News Release

Smoking associated with lower Parkinson's disease risk

Peer-Reviewed Publication

JAMA Network

A pooled analysis of data from previous studies suggests that cigarette smoking appears to be associated with a reduced risk for developing Parkinson’s 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 Parkinson’s disease are less likely to be smokers, according to background information in the article. “Recent studies also suggested that Parkinson’s 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 Parkinson’s disease treatment and prevention.” However, the number of participants in most Parkinson’s 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 Parkinson’s disease and 8,993 controls of the same age and sex but without Parkinson’s disease) involved in 11 studies conducted between 1960 and 2004.

“Our analyses confirmed prior reports of an inverse association between cigarette smoking and Parkinson’s 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 Parkinson’s 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 Parkinson’s disease diagnosis.” Other tobacco products also appeared to be protective—men 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 Parkinson’s 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 Parkinson’s 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 Parkinson’s disease,” they conclude. “In the meantime, there is more to learn from epidemiologic studies with enough statistical power to examine Parkinson’s 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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(Arch Neurol. 2007;64(7):990-997. Available pre-embargo to the media at www.jamamedia.org.)

Editor’s Note: Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.

For more information, contact JAMA/Archives Media Relations at 312/464-JAMA (5262) or e-mail mediarelations@jama-archives.org.


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