Caffeine consumption and the 4-year progression of de novo Parkinson's disease


      • Caffeine consumption was associated with a reduced accrual of PD motor disability.
      • PD patients with higher caffeine use presented a reduced need for l-Dopa treatment.
      • Non-motor symptoms presented a milder progression among PD patients using caffeine.



      Higher caffeine consumption has been associated with reduced risk of Parkinson's disease (PD), and with a more benign progression of motor and non-motor symptoms (NMS). The present observational cohort study investigated motor and non-motor correlates of caffeine consumption in de novo PD.


      79 newly diagnosed, drug naïve PD patients have been included and followed up for 4 years. The total caffeine use was calculated with the Caffeine Consumption Questionnaire. Following study variables were recorded at baseline, and after 2 and 4 years: UPDRS part III, UPDRS part IV, l-dopa Equivalent Daily Dose (LEDD), NMS Questionnaire (NMSQuest), and the time occurring from PD diagnosis to the need for l-dopa treatment. Age, gender and disease duration were included as covariates in the statistical models.


      The average daily caffeine consumption was 296.1 ± 157.2 mg. At Cox regression models, higher caffeine consumption was associated with a lower rate of starting l-Dopa treatment (HR = 0.630; 95%CI = 0.382–0.996). At the mixed-effects linear regression models considering the whole study period, each additional espresso cup per day (50 mg of caffeine) was more likely associated with 5-point lower UPDRS part III total score (Coef = −0.01; 95%CI = −0.02 to 0.00), with 50% reduced LEDD (Coef = −0.01; 95%CI = −0.15 to 0.00; p = 0.021), and with 5-point lower NMSQuest total score (Coef = −0.01; 95%CI = −0.01 to 0.00), but not with UPDRS part IV total score (Coef = −0.00; 95%CI = −0.00 to 0.00).


      Caffeine consumption was associated with a reduced accrual of motor and non-motor disability during 4-year follow-up in de novo PD, highlighting the rationale for using adenosine A2A antagonists since the early phases of PD.


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