Investigating the causal interplay between sleep traits and risk of acute myocardial infarction: a Mendelian randomization study
Abstract Background Few studies have investigated the joint effects of sleep traits on the risk of acute myocardial infarction (AMI). No previous study has used factorial Mendelian randomization (MR) which may reduce confounding, reverse causation, and measurement error. Thus, it is prudent to study...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
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BMC
2023-10-01
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| Series: | BMC Medicine |
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| Online Access: | https://doi.org/10.1186/s12916-023-03078-0 |
| _version_ | 1827710641753817088 |
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| author | Nikhil Arora Laxmi Bhatta Eivind Schjelderup Skarpsno Håvard Dalen Bjørn Olav Åsvold Ben Michael Brumpton Rebecca Claire Richmond Linn Beate Strand |
| author_facet | Nikhil Arora Laxmi Bhatta Eivind Schjelderup Skarpsno Håvard Dalen Bjørn Olav Åsvold Ben Michael Brumpton Rebecca Claire Richmond Linn Beate Strand |
| author_sort | Nikhil Arora |
| collection | DOAJ |
| description | Abstract Background Few studies have investigated the joint effects of sleep traits on the risk of acute myocardial infarction (AMI). No previous study has used factorial Mendelian randomization (MR) which may reduce confounding, reverse causation, and measurement error. Thus, it is prudent to study joint effects using robust methods to propose sleep-targeted interventions which lower the risk of AMI. Methods The causal interplay between combinations of two sleep traits (including insomnia symptoms, sleep duration, or chronotype) on the risk of AMI was investigated using factorial MR. Genetic risk scores for each sleep trait were dichotomized at their median in UK Biobank (UKBB) and the second survey of the Trøndelag Health Study (HUNT2). A combination of two sleep traits constituting 4 groups were analyzed to estimate the risk of AMI in each group using a 2×2 factorial MR design. Results In UKBB, participants with high genetic risk for both insomnia symptoms and short sleep had the highest risk of AMI (hazard ratio (HR) 1.10; 95% confidence interval (CI) 1.03, 1.18), although there was no evidence of interaction (relative excess risk due to interaction (RERI) 0.03; 95% CI −0.07, 0.12). These estimates were less precise in HUNT2 (HR 1.02; 95% CI 0.93, 1.13), possibly due to weak instruments and/or small sample size. Participants with high genetic risk for both a morning chronotype and insomnia symptoms (HR 1.09; 95% CI 1.03, 1.17) and a morning chronotype and short sleep (HR 1.11; 95% CI 1.04, 1.19) had the highest risk of AMI in UKBB, although there was no evidence of interaction (RERI 0.03; 95% CI −0.06, 0.12; and RERI 0.05; 95% CI –0.05, 0.14, respectively). Chronotype was not available in HUNT2. Conclusions This study reveals no interaction effects between sleep traits on the risk of AMI, but all combinations of sleep traits increased the risk of AMI except those with long sleep. This indicates that the main effects of sleep traits on AMI are likely to be independent of each other. |
| first_indexed | 2024-03-10T17:40:47Z |
| format | Article |
| id | doaj.art-64f65d95425943e189019cc7b8e8e08b |
| institution | Directory Open Access Journal |
| issn | 1741-7015 |
| language | English |
| last_indexed | 2024-03-10T17:40:47Z |
| publishDate | 2023-10-01 |
| publisher | BMC |
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| series | BMC Medicine |
