CHICAGO (Reuters Health) - Boosting nicotine levels in smokers may actually help them reduce their smoking, perhaps even easing the path to smoking cessation, according to research presented Monday at the 11th World Conference on Tobacco OR Health in Chic

Dr. Rachel Tyndale, associate professor at the University of Toronto's Center for Addictions and Mental Health in Canada, said genetic clues led her team to experiment with a new approach to nicotine replacement compound. In a short-term study, the new compound reduced smoking by 50% compared with (an inactive) placebo. The key to success is an enzyme inhibitor that slows the inactivation of nicotine in the liver. Until now, nicotine pill development has been stymied by the fact that the liver metabolizes 70% of ingested nicotine before it can reach the brain. Their genetic work on the CYP2A6 enzyme, which is involved in nicotine metabolism, inspired Tyndale's team to study the new nicotine and enzyme inhibitor combination. Earlier studies demonstrated that smokers who have genetic variations that produce lower levels of the CYP2A6 enzyme smoke fewer cigarettes and space them farther apart than smokers with two functional CYP2A6 genes. The enzyme inhibitor was combined with 4 milligrams of nicotine into a pill given to current smokers. ``And what we found in that study was a 50% decrease in smoking compared to the placebo-placebo arm,'' Tyndale told Reuters Health. The researchers used blood carbon monoxide levels to monitor smoking behavior. Their results appear to be somewhat better than those of similar trials of nicotine gum, she noted. ``We think that's because we're not only getting the nicotine into the system, but now we're actually keeping the nicotine in the system because the inhibitor keeps it there for considerably longer,'' Tyndale explained. The reduction in smoking involved a combination of fewer cigarettes as well as shallower and fewer puffs per cigarette; thus smokers satisfied their craving for nicotine, while reducing their exposure to harmful components of tobacco smoke. Tyndale also previewed data from ongoing studies indicating substantial ethnic variability in CYP2A6 enzyme activity. Variations in the persistence of nicotine in the bloodstream might play a role in ethnic differences in smoking behavior, she said, as well as exposure to carcinogens and other toxins in smoke, and ultimately to differences in tobacco-related disease rates between ethnic groups.

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