results highlight the need to consider the complex nature of the relationship between smoking and depressive symptoms in prevention, treatment, and rehabilitation efforts. This complexity seems to involve reciprocal association, which is likely to be partly causal but partly explained by familial and/or other factors. Further, intervention efforts should consider that smoking may be an indicator of liability to depressive symptoms, and likewise, depression an indicator of liability to smoking.