Yi-Shian Liu, Yu-Chun Lin, Meng-Chih Lin, Chao-Chien Wu, Tsu-Nai Wang
{"title":"血脂与哮喘的关系:双向双样本孟德尔随机研究","authors":"Yi-Shian Liu, Yu-Chun Lin, Meng-Chih Lin, Chao-Chien Wu, Tsu-Nai Wang","doi":"10.1111/ahg.12545","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Background</h3>\n \n <p>Observational studies and meta-analyses have indicated associations between blood lipid profiles and asthma. However, the causal association is unknown. Therefore, this study investigated the causal relationship between blood lipid profiles and asthma using bidirectional Mendelian randomization analysis.</p>\n </section>\n \n <section>\n \n <h3> Methods and materials</h3>\n \n <p>Our analyses were performed using individual data from the Taiwan Biobank and summary statistics from the Asian Genetic Epidemiology Network (AGEN). The causal estimates between all genetic variants, exposures of interest and asthma were calculated using an inverse-variance weighted method based on Taiwan Biobank data from 24,853 participants (mean age, 48.8 years; 49.8% women). Sensitivity analyses, including the weighted median, MR Egger regression, MR-PRESSO, mode-based estimate, contamination mixture methods, and leave-one-out analysis, were applied to validate the results and detect pleiotropy.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>In the inverse-variance weighted (IVW) analyses, we found evidence of a significant causal effect of an increased level of low-density lipoprotein cholesterol on asthma risk (<i>β</i><sub>IVW</sub> = 1.338, <i>p</i> = 0.001). A genetically decreased level of high-density lipoprotein cholesterol was also associated with asthma risk (<i>β</i><sub>IVW</sub> = −0.338, <i>p</i> = 0.01). We also found that an increased level of total cholesterol was associated with an increased risk of asthma (<i>β</i><sub>IVW</sub> = 1.343, <i>p</i> = 0.001). Several sensitivity analyses generated consistent findings. We did not find evidence to support the causality between asthma and blood lipid profiles in either direction.</p>\n </section>\n \n <section>\n \n <h3> Conclusion</h3>\n \n <p>Our results supported the causal relationship between higher levels of LDL cholesterol and total cholesterol and lower levels of HDL cholesterol with an increased risk of asthma.</p>\n </section>\n </div>","PeriodicalId":8085,"journal":{"name":"Annals of Human Genetics","volume":"88 4","pages":"307-319"},"PeriodicalIF":1.0000,"publicationDate":"2024-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Association of blood lipid profiles and asthma: A bidirectional two-sample Mendelian randomization study\",\"authors\":\"Yi-Shian Liu, Yu-Chun Lin, Meng-Chih Lin, Chao-Chien Wu, Tsu-Nai Wang\",\"doi\":\"10.1111/ahg.12545\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n \\n <section>\\n \\n <h3> Background</h3>\\n \\n <p>Observational studies and meta-analyses have indicated associations between blood lipid profiles and asthma. However, the causal association is unknown. Therefore, this study investigated the causal relationship between blood lipid profiles and asthma using bidirectional Mendelian randomization analysis.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Methods and materials</h3>\\n \\n <p>Our analyses were performed using individual data from the Taiwan Biobank and summary statistics from the Asian Genetic Epidemiology Network (AGEN). The causal estimates between all genetic variants, exposures of interest and asthma were calculated using an inverse-variance weighted method based on Taiwan Biobank data from 24,853 participants (mean age, 48.8 years; 49.8% women). Sensitivity analyses, including the weighted median, MR Egger regression, MR-PRESSO, mode-based estimate, contamination mixture methods, and leave-one-out analysis, were applied to validate the results and detect pleiotropy.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Results</h3>\\n \\n <p>In the inverse-variance weighted (IVW) analyses, we found evidence of a significant causal effect of an increased level of low-density lipoprotein cholesterol on asthma risk (<i>β</i><sub>IVW</sub> = 1.338, <i>p</i> = 0.001). A genetically decreased level of high-density lipoprotein cholesterol was also associated with asthma risk (<i>β</i><sub>IVW</sub> = −0.338, <i>p</i> = 0.01). We also found that an increased level of total cholesterol was associated with an increased risk of asthma (<i>β</i><sub>IVW</sub> = 1.343, <i>p</i> = 0.001). Several sensitivity analyses generated consistent findings. We did not find evidence to support the causality between asthma and blood lipid profiles in either direction.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Conclusion</h3>\\n \\n <p>Our results supported the causal relationship between higher levels of LDL cholesterol and total cholesterol and lower levels of HDL cholesterol with an increased risk of asthma.</p>\\n </section>\\n </div>\",\"PeriodicalId\":8085,\"journal\":{\"name\":\"Annals of Human Genetics\",\"volume\":\"88 4\",\"pages\":\"307-319\"},\"PeriodicalIF\":1.0000,\"publicationDate\":\"2024-02-02\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Annals of Human Genetics\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/ahg.12545\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"GENETICS & HEREDITY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annals of Human Genetics","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/ahg.12545","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
Association of blood lipid profiles and asthma: A bidirectional two-sample Mendelian randomization study
Background
Observational studies and meta-analyses have indicated associations between blood lipid profiles and asthma. However, the causal association is unknown. Therefore, this study investigated the causal relationship between blood lipid profiles and asthma using bidirectional Mendelian randomization analysis.
Methods and materials
Our analyses were performed using individual data from the Taiwan Biobank and summary statistics from the Asian Genetic Epidemiology Network (AGEN). The causal estimates between all genetic variants, exposures of interest and asthma were calculated using an inverse-variance weighted method based on Taiwan Biobank data from 24,853 participants (mean age, 48.8 years; 49.8% women). Sensitivity analyses, including the weighted median, MR Egger regression, MR-PRESSO, mode-based estimate, contamination mixture methods, and leave-one-out analysis, were applied to validate the results and detect pleiotropy.
Results
In the inverse-variance weighted (IVW) analyses, we found evidence of a significant causal effect of an increased level of low-density lipoprotein cholesterol on asthma risk (βIVW = 1.338, p = 0.001). A genetically decreased level of high-density lipoprotein cholesterol was also associated with asthma risk (βIVW = −0.338, p = 0.01). We also found that an increased level of total cholesterol was associated with an increased risk of asthma (βIVW = 1.343, p = 0.001). Several sensitivity analyses generated consistent findings. We did not find evidence to support the causality between asthma and blood lipid profiles in either direction.
Conclusion
Our results supported the causal relationship between higher levels of LDL cholesterol and total cholesterol and lower levels of HDL cholesterol with an increased risk of asthma.
期刊介绍:
Annals of Human Genetics publishes material directly concerned with human genetics or the application of scientific principles and techniques to any aspect of human inheritance. Papers that describe work on other species that may be relevant to human genetics will also be considered. Mathematical models should include examples of application to data where possible.
Authors are welcome to submit Supporting Information, such as data sets or additional figures or tables, that will not be published in the print edition of the journal, but which will be viewable via the online edition and stored on the website.