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Nicotine metabolism defect reduces smoking

Author

Listed:
  • 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)

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.

Suggested Citation

  • Michael L. Pianezza & Edward M. Sellers & Rachel F. Tyndale, 1998. "Nicotine metabolism defect reduces smoking," Nature, Nature, vol. 393(6687), pages 750-750, June.
    • Handle: RePEc:nat:nature:v:393:y:1998:i:6687:d:10.1038_31623
    DOI: 10.1038/31623
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    Cited by:

    1. George Wehby & Allen Wilcox & Rolv Lie, 2013. "The impact of cigarette quitting during pregnancy on other prenatal health behaviors," Review of Economics of the Household, Springer, vol. 11(2), pages 211-233, June.

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