Some individuals carry a gene variant that may help protect them from becoming addicted to nicotine, according to a new study funded in part by the National Institute on Drug Abuse, National Institutes of Health, and published in the June 25 issue of Nature. The study found that individuals with a genetic variant in a particular enzyme break nicotine more slowly than those who do not. They have greater resistance to nicotine addiction and, if they do smoke, they smoke fewer cigarettes than individuals without the impairment.
Nicotine, the addictive component in tobacco products, is metabolized or broken down primarily by an enzyme in the liver known as CYP2A6. In this study, University of Toronto researchers, led by Dr. Rachel F. Tyndale, observed that variations in the gene for CYP2A6 affect how individuals metabolize nicotine. People with decreased functional CYP2A6 are less likely to become addicted to it.
Dr. Alan I. Leshner, Director of NIDA, said, "We are very excited about the findings from this study and its implications for understanding and treating nicotine addiction. We have long known that individuals vary in their vulnerability to becoming addicted, and this study identifies one gene involved in those individual differences. In addition, understanding the critical role this enzyme plays in nicotine addiction gives a new target for developing more effective medications to help people stop smoking."
Researchers found three different gene types (alleles) for the enzyme
CYP2A6, including a normal, or wild-type allele that is fully functional, and
two null or inactive alleles. People with the null alleles functionally lack
the enzyme and are unable to break down nicotine to cotinine. When comparing a
group of smokers to a group that had tried tobacco but had never become addicted
to it, they found individuals in the non-addicted group were much more likely to
have impaired nicotine metabolism (a
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