Jung-Chen Chang, Amy Ming-Fang Yen, Sam Li-Sheng Chen, Horng-Huei Liou, Tony Hsiu-Hsi Chen
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引用次数: 0
Abstract
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.Plain language summary titleBecause Parkinson's disease develops slowly, early drinking may matter later in life.
背景:将饮酒与帕金森病(PD)联系起来的观察性证据是不一致的,可能是因为传统的分析没有考虑到饮酒与临床发病或诊断之间的长潜伏期。目的检验潜伏期感知模型是否改变酒精与帕金森病的关联,以及早期启动是否会增加终生风险。方法:我们在台湾的两个纵向社区筛查队列中应用潜伏期显式半马尔可夫框架。模型开发采用基隆队列(社区A; n = 23,475;年龄≥60岁;2002-2005),外用彰化队列(社区B; n = 90,129;年龄≥50岁;2005-2022)。我们比较了传统的逻辑回归与潜伏期调整相对率,进行了吸烟分层分析,并根据独立的挨家挨户PD调查对特定年龄的基准预测进行了比较。结果在社区A中,常规回归显示两者呈负相关(优势比0.69,95%可信区间0.53-0.91),而潜伏期调整模型显示饮酒者患帕金森病的风险较高(相对比率1.61,95%可信区间1.32-1.95)。过量风险分别在20岁、30岁和40岁发病后的25、35和45年出现;90岁时的酒精归因风险分别为32.1%、20.7%和4.9%。吸烟使估计潜伏期缩短了5年。在B社区,酗酒者的PD发病率高于非饮酒者,年龄越大分离越广(70-74岁:58.6 vs 46.0 / 100000)。结论:考虑到暴露时间和潜伏期逆转了明显的保护信号,并支持酒精使用的更高的模型终身PD风险,特别是早期开始。考虑潜伏期可以加强病因推断,并为长期预防策略提供信息。
期刊介绍:
The Journal of Parkinson''s Disease (JPD) publishes original research in basic science, translational research and clinical medicine in Parkinson’s disease in cooperation with the Journal of Alzheimer''s Disease. It features a first class Editorial Board and provides rigorous peer review and rapid online publication.