Genetic study of the causal effect of lipid profiles on insomnia risk: a Mendelian randomization trial
Abstract Objectives In response to the controversy surrounding observational studies of the association between lipid profiles and the risk of insomnia, the aim of this study was to analyze lipid profiles, including triglycerides (TG), apolipoprotein A-1 (ApoA-1), apolipoprotein B (ApoB) and lipopro...
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| Format: | Article |
| Language: | English |
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BMC
2023-12-01
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| Series: | BMC Medical Genomics |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s12920-023-01761-y |
| _version_ | 1797387994823393280 |
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| author | Quancai Gong Canshou Guo |
| author_facet | Quancai Gong Canshou Guo |
| author_sort | Quancai Gong |
| collection | DOAJ |
| description | Abstract Objectives In response to the controversy surrounding observational studies of the association between lipid profiles and the risk of insomnia, the aim of this study was to analyze lipid profiles, including triglycerides (TG), apolipoprotein A-1 (ApoA-1), apolipoprotein B (ApoB) and lipoprotein A (LPA), in a European population to further assess the causal relationship between these lipid types and insomnia. Materials and methods This study explores the causal effect of lipid profiles on insomnia based on a genome-wide association study (GWAS)-derived public dataset using two-sample and multivariate Mendelian randomization (MVMR) analysis. The main MR analyses used inverse variance weighting (IVW) odds ratio (OR), and the sensitivity analyses included weighted median (WM) and MR‒Egger. Results Both MR and MVMR showed that lowering ApoA-1 and LPA levels had causal effects on the risk of insomnia [MR: per 10 units, ApoA-1: OR: 0.7546, 95% CI: 0.6075–0.9372, P = 0.011; LPA: OR: 0.8392, 95% CI: 0.7202–0.9778, P = 0.025; MVMR: per 10 units, ApoA-1: OR: 0.7600, 95% CI: 0.6362–0.9079, P = 0.002; LPA, OR: 0.903, 95% CI: 0.8283–0.9845, P = 0.021]. There were no causal effects of TG or ApoB on insomnia (all P > 0.05). The MR‒Egger intercept test, funnel plot, and IVW methods all suggested an absence of strong directional pleiotropy, and leave-one-out permutation analysis did not detect any single single-nucleotide polymorphism that had a strong influence on the results. Conclusion Elevated levels of ApoA-1 and LPA were independently and causally associated with the risk of insomnia, suggesting that elevated ApoA-1 and LPA levels may contribute to a reduced risk of insomnia. |
| first_indexed | 2024-03-08T22:34:15Z |
| format | Article |
| id | doaj.art-5526ffff003c4558a3a1b8d4e97dcf9a |
| institution | Directory Open Access Journal |
| issn | 1755-8794 |
| language | English |
| last_indexed | 2024-03-08T22:34:15Z |
| publishDate | 2023-12-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Medical Genomics |
| spelling | doaj.art-5526ffff003c4558a3a1b8d4e97dcf9a2023-12-17T12:32:51ZengBMCBMC Medical Genomics1755-87942023-12-0116111110.1186/s12920-023-01761-yGenetic study of the causal effect of lipid profiles on insomnia risk: a Mendelian randomization trialQuancai Gong0Canshou Guo1Department of Neurology, Affiliated Hospital of Jianghan UniversityDepartment of Neurology, Affiliated Hospital of Jianghan UniversityAbstract Objectives In response to the controversy surrounding observational studies of the association between lipid profiles and the risk of insomnia, the aim of this study was to analyze lipid profiles, including triglycerides (TG), apolipoprotein A-1 (ApoA-1), apolipoprotein B (ApoB) and lipoprotein A (LPA), in a European population to further assess the causal relationship between these lipid types and insomnia. Materials and methods This study explores the causal effect of lipid profiles on insomnia based on a genome-wide association study (GWAS)-derived public dataset using two-sample and multivariate Mendelian randomization (MVMR) analysis. The main MR analyses used inverse variance weighting (IVW) odds ratio (OR), and the sensitivity analyses included weighted median (WM) and MR‒Egger. Results Both MR and MVMR showed that lowering ApoA-1 and LPA levels had causal effects on the risk of insomnia [MR: per 10 units, ApoA-1: OR: 0.7546, 95% CI: 0.6075–0.9372, P = 0.011; LPA: OR: 0.8392, 95% CI: 0.7202–0.9778, P = 0.025; MVMR: per 10 units, ApoA-1: OR: 0.7600, 95% CI: 0.6362–0.9079, P = 0.002; LPA, OR: 0.903, 95% CI: 0.8283–0.9845, P = 0.021]. There were no causal effects of TG or ApoB on insomnia (all P > 0.05). The MR‒Egger intercept test, funnel plot, and IVW methods all suggested an absence of strong directional pleiotropy, and leave-one-out permutation analysis did not detect any single single-nucleotide polymorphism that had a strong influence on the results. Conclusion Elevated levels of ApoA-1 and LPA were independently and causally associated with the risk of insomnia, suggesting that elevated ApoA-1 and LPA levels may contribute to a reduced risk of insomnia.https://doi.org/10.1186/s12920-023-01761-yGeneticsInsomniaLipid profilesMultivariable mendelian randomizationApolipoprotein A-1lipoprotein-a |
| spellingShingle | Quancai Gong Canshou Guo Genetic study of the causal effect of lipid profiles on insomnia risk: a Mendelian randomization trial BMC Medical Genomics Genetics Insomnia Lipid profiles Multivariable mendelian randomization Apolipoprotein A-1 lipoprotein-a |
| title | Genetic study of the causal effect of lipid profiles on insomnia risk: a Mendelian randomization trial |
| title_full | Genetic study of the causal effect of lipid profiles on insomnia risk: a Mendelian randomization trial |
| title_fullStr | Genetic study of the causal effect of lipid profiles on insomnia risk: a Mendelian randomization trial |
| title_full_unstemmed | Genetic study of the causal effect of lipid profiles on insomnia risk: a Mendelian randomization trial |
| title_short | Genetic study of the causal effect of lipid profiles on insomnia risk: a Mendelian randomization trial |
| title_sort | genetic study of the causal effect of lipid profiles on insomnia risk a mendelian randomization trial |
| topic | Genetics Insomnia Lipid profiles Multivariable mendelian randomization Apolipoprotein A-1 lipoprotein-a |
| url | https://doi.org/10.1186/s12920-023-01761-y |
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