Smoking associated with lower Parkinson's disease risk
Jul 9, 2007 - 4:00:00 AM
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The biochemical basis for possible preventative effects of smoking, or of a substance delivered through cigarette smoke, is not well understood, but animal studies have indicated two possible mechanisms: chemical or biochemical processes may exist by which substances contained in cigarette smoke such as nicotine or carbon monoxide exert a protective effect and promote survival of dopaminergic neurons; or cigarette smoke alters the activity of metabolic enzymes or competes with other substrates for these enzymes and thereby alters the production of toxic endogenous (dopamine quinones) or exogenous (MPP+) metabolites, the authors write.
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By JAMA and Archives Journals,
[RxPG] A pooled analysis of data from previous studies suggests that cigarette smoking appears to be associated with a reduced risk for developing Parkinsons disease, with long-term and current smokers at the lowest risk, according to a report in the July issue of Archives of Neurology, one of the JAMA/Archives journals.
Several studies have suggested that patients with Parkinsons disease are less likely to be smokers, according to background information in the article. Recent studies also suggested that Parkinsons disease risk is particularly low in active smokers with a long history of intense smoking; some even suggested dose-related risk reductions with increasing pack-years of smoking, the authors write. This prompted speculation as to whether and how these observations might inform Parkinsons disease treatment and prevention. However, the number of participants in most Parkinsons disease studies is too small to answer important questions about the role of smoking.
Beate Ritz, M.D., Ph.D., of the UCLA School of Public Health, Los Angeles, and colleagues pooled data from 11,809 individuals (2,816 individuals with Parkinsons disease and 8,993 controls of the same age and sex but without Parkinsons disease) involved in 11 studies conducted between 1960 and 2004.
Our analyses confirmed prior reports of an inverse association between cigarette smoking and Parkinsons disease similar in size to those reported in a recent meta-analysis, the authors write. We also showed that associations did not differ by sex or educational status. Although we found that current smokers and those who had continued to smoke to within five years of Parkinsons disease diagnosis exhibited the lowest risk, a decrease in risk (13 percent to 32 percent) was also observed in those who had quit smoking up to 25 years prior to Parkinsons disease diagnosis. Other tobacco products also appeared to be protectivemen who smoked pipes or cigars had a 54 percent lower risk. The number of chewing tobacco users was small, but there was a suggestion of reduced risk associated with this product.
The researchers found no association between smoking and Parkinsons disease risk in individuals older than 75. In addition, while the association was strong in white and Asian-American individuals, no association was observed in Hispanic or African-American participants. This could be because these groups have more undiagnosed cases of Parkinsons disease than others, or because of genetic characteristics and their interaction with the environment.
The biochemical basis for possible preventative effects of smoking, or of a substance delivered through cigarette smoke, is not well understood, but animal studies have indicated two possible mechanisms: chemical or biochemical processes may exist by which substances contained in cigarette smoke such as nicotine or carbon monoxide exert a protective effect and promote survival of dopaminergic neurons; or cigarette smoke alters the activity of metabolic enzymes or competes with other substrates for these enzymes and thereby alters the production of toxic endogenous (dopamine quinones) or exogenous (MPP+) metabolites, the authors write.
Ultimately, only randomized intervention trials can confirm that some components in tobacco are truly neuroprotective, negating the possibility that a premorbid personality influences smoking behavior among those who later develop Parkinsons disease, they conclude. In the meantime, there is more to learn from epidemiologic studies with enough statistical power to examine Parkinsons disease associations in sub-groups such as users of chewing tobacco or nicotine gums and patches, people exposed to second-hand smoke or groups that metabolize nicotine or other tobacco constituents at different rates.
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