Introduction: 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. Methods: 79 newly diagnosed, drug na ve 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. Results: 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 = 0382-0.996). 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%Cl = -0.00 to 0.00). Conclusion: 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. (C) 2016 Published by Elsevier Ltd
Caffeine consumption and the 4-year progression of de novo Parkinson's disease
ERRO, ROBERTO;
2016-01-01
Abstract
Introduction: 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. Methods: 79 newly diagnosed, drug na ve 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. Results: 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 = 0382-0.996). 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%Cl = -0.00 to 0.00). Conclusion: 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. (C) 2016 Published by Elsevier LtdI documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.