BackgroundObservational evidence linking alcohol consumption to Parkinson's disease (PD) is inconsistent, potentially because conventional analyses do not account for the long latency between alcohol initiation and clinical onset or diagnosis.ObjectiveTo test whether latency-aware modeling changes alcohol-PD associations and whether earlier initiation increases lifetime risk.MethodsWe applied a latency-explicit semi-Markov framework in two longitudinal, community-based screening cohorts in Taiwan. The Keelung cohort (Community A; n = 23,475; aged ≥60 years; 2002-2005) was used for model development, and the Changhua cohort (Community B; n = 90,129; aged ≥50 years; 2005-2022) was used for external application. We compared conventional logistic regression with latency-adjusted relative rates, conducted smoking-stratified analyses, and benchmarked age-specific projections against an independent door-to-door PD survey.ResultsIn Community A, conventional regression suggested an inverse association (odds ratio 0.69; 95% confidence interval 0.53-0.91), whereas latency-adjusted modeling indicated higher PD risk among drinkers (relative rate 1.61; 95% confidence interval 1.32-1.95). Excess risk emerged ∼25, ∼35, and ∼45 years after initiation at ages 20, 30, and 40 years, respectively; alcohol-attributable risk by age 90 was 32.1%, 20.7%, and 4.9%. Smoking shortened estimated latency by 5 years. In Community B, PD incidence was higher among drinkers than non-drinkers, with wider separation at older ages (70-74 years: 58.6 vs 46.0 per 100,000).ConclusionAccounting for exposure timing and latency reversed the apparent protective signal and supported a higher modeled lifetime PD risk with alcohol use, particularly earlier initiation. Incorporating latency may strengthen etiologic inference and inform long-horizon prevention strategies.