Frailty and risk of systemic atherosclerosis: A bidirectional Mendelian randomization study
Numerous observational studies have reported an association between frailty and atherosclerosis. However, the causal relationship between frailty and the occurrence of atherosclerosis in different anatomical sites remains unclear. we conducted a bidirectional Mendelian randomization (MR) study to ev...
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| description | Numerous observational studies have reported an association between frailty and atherosclerosis. However, the causal relationship between frailty and the occurrence of atherosclerosis in different anatomical sites remains unclear. we conducted a bidirectional Mendelian randomization (MR) study to evaluate the causal relationship between the frailty index (FI), and both systemic atherosclerosis and lipids.
We obtained summary statistics from large-scale genome-wide association studies (GWAS) of various phenotypes, including frailty (n = 175,226), coronary atherosclerosis (n = 56,685), cerebral atherosclerosis (n = 150,765), peripheral arterial disease (PAD) (n = 361,194), atherosclerosis at other sites (n = 17,832), LDL-C (n = 201,678), HDL-C (n = 77,409), and triglycerides (n = 78,700). The primary MR analysis employed the inverse variance weighted (IVW) method. Furthermore, to assess reverse causality, we employed inverse MR and multivariate MR analysis.
Genetically predicted FI showed positive associations with the risk of coronary atherosclerosis (OR = 1.47, 95% CI 1.12-1.93) and cerebral atherosclerosis (OR = 1.99, 95% CI 1.05-3.78), with no significant association (p >0.05) applied to peripheral arterial disease and atherosclerosis at other sites. Genetically predicted FI was positively associated with the risk of triglycerides (OR = 1.31, 95% CI 1.08-1.59), negatively associated with the risk of LDL-C (OR = 0.87, 95% CI 0.78-0.97), and showed no significant association with the risk of HDL-C (p >0.05). Furthermore, both reverse MR and multivariate MR analyses demonstrated a correlation between systemic atherosclerosis, lipids, and increased FI.
Our study elucidated that genetically predicted FI is associated with the risk of coronary atherosclerosis and cerebral atherosclerosis by the MR analysis method, and they have a bidirectional causal relationship. Moreover, genetically predicted FI was causally associated with triglyceride and LDL-C levels. Further understanding of this association is crucial for optimizing medical practice and care models specifically tailored to frail populations. |
| doi_str_mv | 10.1371/journal.pone.0304300 |
| format | Article |
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We obtained summary statistics from large-scale genome-wide association studies (GWAS) of various phenotypes, including frailty (n = 175,226), coronary atherosclerosis (n = 56,685), cerebral atherosclerosis (n = 150,765), peripheral arterial disease (PAD) (n = 361,194), atherosclerosis at other sites (n = 17,832), LDL-C (n = 201,678), HDL-C (n = 77,409), and triglycerides (n = 78,700). The primary MR analysis employed the inverse variance weighted (IVW) method. Furthermore, to assess reverse causality, we employed inverse MR and multivariate MR analysis.
Genetically predicted FI showed positive associations with the risk of coronary atherosclerosis (OR = 1.47, 95% CI 1.12-1.93) and cerebral atherosclerosis (OR = 1.99, 95% CI 1.05-3.78), with no significant association (p >0.05) applied to peripheral arterial disease and atherosclerosis at other sites. Genetically predicted FI was positively associated with the risk of triglycerides (OR = 1.31, 95% CI 1.08-1.59), negatively associated with the risk of LDL-C (OR = 0.87, 95% CI 0.78-0.97), and showed no significant association with the risk of HDL-C (p >0.05). Furthermore, both reverse MR and multivariate MR analyses demonstrated a correlation between systemic atherosclerosis, lipids, and increased FI.
