Implications of gene-drug interactions in smoking cessation for improving the prevention of chronic degenerative diseases.

2.50
Hdl Handle:
http://hdl.handle.net/10146/82637
Title:
Implications of gene-drug interactions in smoking cessation for improving the prevention of chronic degenerative diseases.
Authors:
Quaak, Marieke; van Schayck, Constant P.; Knaapen, Ad M.; van Schooten, Frederik J.
Abstract:
Tobacco smoking continues to be the major preventable cause of premature morbidity and mortality throughout the world. Recent research strongly suggests that genetic background is associated with several aspects of smoking (e.g. initiation, maintenance, cessation, number of cigarettes smoked, indicators of nicotine dependence (ND) and nicotine withdrawal). Variations in two broad classes of genes have been shown to influence smoking: (1) genes that may influence the response to nicotine (e.g. nicotine metabolism, nicotinic receptors) and (2) genes that may predispose to addictive behaviour via their effects on key neurotransmitter pathways (e.g. dopamine, serotonin and opioid). Since these genetic variants might also influence the response to smoking cessation pharmacotherapies, smoking cessation rates might be increased by determining which treatment would be most effective based on the smoker's genetic background. This is expected to result in a more efficient use of smoking cessation therapies, increased cessation rates and ultimately, in reduced deaths from smoking. Until now, most research on the influence of genetic variation on smoking cessation pharmacotherapy has been directed to the two most widely accepted and licensed forms of smoking cessation therapy: nicotine replacement therapy (NRT) and the antidepressant bupropion. Overall, genotypes associated with increased dopamine availability seem to predict a better response to bupropion, while smokers with genotypes associated with reduced dopamine levels probably achieve better quit rates with NRT. A decreased metabolism for the drug used (e.g. bupropion or NRT), results in increased cessation rates as well. Furthermore, smokers with reduced dopaminergic and nicotinic receptor activity variants may experience greater benefit from nicotine spray, while smokers with increased activity variants in the opioid receptor may have greater success with transdermal patches. Thus it seems that genetic information may give directions in determining which treatment would be most effective for an individual smoker. However, several challenges will still have to be overcome before genetically tailored smoking cessation therapy can be implemented in standard clinical practice.
Citation:
Mutat. Res. 2009, 667 (1-2):44-57
Journal:
Mutation research
Issue Date:
10-Jul-2009
URI:
http://hdl.handle.net/10146/82637
DOI:
10.1016/j.mrfmmm.2008.10.015
PubMed ID:
19028511
Additional Links:
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T2C-4TVHSX6-1&_user=1843694&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000055040&_version=1&_urlVersion=0&_userid=1843694&md5=a9be00c5143b7674d6e95ef76e1c04c9
Type:
Article
Language:
en
ISSN:
0027-5107
Sponsors:
Sources of support: ZonMW, Project No. 50-50101-96-404 and ECNIS, sixth Framework programma (FP6), Food-CT-2005-513943.
Appears in Collections:
Articles

Full metadata record

DC FieldValue Language
dc.contributor.authorQuaak, Mariekeen
dc.contributor.authorvan Schayck, Constant P.en
dc.contributor.authorKnaapen, Ad M.en
dc.contributor.authorvan Schooten, Frederik J.en
dc.date.accessioned2009-09-25T08:13:46Z-
dc.date.available2009-09-25T08:13:46Z-
dc.date.issued2009-07-10-
dc.identifier.citationMutat. Res. 2009, 667 (1-2):44-57en
dc.identifier.issn0027-5107-
dc.identifier.pmid19028511-
dc.identifier.doi10.1016/j.mrfmmm.2008.10.015-
dc.identifier.urihttp://hdl.handle.net/10146/82637-
dc.description.abstractTobacco smoking continues to be the major preventable cause of premature morbidity and mortality throughout the world. Recent research strongly suggests that genetic background is associated with several aspects of smoking (e.g. initiation, maintenance, cessation, number of cigarettes smoked, indicators of nicotine dependence (ND) and nicotine withdrawal). Variations in two broad classes of genes have been shown to influence smoking: (1) genes that may influence the response to nicotine (e.g. nicotine metabolism, nicotinic receptors) and (2) genes that may predispose to addictive behaviour via their effects on key neurotransmitter pathways (e.g. dopamine, serotonin and opioid). Since these genetic variants might also influence the response to smoking cessation pharmacotherapies, smoking cessation rates might be increased by determining which treatment would be most effective based on the smoker's genetic background. This is expected to result in a more efficient use of smoking cessation therapies, increased cessation rates and ultimately, in reduced deaths from smoking. Until now, most research on the influence of genetic variation on smoking cessation pharmacotherapy has been directed to the two most widely accepted and licensed forms of smoking cessation therapy: nicotine replacement therapy (NRT) and the antidepressant bupropion. Overall, genotypes associated with increased dopamine availability seem to predict a better response to bupropion, while smokers with genotypes associated with reduced dopamine levels probably achieve better quit rates with NRT. A decreased metabolism for the drug used (e.g. bupropion or NRT), results in increased cessation rates as well. Furthermore, smokers with reduced dopaminergic and nicotinic receptor activity variants may experience greater benefit from nicotine spray, while smokers with increased activity variants in the opioid receptor may have greater success with transdermal patches. Thus it seems that genetic information may give directions in determining which treatment would be most effective for an individual smoker. However, several challenges will still have to be overcome before genetically tailored smoking cessation therapy can be implemented in standard clinical practice.en
dc.description.sponsorshipSources of support: ZonMW, Project No. 50-50101-96-404 and ECNIS, sixth Framework programma (FP6), Food-CT-2005-513943.en
dc.language.isoenen
dc.relation.urlhttp://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T2C-4TVHSX6-1&_user=1843694&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000055040&_version=1&_urlVersion=0&_userid=1843694&md5=a9be00c5143b7674d6e95ef76e1c04c9en
dc.subjectSmoking behaviouren
dc.subjectNicotine dependenceen
dc.subjectCessation therapyen
dc.subjectPharmacogeneticsen
dc.subject.meshChronic Diseaseen
dc.subject.meshDopamineen
dc.subject.meshGenotypeen
dc.subject.meshHumansen
dc.subject.meshNicotineen
dc.titleImplications of gene-drug interactions in smoking cessation for improving the prevention of chronic degenerative diseases.en
dc.typeArticleen
dc.identifier.journalMutation researchen

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