Genetics of smoking and depression

Abstract

Smoking and depression are significant public health problems with multiple etiological dimensions and outcomes. Although each condition is important by itself, they are important because they often potentiate each other. Consequently, it is also essential to understand the nature their relationship. This representative review focuses on the genetic etiology of the relationship in the context of reviewing first the epidemiology of depression and smoking, and then by exploring behavioral and molecular genetic studies, and other psychiatric and medical comorbidities. At this point, epidemiological evidence for a relationship between depression and smoking/nicotine dependence is compelling. Although behavioral genetic results differ somewhat by gender and in accordance with specific definitions of depression and smoking variables, recent studies show converging evidence for common genetic factors underlying the relationship, often in addition to non-shared environmental factors. The search for underlying genes and genetic mechanisms is at an early stage, but shows promising candidate genes and genetic approaches for future studies.

Factors associated with cessation of smoking among Swiss adults between 1991 and 2011: results from the SAPALDIA cohort

“…Similar to our results, the aforementioned intervention study in Basel showed that smokers with a history of depression or current use of antidepressants were less likely to quit [34]. This may be related to common genetic mechanisms behind smoking initiation, nicotine dependence and depressive disorders [36,37]. According to the European Respiratory Society-Task force guidelines, respiratory patients who smoke are a difficult target group for smoking cessation, as they tend to minimise their own perceived risk of disease.…”

STin2 VNTR polymorphism is associated with comorbid tobacco use and mood disorders

“…the first type is associated with mood disorders and the STin2 polymorphism, and the second type occurs independently from mood disorders and STin2 polymorphism but is associated with a TUD family history. These findings extend those of previous reports showing that the comorbidity between depression/bipolar disorder and TUD may reflect shared neurobiological endophenotypes (Tsuang et al, 2012). Thus, common genetic familial factors may be related to a life history of TUD and depression (Kendler et al, 1993).…”

“…Potential mechanisms underlying the relationship between TUD and mood disorders, either bipolar disorder or depression, may be explained by common risk factors, including environmental and genetic factors or gene by environmental interactions (Heffner et al, 2011;Kendler et al, 1993;Lyons et al, 2008;McCaffery et al, 2008;Tsuang et al, 2012). Likewise, the comorbidity between both disorders is thought to be determined at least in part by neurobiological endophenotypes (Tsuang et al, 2012).…”

“…Likewise, the comorbidity between both disorders is thought to be determined at least in part by neurobiological endophenotypes (Tsuang et al, 2012). Shared candidate genes for mood disorders and TUD have been identified, including genes that encode catechol-O-methyltransferase (COMT) and the dopamine and serotonin (5-HT) transporter (McEachin et al, 2010).…”

“…The SLC6A4 gene, mapped on chromosome 17, encodes the 5-HTT (Lesch et al, 1994) and a polymorphism in the promoter region of the SLC6A4 gene was used to characterize genetic vulnerability to mood disorders (Caspi et al, 2003;Kaufman et al, 2004;Risch et al, 2009) and TUD (Lerman et al, 1998(Lerman et al, , 2000Ishikawa et al, 1999;Hu et al, 2000;Eddahibi et al, 2003;Brody et al, 2005;Kremmer et al, 2005;Munafò et al, 2005Munafò et al, , 2006Skowronek et al, 2006;Trummer et al, 2006;David et al, 2007;Han et al, 2008;Sieminska et al, 2008;Watanabe et al, 2011;Ishii et al, 2011;Tsuang et al, 2012;Yang et al, 2013).…”