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Sunday, November 10, 2002During the study, Lerman's team worked with 426 white smokers who were trying to kick the habit. All participants smoked at least 10 cigarettes per day. They received either bupropion (Zyban)--an antidepressant known to help smokers quit--or an inactive drug for 10 weeks, and also participated in seven sessions of group therapy. All were told they had to quit smoking 2 weeks after starting medication. The investigators also took blood samples from the smokers and noted which type of the gene known as CYP2B6 they carried. CYP2B6 encodes an enzyme that research suggests plays a role in the metabolism of nicotine in the brain. Lerman and her colleagues found that people who carried a form of CYP2B6 that produces an enzyme with decreased activity reported a larger increase in their cravings of cigarettes after their quit-date than did those with the more common form of the gene. Carriers of the less active form of CYP2B6 were also 50% more likely to start smoking again during the treatment. About 25% of the population carry this form of the gene. The researchers also discovered that among women who carried the less active form of CYP2B6, 54% of those who took bupropion had continued to resist cigarettes by the end of the study, an achievement noted in only 19% of those who received the inactive drug. The findings will be published in the upcoming issue of Pharmacogenetics. This doesn't negate the role of the will in smoking cessation, however. (The article doesn't say what percentage of people with the defective gene successfully quit compared to those with the normal gene. It only comments on the effect of bupropion on their efforts.) The symptom reported by carriers of the defective gene was craving, and cravings can be safely ignored. It may make it harder to quit, but it certainly doesn't make it impossible. posted by Sydney on 11/10/2002 09:17:00 AM 0 comments 0 Comments: |
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