Levels of caffeine consumption and lower blood urate were both inversely associated with the risk of Parkinson disease, highlighting the benefit derived from sufficient levels of both components, according to study findings.
Levels of caffeine consumption and lower blood urate were both inversely associated with the risk of Parkinson disease (PD), highlighting the benefit derived from sufficient levels of both components, according to study findings published this week in the Journal of Parkinson Disease.
The neuroprotective properties of not only caffeine, but urate as well, were suggested by lead investigator Rachit Bakshi, PhD, of Harvard Medical School and the Department of Neurology at Massachusetts General Hospital, to be caused by the adenosine receptor antagonist and antioxidant actions. “They both have protective properties in animal models of PD, raising the possibility of their disease-slowing potential,” expanded Bakshi. In fact, the link between caffeine intake and PD has been addressed in prior studies, with research suggesting that coffee consumption leads to reduced severity of tremors in men with PD.
Researchers sought to further investigate the association between both purines and PD among participants of the Harvard Biomarkers Study (HBS), a longitudinal study designed to expedite the discovery and validation of molecular, diagnostic, and progression markers of early-stage PD. The cross-sectional, case-control study examined the urate collected in plasma samples from the initial HBS visit of 369 participants with idiopathic PD and 197 healthy controls.
Additionally, caffeine intake was assessed at the initial HBS visit via a semi-quantitative questionnaire that inquired about each participants’ typical consumption of caffeinated and decaffeinated coffee, tea, and soft drinks in the past 12 months. Responses were categorized into 9 possible frequencies, ranging from never to 6 or more cups/cans per day. Both analyses were stratified for sex and adjusted for age and body mass index.
When examining patients with idiopathic PD, male patients were found to have significantly lower caffeine intake compared with healthy controls (mean difference, —125 mg/day; P <.001). However, this trend was not observed for female patients (mean difference, —30 mg/day; P = .29). Compared with the lowest quartile of caffeine intake, the prevalence of PD was more than 70% lower in the highest quartile. Moreover, plasma urate levels of both male (mean difference, —0.46 mg/dL; P = .017) and female (mean difference, —0.45 mg/dL; P = .001) patients exhibited a strong inverse association with risk of PD.
“Identifying factors that are linked to lower likelihood of PD, such as caffeine consumption, offer a unique opportunity to understand the disease, and if the link were causal, then possibly to slow the disease,” concluded Bakshi.
While promising, researchers cautioned that a recent large clinical trial of a urate-elevating treatment did not demonstrate a benefit for patients with PD over months to years. As caffeine has yet to be extensively studied in a long-term PD trial, increasing caffeine intake remains a potentially therapeutic, albeit unproven, option, noted the study authors.
Bakshi R, Macklin EA, Hung AY. Associations of lower caffeine intake and plasma urate levels with idiopathic Parkinson’s disease in the Harvard Biomarkers Study [published May 3, 2020]. J Parkinsons Dis. doi: 10.3233/JPD-191882.