Our study elucidated that genetically predicted FI is associated with the risk of coronary atherosclerosis and cerebral atherosclerosis by the MR analysis method, and they have a bidirectional causal relationship. Moreover, genetically predicted FI was causally associated with triglyceride and LDL-C levels. Further understanding of this association is crucial for optimizing medical practice and care models specifically tailored to frail populations.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0304300</identifier><identifier>PMID: 38781179</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Aged ; Arteriosclerosis ; Atherosclerosis ; Atherosclerosis - genetics ; Biobanks ; Biology and Life Sciences ; Cardiovascular disease ; Cholesterol, HDL - blood ; Cholesterol, LDL - blood ; Chronic illnesses ; Confounding (Statistics) ; Coronary Artery Disease - genetics ; Coronary vessels ; Epidemiology ; Estimates ; Female ; Frailty ; Frailty - genetics ; Genome-wide association studies ; Genome-Wide Association Study ; Genomes ; Genomics ; High density lipoprotein ; Humans ; Hypotheses ; Ischemia ; Lipids ; Low density lipoprotein ; Low density lipoproteins ; Male ; Medicine and Health Sciences ; Mendelian Randomization Analysis ; Multivariate analysis ; Observational studies ; Phenotypes ; Polymorphism, Single Nucleotide ; Randomization ; Risk ; Risk Factors ; Statistical analysis ; Statistics ; Triglycerides ; Triglycerides - blood ; Variables ; Veins & arteries</subject><ispartof>PloS one, 2024-05, Vol.19 (5), p.e0304300-e0304300</ispartof><rights>Copyright: © 2024 Xu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</rights><rights>COPYRIGHT 2024 Public Library of Science</rights><rights>2024 Xu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2024 Xu et al 2024 Xu et al</rights><rights>2024 Xu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c642t-f34f7cd0ba4887b44b27f40408b9c85663cb02bce94b05bade353ca7915d09413</cites><orcidid>0009-0004-5111-0936</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11115302/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11115302/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38781179$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Khalaji, Amirmohammad</contributor><creatorcontrib>Xu, Liugang</creatorcontrib><creatorcontrib>Wang, Yajun</creatorcontrib><creatorcontrib>Ji, Hongyun</creatorcontrib><creatorcontrib>Du, Wei</creatorcontrib><creatorcontrib>You, Chunhui</creatorcontrib><creatorcontrib>Chen, Jin</creatorcontrib><creatorcontrib>Jiang, Jianyu</creatorcontrib><creatorcontrib>Shan, Yisi</creatorcontrib><creatorcontrib>Pan, Qian</creatorcontrib><creatorcontrib>Cao, Ruihong</creatorcontrib><title>Frailty and risk of systemic atherosclerosis: A bidirectional Mendelian randomization study</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Numerous observational studies have reported an association between frailty and atherosclerosis. However, the causal relationship between frailty and the occurrence of atherosclerosis in different anatomical sites remains unclear. we conducted a bidirectional Mendelian randomization (MR) study to evaluate the causal relationship between the frailty index (FI), and both systemic atherosclerosis and lipids.
We obtained summary statistics from large-scale genome-wide association studies (GWAS) of various phenotypes, including frailty (n = 175,226), coronary atherosclerosis (n = 56,685), cerebral atherosclerosis (n = 150,765), peripheral arterial disease (PAD) (n = 361,194), atherosclerosis at other sites (n = 17,832), LDL-C (n = 201,678), HDL-C (n = 77,409), and triglycerides (n = 78,700). The primary MR analysis employed the inverse variance weighted (IVW) method. Furthermore, to assess reverse causality, we employed inverse MR and multivariate MR analysis.
Genetically predicted FI showed positive associations with the risk of coronary atherosclerosis (OR = 1.47, 95% CI 1.12-1.93) and cerebral atherosclerosis (OR = 1.99, 95% CI 1.05-3.78), with no significant association (p >0.05) applied to peripheral arterial disease and atherosclerosis at other sites. Genetically predicted FI was positively associated with the risk of triglycerides (OR = 1.31, 95% CI 1.08-1.59), negatively associated with the risk of LDL-C (OR = 0.87, 95% CI 0.78-0.97), and showed no significant association with the risk of HDL-C (p >0.05). Furthermore, both reverse MR and multivariate MR analyses demonstrated a correlation between systemic atherosclerosis, lipids, and increased FI.
Our study elucidated that genetically predicted FI is associated with the risk of coronary atherosclerosis and cerebral atherosclerosis by the MR analysis method, and they have a bidirectional causal relationship. Moreover, genetically predicted FI was causally associated with triglyceride and LDL-C levels. Further understanding of this association is crucial for optimizing medical practice and care models specifically tailored to frail populations.</description><subject>Aged</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - genetics</subject><subject>Biobanks</subject><subject>Biology and Life Sciences</subject><subject>Cardiovascular disease</subject><subject>Cholesterol, HDL - blood</subject><subject>Cholesterol, LDL - blood</subject><subject>Chronic illnesses</subject><subject>Confounding (Statistics)</subject><subject>Coronary Artery Disease - genetics</subject><subject>Coronary vessels</subject><subject>Epidemiology</subject><subject>Estimates</subject><subject>Female</subject><subject>Frailty</subject><subject>Frailty - genetics</subject><subject>Genome-wide association studies</subject><subject>Genome-Wide Association Study</subject><subject>Genomes</subject><subject>Genomics</subject><subject>High density lipoprotein</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Ischemia</subject><subject>Lipids</subject><subject>Low density lipoprotein</subject><subject>Low density lipoproteins</subject><subject>Male</subject><subject>Medicine and Health Sciences</subject><subject>Mendelian Randomization Analysis</subject><subject>Multivariate analysis</subject><subject>Observational studies</subject><subject>Phenotypes</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Randomization</subject><subject>Risk</subject><subject>Risk Factors</subject><subject>Statistical analysis</subject><subject>Statistics</subject><subject>Triglycerides</subject><subject>Triglycerides - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xu, Liugang</au><au>Wang, Yajun</au><au>Ji, Hongyun</au><au>Du, Wei</au><au>You, Chunhui</au><au>Chen, Jin</au><au>Jiang, Jianyu</au><au>Shan, Yisi</au><au>Pan, Qian</au><au>Cao, Ruihong</au><au>Khalaji, Amirmohammad</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Frailty and risk of systemic atherosclerosis: A bidirectional Mendelian randomization study</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2024-05-23</date><risdate>2024</risdate><volume>19</volume><issue>5</issue><spage>e0304300</spage><epage>e0304300</epage><pages>e0304300-e0304300</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Numerous observational studies have reported an association between frailty and atherosclerosis. However, the causal relationship between frailty and the occurrence of atherosclerosis in different anatomical sites remains unclear. we conducted a bidirectional Mendelian randomization (MR) study to evaluate the causal relationship between the frailty index (FI), and both systemic atherosclerosis and lipids.
