Sleep Duration and Stroke: A Mendelian Randomization Study
Study Objectives: To clarify the effects of sleep duration on stroke and stroke subtypes, we adopted a Mendelian randomization (MR) approach to evaluate their causal relationship.Methods: A genome-wide association study including 446,118 participants from UK biobank was used to identify instruments...
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Frontiers Media S.A.
2020-10-01
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Online Access: | https://www.frontiersin.org/article/10.3389/fneur.2020.00976/full |
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author | Hui Lu Peng-Fei Wu Peng-Fei Wu Rui-Zhuo Li Wan Zhang Wan Zhang Guo-xiang Huang |
author_facet | Hui Lu Peng-Fei Wu Peng-Fei Wu Rui-Zhuo Li Wan Zhang Wan Zhang Guo-xiang Huang |
author_sort | Hui Lu |
collection | DOAJ |
description | Study Objectives: To clarify the effects of sleep duration on stroke and stroke subtypes, we adopted a Mendelian randomization (MR) approach to evaluate their causal relationship.Methods: A genome-wide association study including 446,118 participants from UK biobank was used to identify instruments for short sleep, long sleep and sleep duration. Summary-level data for all stroke, ischemic stroke, intracerebral hemorrhage, and their subtypes were obtained from meta-analyses conducted by the MEGASTROKE consortium. MR analyses were performed using the inverse-variance-weighted method, weighted median estimator, MR pleiotropy residual sum and outlier (MR-PRESSO) test, and MR-Egger regression. Sensitivity analyses were further performed using leave-one-out analysis, MR-PRESSO global test and Cochran's Q test to verify the robustness of our findings.Results: By two-sample MR, we didn't find causal associations between sleep duration and risk of stroke. However, in the subgroup analysis, we found weak evidence for short sleep in increasing risk of cardio-embolic stroke (odds ratio [OR], 1.33; 95% confidence interval [CI], 1.11–1.60; P = 0.02) and long sleep in increasing risk of large artery stroke [OR, 1.41; 95% CI, 1.02–1.95; P = 0.04]. But the associations were not significant after Bonferroni correction for multiple comparisons.Conclusions: Our study suggests that sleep duration is not causally associated with risk of stroke and its subtypes. |
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issn | 1664-2295 |
language | English |
last_indexed | 2024-12-11T13:05:18Z |
publishDate | 2020-10-01 |
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spelling | doaj.art-4cbde153506743af8c54f691730823f62022-12-22T01:06:20ZengFrontiers Media S.A.Frontiers in Neurology1664-22952020-10-011110.3389/fneur.2020.00976577059Sleep Duration and Stroke: A Mendelian Randomization StudyHui Lu0Peng-Fei Wu1Peng-Fei Wu2Rui-Zhuo Li3Wan Zhang4Wan Zhang5Guo-xiang Huang6Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, ChinaCenter for Medical Genetics & Hunan Provincial Key Laboratory for Medical Genetics, School of Life Sciences, Central South University, Changsha, ChinaDepartment of Neurology, Beth Israel Deaconess Medical Center & Harvard Medical School, Boston, MA, United StatesSchool of Medicine, South China University of Technology, Guangzhou, ChinaDepartment of Neurology, Beth Israel Deaconess Medical Center & Harvard Medical School, Boston, MA, United StatesBiology Department, College of Arts & Sciences, Boston University, Boston, MA, United StatesDepartment of Neurology, Affiliated Hospital of Nantong University, Nantong, ChinaStudy Objectives: To clarify the effects of sleep duration on stroke and stroke subtypes, we adopted a Mendelian randomization (MR) approach to evaluate their causal relationship.Methods: A genome-wide association study including 446,118 participants from UK biobank was used to identify instruments for short sleep, long sleep and sleep duration. Summary-level data for all stroke, ischemic stroke, intracerebral hemorrhage, and their subtypes were obtained from meta-analyses conducted by the MEGASTROKE consortium. MR analyses were performed using the inverse-variance-weighted method, weighted median estimator, MR pleiotropy residual sum and outlier (MR-PRESSO) test, and MR-Egger regression. Sensitivity analyses were further performed using leave-one-out analysis, MR-PRESSO global test and Cochran's Q test to verify the robustness of our findings.Results: By two-sample MR, we didn't find causal associations between sleep duration and risk of stroke. However, in the subgroup analysis, we found weak evidence for short sleep in increasing risk of cardio-embolic stroke (odds ratio [OR], 1.33; 95% confidence interval [CI], 1.11–1.60; P = 0.02) and long sleep in increasing risk of large artery stroke [OR, 1.41; 95% CI, 1.02–1.95; P = 0.04]. But the associations were not significant after Bonferroni correction for multiple comparisons.Conclusions: Our study suggests that sleep duration is not causally associated with risk of stroke and its subtypes.https://www.frontiersin.org/article/10.3389/fneur.2020.00976/fullstrokesleep durationmendelian randomizationgenome-wide association studysingle nucleotide polymorphism |
spellingShingle | Hui Lu Peng-Fei Wu Peng-Fei Wu Rui-Zhuo Li Wan Zhang Wan Zhang Guo-xiang Huang Sleep Duration and Stroke: A Mendelian Randomization Study Frontiers in Neurology stroke sleep duration mendelian randomization genome-wide association study single nucleotide polymorphism |
title | Sleep Duration and Stroke: A Mendelian Randomization Study |
title_full | Sleep Duration and Stroke: A Mendelian Randomization Study |
title_fullStr | Sleep Duration and Stroke: A Mendelian Randomization Study |
title_full_unstemmed | Sleep Duration and Stroke: A Mendelian Randomization Study |
title_short | Sleep Duration and Stroke: A Mendelian Randomization Study |
title_sort | sleep duration and stroke a mendelian randomization study |
topic | stroke sleep duration mendelian randomization genome-wide association study single nucleotide polymorphism |
url | https://www.frontiersin.org/article/10.3389/fneur.2020.00976/full |
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