Dietary Factors and Parkinson's Disease Risk: Systematic Review of Verified Observational Evidence

Abstract

Background: Dietary exposures have been proposed as modifiable factors influencing Parkinson’s disease (PD) risk, yet observational evidence remains heterogeneous and often inconsistent. Methods: We conducted a systematic review of PubMed, Embase, and Web of Science for studies published between January 1, 2015, and June 30, 2025. Eligible studies included prospective cohorts, case–control, and cross-sectional studies that used validated or semi-validated dietary assessment instruments to evaluate dietary intake in relation to PD. Studies lacking verifiable publication metadata (DOI, PMID, or retrievable records) were excluded. Data extraction was performed independently in duplicate. Study quality was assessed using a modified Newcastle-Ottawa Scale and the ROBINS-I framework, with certainty of evidence evaluated via GRADE. Due to anticipated heterogeneity in exposures, outcomes, and study designs, a narrative thematic synthesis was pre-specified as the primary analytic approach. Heterogeneity was not quantitatively pooled in this review; the included meta-analysis (Hong et al.) reported I² = 58%. Formal sensitivity analysis excluding unverifiable studies was not feasible (they were excluded a priori), but comparison of exposure categories showed no unique dietary domains among unverifiable reports. Results: Six verified studies (total n >1.2 million participants; >25,000 incident PD cases) and one meta-analysis met inclusion criteria. Consistent evidence from high-quality prospective cohorts indicated that higher coffee or caffeine consumption was inversely associated with PD risk. In contrast, frequent dairy intake, particularly low-fat milk, was associated with modestly elevated risk. Evidence regarding alcohol, dietary fats, micronutrients, and overall dietary patterns was limited, heterogeneous, or of lower certainty. Most studies were rated moderate risk of bias, with large prospective cohorts providing the most robust findings. Conclusions: Verified observational evidence suggests that habitual caffeine intake may confer neuroprotective effects, whereas high consumption of specific dairy products may modestly increase PD risk. Associations for other dietary exposures remain inconclusive. Future studies should incorporate biomarker-validated dietary assessment, mechanistic endpoints, and harmonized cohort designs to clarify causal pathways and inform evidence-based dietary guidance for PD prevention.