Colonoscopy and Subsequent Risk of Parkinson's Disease.

Background: Parkinson's disease (PD) is caused by the misfolding and aggregation of α-synuclein in neurons into toxic oligomers and fibrils that have prion-like properties allowing them to infect healthy neurons and to be transmitted to animal models of PD by injection or oral exposure. Given α-synuclein fibrils' potential transmission on the gut-brain axis, α-synuclein may be transmitted through colonoscopy procedures. Objective: This study examines a possible association between colonoscopy and PD. Methods: Longitudinal health insurance data of 250,000 individuals aged 50+ from 2004-2019 was analyzed. Cox proportional hazard and competing risk models with death as a competing event were estimated to calculate the risk of PD. Colonoscopy was categorized as never receiving colonoscopy, colorectal cancer (CRC) screening without or with biopsy, destruction or excision (BDE), and diagnostic colonoscopy without or with BDE. Results: We identified 6,422 new cases of PD among 221,582 individuals. The Cox model revealed a significantly increased risk of PD for patients who ever had a diagnostic colonoscopy without or with BDE (HR = 1.31; 95% CI: [1.23-1.40]; HR = 1.32 [1.22-1.42]) after adjustment for age and sex. After controlling for covariates and death, persons who ever underwent CRC screening had a 40% reduced risk of PD (CRHR = 0.60 [0.54-0.67]), while persons who underwent diagnostic colonoscopy had a 20% reduced risk of PD (CRHR = 0.81 [0.75-0.88]). Conclusions: Colonoscopy does not increase the risk of PD, after adjusting for death and covariates. Individuals who underwent only CRC screening had the lowest risk of PD, which may be a result of a more health-conscious lifestyle.

Contributions of causes of death to differentials in life expectancy by internal migrant status in the Netherlands. A population register based study, 2015-2019.

Important health differences exist in the context of international migration and residential mobility. Less is known about health differences regarding the medium-distance level of internal migration. This study examines life expectancy gaps between internal movers and stayers in the Netherlands and their underlying processes by assessing the contribution of different causes of death by age and sex. It uses individually-linked death counts and population exposures extracted from population registers, covering the native Dutch population aged 10+ from 2015 to 2019. The pooled data were disaggregated by causes-of-death group (neurodegenerative diseases, cardiovascular diseases, lifestyle-related mortality, external causes, and other causes), internal migrant status (movers and stayers, based on past 10-year residence in the 40 NUTS-3 [Nomenclature of Territorial Units for Statistics, level 3] regions), age, and sex. Comparing movers and stayers, we computed life expectancy at age 10 (e10), age- and cause-specific mortality risks, and applied decomposition methods to assess contributions of causes of death to e10 gaps. In the Netherlands in 2015-2019, e10 was lower for movers between NUTS-3 regions than stayers (males: 2.49 years; females: 3.51 years), due to excess mortality for movers at most ages. Movers only had a lower mortality than stayers at younger working ages (males: ages 20-44; females: ages 20-34). Mortality from neurodegenerative diseases and cardiovascular diseases were the largest contributors to the e10 gap, especially at ages 75+ and for females. Mortality from lifestyle-related and external causes of death contributed less, with the largest contributions for females aged 75-89 and males aged 45-69. The lower e10 of movers in the Netherlands is likely explained by health selection effects-in particular care-related moves as coping behaviour-rather than by causal effects through risk accumulation. Research focusing on regional or spatial heterogeneity of the mover-stayer health gap would be insightful to further understand these processes.