Those who reported tobacco use had a later median age at onset — 63.5 years — compared to 60.8 years for nonusers. The number of cigarettes per day also was linked to later age of onset, despite making only a small difference. Likewise, a longer duration of smoking resulted in a positive correlation with age of onset, but with a small effect size as well.
However, smoking was linked to more severe motor symptoms. Smokers also reported anxiety, depression, and other nonmotor symptoms such as inexplicable aches and memory problems vs nonsmokers.
Participants were deemed to be coffee drinkers if they regularly consumed caffeinated coffee at a minimum of once per week during at least a 6-month period. The same classification applied to caffeinated black tea.
Patients who consumed coffee regularly had a later age at onset of PD — 61.9 years compared to 59.4 years for those who did not drink coffee. There was also a small possible coffee dosage effect from the number of cups consumed per week, as well as a positive correlation with longer coffee-drinking duration. In addition, coffee drinking was associated with less severe motor scores.
In evaluating the effect of anti-inflammatory medication on age at onset of PD, aspirin showed the most significant difference. Individuals were considered aspirin users if they took at least two pills per week over a minimum of 6 months.
Those who reported aspirin use had a 5-year later age at onset — 64.0 years compared to 59.1 years for patients who did not take aspirin. However, aspirin’s effect lessened as an independent predictor of PD onset after accounting for the comorbidities of heart disease and arthritis.
Trinh said the project “helps to improve understanding of PD and could have an impact on therapeutics designed to push back the disease onset and further adjustment for treatment outcome in the future.”
Mechanisms Remain a Mystery
Commenting on the findings for Medscape Medical News, Clemens Scherzer, MD, professor of neurology, Harvard Medical School in Boston, said, “we have known for some time that coffee drinking and smoking are strongly associated with reduced risk of developing PD, although the exact mechanisms and the exact chemicals at play remain mysterious.”
Overall, “the data did not provide a clear answer” on aspirin’s possible effects, said Scherzer, who is also director, American Parkinson Disease Association Center for Advanced Research at Brigham & Women’s Hospital, attributing the uncertainty to the type of analysis, confounding variables, and the study’s retrospective design.
“Instead,” he added, “the results suggest that this might be a clue worthy of further investigation and clarification.”
While noting the study’s observations are exploratory and preliminary, Scherzer, who was not involved in the research, noted “coffee lovers, however, can feel good about this study. Risk is reduced and Parkinson’s disease might start later in people who drink coffee.”
Also commenting on the research, Andrew Siderowf, MD, professor of neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, who was not involved in the study, urged caution in interpreting the findings.
“The protective effect of smoking suggested by these results is not proven, and the detrimental health effects of smoking vastly outweigh any potential benefits for Parkinson’s disease,” said Siderowf. “I strongly discourage my Parkinson patients from taking up smoking.”
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