Smoking cigarettes, consuming caffeine and taking non-steroidal anti-inflammatory (NSAID) medications (such as aspirin, ibuprofen and naproxen) have been reported to protect individuals from developing Parkinson's disease, according to background information in the article. However, little family-based research has examined these associations. Studying individuals with Parkinson's disease and their families enables scientists to limit the number of unknown genetic and environmental factors influencing the development of the condition.

Dana B. Hancock, B.S., of Duke University Medical Center, Durham, N.C., and colleagues assessed the associations between smoking, caffeine and NSAID use and Parkinson's disease in 356 Parkinson's disease patients (average age 66.1) and 317 family members without the disease (average age 63.7). Participants were evaluated clinically to confirm their Parkinson's disease status and then interviewed by phone to determine their exposure to environmental factors.

"Individuals with Parkinson's disease were .56 times as likely to report ever smoking and .30 times as likely to report current smoking compared with unaffected relatives," the authors write. "Increasing intensity of coffee drinking was inversely associated with Parkinson's disease. Increasing dosage and intensity of total caffeine consumption were also inversely associated, with high dosage presenting a significant inverse association with Parkinson's disease." There was no link between NSAID use and Parkinson's disease.

The biological mechanisms through which smoking and caffeine might work in individuals at risk of Parkinson's disease is unknown, the authors note. "Given the complexity of Parkinson's disease, these environmental factors likely do not exert their effects in isolation, thus highlighting the importance of gene-environment interactions in determining Parkinson's disease susceptibility," they conclude. "Smoking and caffeine possibly modify genetic effects in families with Parkinson's disease and should be considered as effect modifiers in candidate gene studies for Parkinson's disease."

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