CYP2A6 Polymorphisms May Strengthen Individualized Treatment for Nicotine Dependence

Each CYP2A6 gene variant metabolizes nicotine differently depending on its enzymatic activities. The normal nicotine metabolizer CYP2A6*1A is associated with high scores of nicotine dependence (5–10) on the Fagerström Test for Nicotine Dependence (FTND) scale because it encodes for enzymes that cata...

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Main Author: Yawo Mawuli Akrodou
Format: Article
Language:English
Published: Wiley 2015-01-01
Series:Scientifica
Online Access:http://dx.doi.org/10.1155/2015/491514
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author Yawo Mawuli Akrodou
author_facet Yawo Mawuli Akrodou
author_sort Yawo Mawuli Akrodou
collection DOAJ
description Each CYP2A6 gene variant metabolizes nicotine differently depending on its enzymatic activities. The normal nicotine metabolizer CYP2A6*1A is associated with high scores of nicotine dependence (5–10) on the Fagerström Test for Nicotine Dependence (FTND) scale because it encodes for enzymes that catalyze nicotine 100%. Slow nicotine metabolizers (i.e., CYP2A6*1H, CYP2A6*4A, CYP2A6*9, and CYP2A6*12A) are associated with underrated nicotine metabolizing activity (50%–75%), linking them to low scores for nicotine dependence (0–4) on the FTND scale. In a clinical trial involving the use of bupropion, people who were carriers of slow nicotine metabolizers were found to have a tendency to maintain abstinence 1.7 times longer than people with normal nicotine metabolizers. An overview of CYP2A6 polymorphism enzymatic activities in nicotine dependence etiology and treatment revealed that slow nicotine metabolizers may strengthen the individualized treatment of nicotine dependence.
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spelling doaj-art-f304e569131b4624adbb2b4ee654fb802025-02-03T01:12:56ZengWileyScientifica2090-908X2015-01-01201510.1155/2015/491514491514CYP2A6 Polymorphisms May Strengthen Individualized Treatment for Nicotine DependenceYawo Mawuli Akrodou0Department of Public Health, College of Health Sciences, Walden University, Minneapolis, MN 55401, USAEach CYP2A6 gene variant metabolizes nicotine differently depending on its enzymatic activities. The normal nicotine metabolizer CYP2A6*1A is associated with high scores of nicotine dependence (5–10) on the Fagerström Test for Nicotine Dependence (FTND) scale because it encodes for enzymes that catalyze nicotine 100%. Slow nicotine metabolizers (i.e., CYP2A6*1H, CYP2A6*4A, CYP2A6*9, and CYP2A6*12A) are associated with underrated nicotine metabolizing activity (50%–75%), linking them to low scores for nicotine dependence (0–4) on the FTND scale. In a clinical trial involving the use of bupropion, people who were carriers of slow nicotine metabolizers were found to have a tendency to maintain abstinence 1.7 times longer than people with normal nicotine metabolizers. An overview of CYP2A6 polymorphism enzymatic activities in nicotine dependence etiology and treatment revealed that slow nicotine metabolizers may strengthen the individualized treatment of nicotine dependence.http://dx.doi.org/10.1155/2015/491514
spellingShingle Yawo Mawuli Akrodou
CYP2A6 Polymorphisms May Strengthen Individualized Treatment for Nicotine Dependence
Scientifica
title CYP2A6 Polymorphisms May Strengthen Individualized Treatment for Nicotine Dependence
title_full CYP2A6 Polymorphisms May Strengthen Individualized Treatment for Nicotine Dependence
title_fullStr CYP2A6 Polymorphisms May Strengthen Individualized Treatment for Nicotine Dependence
title_full_unstemmed CYP2A6 Polymorphisms May Strengthen Individualized Treatment for Nicotine Dependence
title_short CYP2A6 Polymorphisms May Strengthen Individualized Treatment for Nicotine Dependence
title_sort cyp2a6 polymorphisms may strengthen individualized treatment for nicotine dependence
url http://dx.doi.org/10.1155/2015/491514
work_keys_str_mv AT yawomawuliakrodou cyp2a6polymorphismsmaystrengthenindividualizedtreatmentfornicotinedependence