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Pharmacogenetics and addiction services

Published online by Cambridge University Press:  02 January 2018

Colin O'Gara*
Affiliation:
Institute of Psychiatry and Smoking Cessation Clinic, Maudsley Hospital, Denmark Hill, London SE5 8AF. E-mail: c.o'[email protected]
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Abstract

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Creative Commons
Creative Common License - CCCreative Common License - BY
This is an Open Access article, distributed under the terms of the Creative Commons Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited.
Copyright
Copyright © 2004. The Royal College of Psychiatrists.

I support the view of Hodgson et al (Psychiatric Bulletin, August 2004, 28, 298-300) that future developments in genetics may lead to tailored treatments for psychiatric patients. Currently in addiction services, these technologies are not yet generally in use. However, recent developments suggest they may soon be available to patients.

Like antipsychotic drugs, nicotine is metabolised by a cytochrome enzyme complex (CYP 2A6). In past years, much attention has focused on the effect of functional variants of the CYP 2A6 gene on smoking status (Reference Pianezza, Sellers and TyndalePianezza et al, 1998). More recent studies have also highlighted the potential of applying pharmacogenetics in clinical addiction services; women receiving nicotine replacement therapy (NRT) possessing a variant of dopamine receptor 2 gene (DRD2) were shown to have significantly different success rates with NRT depending on their DRD2 genotype (Yudkin et al, 2004).

This and other findings (Reference Lerman, Shields and WileytoLerman et al, 2002) raise the issue of screening smokers with the intention of informing them which treatments they are most likely to benefit from. With rapid advances in genomic information and high throughput genotype screening techniques, more relevant functional genomic information is becoming available. Hodgson et al correctly infer that a thorough development phase is needed before this approach can be translated into wide-spread clinical applications.

In addition it will be important to protect patients against possible premature exposure to private genetic screening and advisory services using preliminary genetic findings which may not be substantiated through rigorous replication studies. With the realistic possibility of commercial involvement in gene based diagnostics, patients may be exposed to marketing strategies offering tailored smoking cessation therapies, based on preliminary/incomplete study results.

References

Lerman, C., Shields, P. G., Wileyto, E. P., et al (2002) Pharmacogenetic investigation of smoking cessation treatment. Pharmacogenetics, 12, 627634.Google Scholar
Pianezza, M. L., Sellers, E. M. & Tyndale, R. F. (1998) Nicotine metabolism defect reduces smoking. Nature, 393, 750.Google Scholar
Yudkin, P. (2004) Effectiveness of nicotine patches in relation to genotype in women versus men: randomised controlled trial. BMJ, 328, 989990.Google Scholar
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