Caffeine consumption and the 4-year progression of de novo Parkinson's disease.
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.
Department of Neuroscience, Reproductive Science and Odontostomatology, Federico II University, Naples, Italy.
Marcello
M
Moccia
Sobell Department of Motor Neuroscience and Movement Disorders, UCL Institute of Neurology, London, United Kingdom; Dipartimento di Scienze Neurologiche e del Movimento, Università di Verona, Verona, Italy.
Roberto
R
Erro
Center for Neurodegenerative Diseases (CEMAND), Department of Medicine and Surgery, Neuroscience Section, University of Salerno, Italy.
Marina
M
Picillo
Department of Motor Sciences, University Parthenope, Naples, Italy; Neurology Clinic, IDC-Hermitage-Capodimonte, Naples, Italy.
Carmine
C
Vitale
Neurology Clinic, IDC-Hermitage-Capodimonte, Naples, Italy.
Katia
K
Longo
Neurology Clinic, IDC-Hermitage-Capodimonte, Naples, Italy.
Marianna
M
Amboni
Center for Neurodegenerative Diseases (CEMAND), Department of Medicine and Surgery, Neuroscience Section, University of Salerno, Italy.
Maria Teresa
MT
Pellecchia
Center for Neurodegenerative Diseases (CEMAND), Department of Medicine and Surgery, Neuroscience Section, University of Salerno, Italy. Electronic address: pbarone@unisa.it.
Paolo
P
Barone
D000368:Aged; D000978:Antiparkinson Agents / Q000627:therapeutic use; D002110:Caffeine / Q000378:metabolism*; D015331:Cohort Studies; D018450:Disease Progression; D005260:Female; D006801:Humans; D053208:Kaplan-Meier Estimate; D007980:Levodopa / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D010300:Parkinson Disease / Q000188:drug therapy / Q000503:physiopathology*; D016016:Proportional Hazards Models; D011788:Quality of Life; D011795:Surveys and Questionnaires; D013997:Time Factors
D000978:Antiparkinson Agents; D002110:Caffeine; D007980:Levodopa
Caffeine; Dopa; Motor; Non-motor; Parkinson; Progression