We confirmed the association between variants within genes that code nicotinic-acetylcholine receptors (-A3, -A5 and -B3), CYP2A6/B6 and tobacco dependence development in the Czech population.
No significant difference of tobacco dependence between normal and reduced metabolizers of CYP2A6 gene was found (FEM: SMD = 0.185, 95%CI = -0.001 to 0.371).
Conversion to TD and TD status were associated with the intensity of recent (that is, past 3-month) cigarette consumption (adjusted incidence rate ratio (aIRR) 1.63 (95% confidence interval (CI) 1.36 to 1.97) and adjusted prevalence odds ratio (aPOR) 1.35 (95% CI 1.23 to 2.48) per 100 cigarettes per month), slowest CYP2A6 activity (aIRR 4.19 (95% CI 1.38 to 12.76) and aPOR 2.30 (95% CI 1.29 to 4.09)), depression score (aIRR 1.61 (95% CI 1.17 to 2.21) and aPOR 1.47 (95% CI 1.22, 1.75) per 1-unit change).
The clinical implications of CYP2A6 polymorphisms have been linked to a decreased risk of tobacco dependence, a decrease in number of cigarettes smoked and reduced risk of tobacco-related cancers.
SNPs within CHRNA5-A3-B4 and CYP2A6/B6 are associated with smoking dependence but not with tobacco dependence treatment outcomes in the Czech population.
Second, genetic variation that modifies noxious responses to nicotine and thereby influences vulnerability to tobacco dependence, in particular variation in the CHRNA5-CHRNA3-CHRNB4 nicotinic acetylcholine receptor (nAChR) subunit gene cluster, will be discussed.
Indeed, genetic variation in the CHRNA5-CHRNA3-CHRNB4 gene cluster, encoding the α5, α3, and β4 nAChR subunits, respectively, has been shown to increase vulnerability to tobacco dependence and smoking-associated diseases including lung cancer.
Indeed, genetic variation in the CHRNA5-CHRNA3-CHRNB4 gene cluster, encoding the α5, α3, and β4 nAChR subunits, respectively, has been shown to increase vulnerability to tobacco dependence and smoking-associated diseases including lung cancer.
Recent human genetic studies also imply that tobacco dependence is affected by polymorphisms in the alpha3/alpha5 subunits of the nAChR (CHRNA3/CHRNA5) gene cluster.
Recent human genetic studies also imply that tobacco dependence is affected by polymorphisms in the alpha3/alpha5 subunits of the nAChR (CHRNA3/CHRNA5) gene cluster.
Role of functional genetic variation in the dopamine D2 receptor (DRD2) in response to bupropion and nicotine replacement therapy for tobacco dependence: results of two randomized clinical trials.