Journal of Addiction Research & Therapy
Open Access

Abstract

Existing nicotine dependence therapies have decreased smoking prevalence in the United States, but the decline in the number of adult smokers is stalling, due, in part, to the limited efficacy of current therapies that lack treatment personalization. Cytochrome P450 2A6 (CYP2A6) gene variants are known to metabolize nicotine and possibly influence nicotine dependence treatment. These gene�s inconsistent information, interindividual variability, interactions with other genes, and environmental factors have made it difficult to use their information to improve nicotine dependence therapy. This cross-sectional study based on behavioral genetic theory stating that environmental and genetic factors cause behavioral disorders, assessed the impact of slow nicotine metabolizers (CYP2A6*1H, CYP2A6*4A, CYP2A6*9, and CYP2A6*12A) and normal (fast) nicotine metabolizers (CYP2A6*1A) gene variants and their interactions with CYP2B*6 associated with nicotine therapy type and nicotine dependence and withdrawal syndromes on nicotine dependence outcome. Results were that CYP2A6*4A (OR=1.60, CI [1.13-1.95]; p<0.001) and CYP2A6*9A (OR=1.47, CI[1.18-1.88]; p<0.001) were the most linked to the highest odds of successful treatment outcome, indicating that carriers of slow nicotine metabolizers were more likely to maintain abstinence 6 months post period treatment than normal(fast) metabolizer CYP2A6*1A (OR=1.35, 95% CI[ 1.11-1.70]; p<0.003) carriers. Study findings may be useful in gene counseling and nicotine gene therapy to tailor individualized nicotine clinical treatments, to increase smoking quit rates, and to induce positive social change by improving the lives of smokers and their families.

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