| spelling | doaj.art-64f65d95425943e189019cc7b8e8e08b2023-11-20T09:41:21ZengBMCBMC Medicine1741-70152023-10-0121111610.1186/s12916-023-03078-0Investigating the causal interplay between sleep traits and risk of acute myocardial infarction: a Mendelian randomization studyNikhil Arora0Laxmi Bhatta1Eivind Schjelderup Skarpsno2Håvard Dalen3Bjørn Olav Åsvold4Ben Michael Brumpton5Rebecca Claire Richmond6Linn Beate Strand7K.G. Jebsen Center for Genetic Epidemiology, Department of Public Health and Nursing, Norwegian University of Science and TechnologyK.G. Jebsen Center for Genetic Epidemiology, Department of Public Health and Nursing, Norwegian University of Science and TechnologyDepartment of Public Health and Nursing, Norwegian University of Science and TechnologyDepartment of Circulation and Medical Imaging, Norwegian University of Science and TechnologyK.G. Jebsen Center for Genetic Epidemiology, Department of Public Health and Nursing, Norwegian University of Science and TechnologyK.G. Jebsen Center for Genetic Epidemiology, Department of Public Health and Nursing, Norwegian University of Science and TechnologyPopulation Health Sciences, Bristol Medical School, University of BristolDepartment of Public Health and Nursing, Norwegian University of Science and TechnologyAbstract Background Few studies have investigated the joint effects of sleep traits on the risk of acute myocardial infarction (AMI). No previous study has used factorial Mendelian randomization (MR) which may reduce confounding, reverse causation, and measurement error. Thus, it is prudent to study joint effects using robust methods to propose sleep-targeted interventions which lower the risk of AMI. Methods The causal interplay between combinations of two sleep traits (including insomnia symptoms, sleep duration, or chronotype) on the risk of AMI was investigated using factorial MR. Genetic risk scores for each sleep trait were dichotomized at their median in UK Biobank (UKBB) and the second survey of the Trøndelag Health Study (HUNT2). A combination of two sleep traits constituting 4 groups were analyzed to estimate the risk of AMI in each group using a 2×2 factorial MR design. Results In UKBB, participants with high genetic risk for both insomnia symptoms and short sleep had the highest risk of AMI (hazard ratio (HR) 1.10; 95% confidence interval (CI) 1.03, 1.18), although there was no evidence of interaction (relative excess risk due to interaction (RERI) 0.03; 95% CI −0.07, 0.12). These estimates were less precise in HUNT2 (HR 1.02; 95% CI 0.93, 1.13), possibly due to weak instruments and/or small sample size. Participants with high genetic risk for both a morning chronotype and insomnia symptoms (HR 1.09; 95% CI 1.03, 1.17) and a morning chronotype and short sleep (HR 1.11; 95% CI 1.04, 1.19) had the highest risk of AMI in UKBB, although there was no evidence of interaction (RERI 0.03; 95% CI −0.06, 0.12; and RERI 0.05; 95% CI –0.05, 0.14, respectively). Chronotype was not available in HUNT2. Conclusions This study reveals no interaction effects between sleep traits on the risk of AMI, but all combinations of sleep traits increased the risk of AMI except those with long sleep. This indicates that the main effects of sleep traits on AMI are likely to be independent of each other.https://doi.org/10.1186/s12916-023-03078-0InsomniaSleep durationChronotypeMyocardial infarctionMendelian randomization |
| spellingShingle | Nikhil Arora Laxmi Bhatta Eivind Schjelderup Skarpsno Håvard Dalen Bjørn Olav Åsvold Ben Michael Brumpton Rebecca Claire Richmond Linn Beate Strand Investigating the causal interplay between sleep traits and risk of acute myocardial infarction: a Mendelian randomization study BMC Medicine Insomnia Sleep duration Chronotype Myocardial infarction Mendelian randomization |
| title | Investigating the causal interplay between sleep traits and risk of acute myocardial infarction: a Mendelian randomization study |
| title_full | Investigating the causal interplay between sleep traits and risk of acute myocardial infarction: a Mendelian randomization study |
| title_fullStr | Investigating the causal interplay between sleep traits and risk of acute myocardial infarction: a Mendelian randomization study |
| title_full_unstemmed | Investigating the causal interplay between sleep traits and risk of acute myocardial infarction: a Mendelian randomization study |
| title_short | Investigating the causal interplay between sleep traits and risk of acute myocardial infarction: a Mendelian randomization study |
| title_sort | investigating the causal interplay between sleep traits and risk of acute myocardial infarction a mendelian randomization study |
| topic | Insomnia Sleep duration Chronotype Myocardial infarction Mendelian randomization |
| url | https://doi.org/10.1186/s12916-023-03078-0 |
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