Nicotine metabolism defect reduces smoking

Michael L. Pianezza, Edward M. Sellers and Rachel F. Tyndale ()
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Michael L. Pianezza: Addiction Research Foundation of Ontario, Centre for Research in Womens Health, Medicine and Psychiatry, University of Toronto
Edward M. Sellers: Addiction Research Foundation of Ontario, Centre for Research in Womens Health, Medicine and Psychiatry, University of Toronto
Rachel F. Tyndale: Addiction Research Foundation of Ontario, Centre for Research in Womens Health, Medicine and Psychiatry, University of Toronto

Nature, 1998, vol. 393, issue 6687, 750-750

Abstract: Abstract Nicotine is the primary compound in tobacco that establishes and maintains tobacco dependence1. Most of this nicotine is metabolized to cotinine by the genetically variable enzyme CYP2A6. Here we show that individuals lacking full functional CYP2A6, who therefore have impaired nicotine metabolism, are significantly protected against becoming tobacco-dependent smokers. In addition, smokers whose nicotine metabolism is thus impaired smoke significantly fewer cigarettes than those with normal nicotine metabolism.

Date: 1998
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DOI: 10.1038/31623

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