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Smoking and Caffeine Inversely Associated with Parkinson's


DURHAM, N.C. -- There is more credibility to the curious finding that Parkinson's disease patients are more likely to be non-smokers and sparing in their consumption of caffeine.

DURHAM, N.C, April 9 -- There is more credibility to the curious finding that patients who develop Parkinson's disease are more likely to be non-smokers and sparing in their consumption of caffeine.

In a case-control study of those with Parkinson's in families, those with the disease were less likely to smoke or consume large amounts of caffeine than other family members, reported William K. Scott, Ph.D., of Duke, now at the University of Miami, and colleagues, in the April issue of Archives of Neurology.

This family-based study corroborated a protective association of smoking and caffeine consumption found in other clinical research, said Dr. Scott. The reasons for the association remain obscure.

However, the study did not back up suggestions that the use of nonsteroidal anti-inflammatory drugs also has a protective effect against Parkinson's disease among family members.

Findings such as these, they added, enable researchers to limit the numbers of unknown genetic and environmental factors involved in genetic studies of Parkinson's.

The family-based case-control study included 356 cases (mean age 66.1) and 317 family controls (mean age 63.7) who self-reported environmental exposures.

Of these, 235 of cases were male (66%) as were 139 (43.9%) of controls. For this reason, sex and age at examination were considered important confounders in the analyses, the researchers said.

Participants were recruited from Duke through physicians and self-referral. Doses and duration (years) of exposures were determined, and intensity (pack-years, cup-years, and NSAID tablet-years) was calculated as the result of dosage and duration.

Those with Parkinson's were significantly less likely to report ever smoking (odds ratio=0.56; 95% confidence interval, 0.41-0.78), and less likely to report current smoking (OR 0.30, CI, 0.17-0.53) compared with unaffected relatives, the researchers reported.

Additional measures of smoking revealed significant inverse associations with Parkinson's (P<.05) and trends in odds ratios (P<.005). Patterns remained significant after stopping exposure at 10 and 20 years before the reference age and adjusting for caffeine and NSAID use, the researchers reported.

Increasing intensity of total coffee drinking was also inversely associated with Parkinson's disease (test for trend P=.05).

Increasing dosage (trend P =.009) and intensity (trend P=.01) of total caffeine consumption were also inversely associated, with high dosage having a significant inverse association with Parkinson's (OR=0.58; CI, 0.34- 0.99).

There was no significant link between NSAID use (aspirin, ibuprofen, and naproxen [Aleve]) and Parkinson's disease, the researchers reported. For high intensity use, the OR was 1.08 (0.59-2.00) and P trend (0.99).

"To our knowledge," the researchers wrote, "our findings represent the first examination of the association between Parkinson's disease and caffeine in a case-family control setting, where cases were well matched to family controls on many unmeasured genetic and environmental factors."

Given this matching, these results may not be generalizable at the population level, they wrote. Nonetheless, the persistence of significant inverse associations for smoking and caffeine in these families suggests that these associations are likely not confounded by familial influences on exposure.

Further, residual confounding, they added, between the environmental factors themselves may lead to spurious associations, particularly with appreciable recall error, but inverse trends for caffeine and smoking remained significant (or nearly significant) after adjustment for one another.

Summing up, the researchers wrote that 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 susceptibility.

This evaluation of potentially inversely associated risk factors

for Parkinson's implicates smoking and caffeine as important environmental exposures even in families with Parkinson's disease, where confounding by unmeasured influences on exposure is reduced, the researchers wrote.

Smoking and caffeine possibly modify genetic effects in these families and should be considered as important covariates in genetic studies, they concluded.

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