We obtained summary statistics from large-scale genome-wide association studies (GWAS) of various phenotypes, including frailty (n = 175,226), coronary atherosclerosis (n = 56,685), cerebral atherosclerosis (n = 150,765), peripheral arterial disease (PAD) (n = 361,194), atherosclerosis at other sites (n = 17,832), LDL-C (n = 201,678), HDL-C (n = 77,409), and triglycerides (n = 78,700). The primary MR analysis employed the inverse variance weighted (IVW) method. Furthermore, to assess reverse causality, we employed inverse MR and multivariate MR analysis.
Genetically predicted FI showed positive associations with the risk of coronary atherosclerosis (OR = 1.47, 95% CI 1.12-1.93) and cerebral atherosclerosis (OR = 1.99, 95% CI 1.05-3.78), with no significant association (p >0.05) applied to peripheral arterial disease and atherosclerosis at other sites. Genetically predicted FI was positively associated with the risk of triglycerides (OR = 1.31, 95% CI 1.08-1.59), negatively associated with the risk of LDL-C (OR = 0.87, 95% CI 0.78-0.97), and showed no significant association with the risk of HDL-C (p >0.05). Furthermore, both reverse MR and multivariate MR analyses demonstrated a correlation between systemic atherosclerosis, lipids, and increased FI.
Our study elucidated that genetically predicted FI is associated with the risk of coronary atherosclerosis and cerebral atherosclerosis by the MR analysis method, and they have a bidirectional causal relationship. Moreover, genetically predicted FI was causally associated with triglyceride and LDL-C levels. Further understanding of this association is crucial for optimizing medical practice and care models specifically tailored to frail populations.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>38781179</pmid><doi>10.1371/journal.pone.0304300</doi><orcidid>https://orcid.org/0009-0004-5111-0936</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2024-05, Vol.19 (5), p.e0304300-e0304300 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_3069289915 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS) Journals Open Access; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Aged Arteriosclerosis Atherosclerosis Atherosclerosis - genetics Biobanks Biology and Life Sciences Cardiovascular disease Cholesterol, HDL - blood Cholesterol, LDL - blood Chronic illnesses Confounding (Statistics) Coronary Artery Disease - genetics Coronary vessels Epidemiology Estimates Female Frailty Frailty - genetics Genome-wide association studies Genome-Wide Association Study Genomes Genomics High density lipoprotein Humans Hypotheses Ischemia Lipids Low density lipoprotein Low density lipoproteins Male Medicine and Health Sciences Mendelian Randomization Analysis Multivariate analysis Observational studies Phenotypes Polymorphism, Single Nucleotide Randomization Risk Risk Factors Statistical analysis Statistics Triglycerides Triglycerides - blood Variables Veins & arteries |
| title | Frailty and risk of systemic atherosclerosis: A bidirectional Mendelian randomization study |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-23T10%3A29%3A16IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Frailty%20and%20risk%20of%20systemic%20atherosclerosis:%20A%20bidirectional%20Mendelian%20randomization%20study&rft.jtitle=PloS%20one&rft.au=Xu,%20Liugang&rft.date=2024-05-23&rft.volume=19&rft.issue=5&rft.spage=e0304300&rft.epage=e0304300&rft.pages=e0304300-e0304300&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0304300&rft_dat=%3Cgale_plos_%3EA795035272%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=3069289915&rft_id=info:pmid/38781179&rft_galeid=A795035272&rft_doaj_id=oai_doaj_org_article_091bd1c2dcbb49058055197b6dda9c0b&rfr_iscdi=true |