Introduction: Nicotine metabolising enzymes CYP2B6 and CYP2A6 have been linked to nicotine addiction treatment. Despite evidence that they may interact to influence nicotine dependence treatment outcomes in terms of nicotine dependence and withdrawal syndromes, as well as therapy kinds (placebo, bupropion, and NRT), their role in nicotine cessation has yet to be thoroughly proven and understood. Methods: A total of 1862 persons, including Caucasians and African Americans, were studied. Nicotine dependence and withdrawal syndrome were assessed using the Fagerström Test for Nicotine Dependency (FTND) and Wisconsin Inventory of Smoking Dependence Motives (WISDM), respectively. Before reporting their quitting status six months later, participants had to smoke at least ten cigarettes per day and use one of three types of therapy (placebo, NRT, or bupropion) for two weeks. For nicotine genotype analysis, participants were also tested for SNPs CYP2A6*1A (rs1137115), *1H (rs616636070),*4A (rs28399434), *9A (rs28399443),*12A (rs28399442), and CYP2B6*6 (rs3745274). With p-values > 0.05, the chi-squared test demonstrated that gene variants were consistently distributed in the population. CYP2A6*4A was most significantly associated with the odds ratio (OR) of quitting smoking in each treatment group with nicotine dependence syndrome (OR=1.61, 95 percent CI 1.31-1.96), and *4A in individuals with nicotine withdrawal syndrome (OR=1.70, 95 percent CI 1.15-1.95), according to logistic regression analysis. The ANOVA test demonstrated a significant main interaction impact between CYP2B6*6, *1A, *4A, and *12A gene variations in the bupropion group. Conclusion: CYP2A6 and CYP2B6*6 may work together to increase nicotine addiction therapy success.
Author(s) Details
Department of Public Health, Walden University Minneapolis, USA.
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