Affiliations: Preventive Neurology Unit, Wolfson Institute of Population Health, Faculty of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, UK
Correspondence:
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Correspondence to: Prof Alastair Noyce, MRCP, PhD, Preventive Neurology Unit, Faculty of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK. Tel.: +44 (0) 207 882 5841; E-mail: a.noyce@qmul.ac.uk.
Abstract: Background:A substantial body of research has examined the relationship between alcohol consumption and risk of Parkinson’s disease (PD). Objective:To provide an updated systematic review and meta-analysis of observational studies examining the relationship between alcohol consumption and risk of PD. Methods:Eligible studies comparing PD risk in ever vs. never alcohol drinkers were sourced from six databases. Outcomes were pooled using standard meta-analysis techniques. Separate female and male estimates were generated from studies reporting sex-specific data. Additionally, cohort studies stratifying participants by quantity of alcohol intake were integrated in a dose-response analysis. Results:52 studies were included, totaling 63,707 PD patients and 9,817,924 controls. Our meta-analysis supported a statistically significant overrepresentation of never drinkers among PD subjects; odds ratio (OR) for ever drinking alcohol 0.84 (95% confidence interval (CI) 0.76 – 0.92). A subgroup analysis revealed similar effect estimates in females and males. A further synthesis of seven cohort studies suggested a negative, dose-dependent association between alcohol and risk of PD. Conclusion:In the absence of a known neuroprotective pathway, there may be reason to doubt a true biological effect. The role of survivor bias, selection and recall bias, misclassification, and residual confounding requires consideration. Alternatively, observations might be attributable to reverse causation if those predestined for PD alter their alcohol habits during the preclinical phase. Major limitations of our study include high between-study heterogeneity (I2 = 93.2%) and lack of adjustment for key confounders, namely smoking status.
