More Evidence Found That Caffeine and Urate Protect Against Parkinson’s
People who drink more caffeinated beverages and have high blood levels of urate appear to have a significantly lower chance of developing Parkinson’s disease, a study has found.
While the research provides further support that caffeine and urate are protective factors against Parkinson’s, scientists caution that the therapeutic potential of these molecules is still not established and recommend against increasing caffeine intake.
Their study, “Associations of Lower Caffeine Intake and Plasma Urate Levels with Idiopathic Parkinson’s Disease in the Harvard Biomarkers Study,” was published in the Journal of Parkinson’s Disease.
Caffeine and urate are two purines that protect nerve cells from damage and have been widely associated with a lower risk of Parkinson’s in prior studies.
“Both caffeine and urate possess neuroprotective properties via adenosine receptor antagonist and antioxidant actions, respectively,” Rachit Bakshi, PhD, lead investigator of the study, said in a press release.
“They both have protective properties in animal models of [Parkinson’s disease], raising the possibility of their disease-slowing potential,” added Bakshi, an instructor in the Department of Neurology at Massachusetts General Hospital and Harvard Medical School.
To further validate these two molecules as protective factors against Parkinson’s, Bakshi and colleagues examined caffeine intake and urate levels in a well-characterized group of people participating in the Harvard Biomarkers Study.
This is a longitudinal study following people with early-stage Parkinson’s or mild cognitive impairment, as well as healthy people used as controls, designed to accelerate the discovery and validation of biomarkers for the disease.
The analysis included 369 patients with idiopathic (of unknown cause) Parkinson’s, with a mean age of 67.3 years, as well as 197 healthy controls, at an average age of 66.3 years. At their initial visit, participants were assessed for blood urate levels and asked about their typical consumption of coffee (with and without caffeine), tea, and soft drinks over the prior year.
According to the results, people with Parkinson’s consumed less caffeine and had lower urate levels than healthy controls. After adjusting for factors such as age and body mass index, however, only men showed significantly less caffeine consumption. Healthy men and women with Parkinson’s did not show any significant differences in their caffeine intake.
Statistical analysis then demonstrated that more caffeine consumption significantly lowered the odds of developing Parkinson’s. When participants were classified into five groups according to their caffeine consumption, people with the highest intake had a 71% lower prevalence of Parkinson’s, compared with those in the lowest intake group.
Similarly, when participants were divided into five groups according to their blood urate levels, Parkinson’s was 69% less prevalent among those with the highest levels than in those in the lowest dose level.
The validation of these biomarkers in a large and well-characterized group of people, “is an important basis to further develop future disease-modifying approaches to slow down the decline of this otherwise relentlessly progressive condition,” said Bas Bloem, MD, PhD, co-editor-in-chief of the Journal of Parkinson’s Disease.
But the researchers emphasize that caution — and more study — is still needed. A large, randomized Phase 3 trial called SURE-PD3 (NCT02642393) failed to demonstrate the benefits of elevating urate levels in Parkinson’s patients, and that no trials have investigated the long-term use of caffeine in these patients. As such, they recommend against increasing patients’ caffeine intake.
“Identifying factors that are linked to lower likelihood of [Parkinson’s disease], such as caffeine consumption, offer a unique opportunity to understand the disease, and if the link were causal, then possibly to slow the disease,” Bakshi said.