番茄社区

VANCOUVER – Dashing hopes raised by an earlier study, a randomized trial reported here found that caffeine didn't help improve motor function in Parkinson's disease.

The CafePD trial was stopped early after finding no difference in Unified Parkinson's Disease Ratings Scale (UPDRS) Part III scores between caffeine pills and placebo taken over 6 months, Ron Postuma, MD, of McGill University in Montreal, and colleagues reported during a poster session at the .

An did show improvement in motor function with caffeine over placebo – but that trial only lasted 6 weeks, and it wasn't powered to detect that endpoint, Postuma told 番茄社区.

"Many Parkinson's patients heard that coffee was good for you, but that was an overinterpretation of a preliminary finding," Postuma said. "Now we can say with some confidence that caffeine is not a drug for treating symptoms of Parkinson's disease."

Numerous epidemiologic studies have linked drinking less coffee with a higher risk of Parkinson's disease: "It's well established that people who drink less coffee are at a higher risk of Parkinson's disease," Postuma said. "There is absolutely no doubt about that. It's been shown in study after study" -- but none were prospective trials.

Postuma said his recent findings are yet another illustration of the difference between observational and randomized controlled trial data: "We have to be careful when looking at epidemiologic findings," he said. "Just because two things are connected does not mean one causes the other."

At the same time, he noted that the study can't answer the question as to whether drinking coffee in the long run, well before Parkinson's disease is manifest, can prevent or slow its development.

"Is there something about people who are going to develop Parkinson's disease that they just don't want coffee?" he noted. "Is there something different about the reward mechanisms that they just don't enjoy coffee?"

He said there's a similar conundrum with nicotine. Epidemiologic evidence has shown smoking to be "protective" against Parkinson's. But again, Postuma said, it could just be that people who will develop Parkinson's lack the reward system needed to enjoy cigarettes.

"It's not so far-fetched," he said. "It may just be part of who they are."

Study Details

Postuma's team planned to enroll 250 patients in the CafePD study, but during an interim analysis at 6 months, they terminated the trial because there was "absolutely no evidence that caffeine can be used as a medication for treating the symptoms of Parkinson's disease or improving motor function directly," Postuma said.

They had enrolled 121 patients at that point, 60 of whom took 200 mg of caffeine twice a day, and 61 who took a matching placebo. The primary outcome was change in motor function as measured by UPDRS-III, and secondary outcomes included safety and tolerability; motor symptoms as measured by UPDRS-II; motor fluctuations, sleep, and non-motor symptoms as measured by the UPDRS-I; cognition as measured by the Montreal Cognitive Assessment; and quality of life.

Although the caffeine was well tolerated, with a similar prevalence of side effects as that seen in the placebo group, there was no improvement in motor function, with only a 0.48-point difference between the two groups on the UPDRS-III at 6 months, the researchers reported.

Nor was there any difference between groups in motor symptoms as measured by the UPDRS-II, or in quality of life, they said.

Although the drug was tied to decreased somnolence – no surprise to coffee drinkers – it was associated with a slight increase in dyskinesia and worse cognitive testing scores compared with placebo, Postuma said.

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