Genetic evidence for protective effects of smoking and drinking behavior on Parkinsons disease: A Mendelian Randomization study
| Autor: | Xianjun Dong, Jue-Sheng Ong, Miguel E. Rentería, Domínguez-Baleón C, Clemens R. Scherzer |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0303 health sciences
medicine.medical_specialty Parkinson's disease business.industry medicine.medical_treatment Confounding Protective factor ADH1B Disease medicine.disease 3. Good health 03 medical and health sciences 0302 clinical medicine Internal medicine Mendelian randomization medicine Smoking cessation Observational study business 030217 neurology & neurosurgery 030304 developmental biology |
| DOI: | 10.1101/2020.04.20.20073247 |
| Popis: | BackgroundObservational studies have identified correlations between environmental and lifestyle factors and Parkinson’s disease (PD). However, the causal direction of many of these relationships remains unclear.ObjectiveTo infer causal relationships between smoking and alcohol intake and PD.MethodsWe use a two-sample Mendelian randomization (MR) experimental design to infer causal relationships between smoking (initiation, age of initiation, heaviness, and cessation) and alcohol (drinks per week) consumption as exposure variables and PD as the health outcome. We also conduct sensitivity analyses, including testing for pleiotropic effects MR-Egger and MR-PRESSO, and multivariable MR to jointly model the effects of drinking and smoking behavior on PD risk.ResultsBoth alcohol intake (OR = 0.69; 95% CI 0.56-0.86; p=0.001). and smoking cessation (comparing current vs. former smokers) (IVW OR = 0.39; 95% CI 0.22 to 0.69; p=0.001) were causally associated with a reduced risk of PD. In addition, our multivariable MR results provide additional assurance that the causal association between drinks per week and PD is unlikely due to confounding by smoking behavior.ConclusionOur findings support the role of smoking as a protective factor against PD, but only when comparing current vs. former smokers. Increased alcohol intake also had a protective effect over PD risk, and the alcohol dehydrogenase 1B (ADH1B) locus is a candidate for further investigating the mechanisms underlying this association. |
| Databáze: | OpenAIRE |
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