Cigarette smoking should be considered a chronic and relapsing disease, with chronic obstructive pulmonary disease (COPD) as one of its complications. An understanding of the physiologic underpinnings of addiction and smoking cessation may help clinicians appreciate not only the difficulties of smoking prevention and cessation but also the potential for future therapies that target these specific pathophysiologies. This article considers 4 elements of smoking as a primary prevention strategy, including (1) smoking initiation and the function of dopaminergic pathways in the brain as a key to nicotine addiction, (2) smoking cessation and the role of various nicotine replacement therapies, (3) relapse prevention and the permanent alteration of brain susceptibility to addiction seen in long-time smokers, and (4) harm reduction techniques and the impending political and social implications of the new "safer" cigarettes. Large studies have convincingly demonstrated that smoking cessation can preserve lung function and alter the natural history of COPD. By improving our understanding of the biology underlying the complex and difficult "quitting" behavior, clinicians will be in a better position to help their patients stop smoking and, thereby, lower the risk for COPD as well as for the many other diseases caused by cigarette smoking.
|Original language||English (US)|
|Journal||Advanced Studies in Medicine|
|Issue number||4 B|
|Publication status||Published - Apr 1 2003|
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