Causal association of plasma n-3 PUFA with peptic ulcer disease: a two-sample Mendelian randomisation study
Dietary n-3 PUFA may have potential benefits in preventing peptic ulcer disease (PUD). However, data from observational epidemiological studies are limited. Thus, we conducted a Mendelian randomisation analysis to reveal the causal impact of n-3 PUFA on PUD. Genetic variants strongly associated with...
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| Veröffentlicht in: | British journal of nutrition 2024-10, Vol.132 (8), p.1014-1021 |
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| creator | Dai, Zebin Wang, Qinjian He, Bingbing Shi, Fang Chen, Wei Jiang, Qingxi Zhou, Dan Xue, Zhanxiong Yang, Bo |
| description | Dietary n-3 PUFA may have potential benefits in preventing peptic ulcer disease (PUD). However, data from observational epidemiological studies are limited. Thus, we conducted a Mendelian randomisation analysis to reveal the causal impact of n-3 PUFA on PUD. Genetic variants strongly associated with plasma levels of total or individual n-3 PUFA including plant-derived α-linolenic acid and marine-derived EPA, DPA and DHA were enrolled as instrumental variables. Effect size estimates of the n-3 PUFA-associated genetic variants with PUD were evaluated using data from the UK biobank. Per one sd increase in the level of total n-3 PUFA in plasma was significantly associated with a lower risk of PUD (OR = 0·91; 95 % CI 0·85, 0·99; P = 0·020). The OR were 0·81 (95 % CI 0·67, 0·97) for EPA, 0·72 (95 % CI 0·58, 0·91) for DPA and 0·87 (95 % CI 0·80, 0·94) for DHA. Genetically predicted α-linolenic acid levels in plasma had no significant association with the risk of PUD (OR = 5·41; 95 % CI 0·70, 41·7). Genetically predicted plasma levels of n-3 PUFA were inversely associated with the risk of PUD, especially marine-based n-3 PUFA. Such findings may have offered an effective and feasible strategy for the primary prevention of PUD. |
| doi_str_mv | 10.1017/S0007114524001752 |
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However, data from observational epidemiological studies are limited. Thus, we conducted a Mendelian randomisation analysis to reveal the causal impact of n-3 PUFA on PUD. Genetic variants strongly associated with plasma levels of total or individual n-3 PUFA including plant-derived α-linolenic acid and marine-derived EPA, DPA and DHA were enrolled as instrumental variables. Effect size estimates of the n-3 PUFA-associated genetic variants with PUD were evaluated using data from the UK biobank. Per one sd increase in the level of total n-3 PUFA in plasma was significantly associated with a lower risk of PUD (OR = 0·91; 95 % CI 0·85, 0·99; P = 0·020). The OR were 0·81 (95 % CI 0·67, 0·97) for EPA, 0·72 (95 % CI 0·58, 0·91) for DPA and 0·87 (95 % CI 0·80, 0·94) for DHA. Genetically predicted α-linolenic acid levels in plasma had no significant association with the risk of PUD (OR = 5·41; 95 % CI 0·70, 41·7). Genetically predicted plasma levels of n-3 PUFA were inversely associated with the risk of PUD, especially marine-based n-3 PUFA. Such findings may have offered an effective and feasible strategy for the primary prevention of PUD.</description><identifier>ISSN: 0007-1145</identifier><identifier>ISSN: 1475-2662</identifier><identifier>EISSN: 1475-2662</identifier><identifier>DOI: 10.1017/S0007114524001752</identifier><identifier>PMID: 39523850</identifier><language>eng</language><publisher>Cambridge, UK: Cambridge University Press</publisher><subject>alpha-Linolenic Acid - blood ; Anti-inflammatory agents ; Biobanks ; Biomarkers ; Confounding (Statistics) ; Diet ; Disease ; Disease prevention ; Eicosapentaenoic Acid - blood ; Epidemiology ; Fatty acids ; Fatty Acids, Omega-3 - blood ; Genetic analysis ; Genetic diversity ; Genetic variance ; Genomes ; Human and Clinical Nutrition ; Humans ; Impact analysis ; Leukocytes ; Linolenic acid ; Mendelian Randomization Analysis ; Observational studies ; Older people ; Peptic Ulcer - blood ; Peptic Ulcer - genetics ; Peptic Ulcer - prevention & control ; Peptic ulcers ; Plants ; Plasma ; Plasma levels ; Polymorphism, Single Nucleotide ; Randomization ; Risk ; Ulcers ; United Kingdom</subject><ispartof>British journal of nutrition, 2024-10, Vol.132 (8), p.1014-1021</ispartof><rights>The Author(s), 2024. 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However, data from observational epidemiological studies are limited. Thus, we conducted a Mendelian randomisation analysis to reveal the causal impact of n-3 PUFA on PUD. Genetic variants strongly associated with plasma levels of total or individual n-3 PUFA including plant-derived α-linolenic acid and marine-derived EPA, DPA and DHA were enrolled as instrumental variables. Effect size estimates of the n-3 PUFA-associated genetic variants with PUD were evaluated using data from the UK biobank. Per one sd increase in the level of total n-3 PUFA in plasma was significantly associated with a lower risk of PUD (OR = 0·91; 95 % CI 0·85, 0·99; P = 0·020). The OR were 0·81 (95 % CI 0·67, 0·97) for EPA, 0·72 (95 % CI 0·58, 0·91) for DPA and 0·87 (95 % CI 0·80, 0·94) for DHA. Genetically predicted α-linolenic acid levels in plasma had no significant association with the risk of PUD (OR = 5·41; 95 % CI 0·70, 41·7). Genetically predicted plasma levels of n-3 PUFA were inversely associated with the risk of PUD, especially marine-based n-3 PUFA. Such findings may have offered an effective and feasible strategy for the primary prevention of PUD.</description><subject>alpha-Linolenic Acid - blood</subject><subject>Anti-inflammatory agents</subject><subject>Biobanks</subject><subject>Biomarkers</subject><subject>Confounding (Statistics)</subject><subject>Diet</subject><subject>Disease</subject><subject>Disease prevention</subject><subject>Eicosapentaenoic Acid - blood</subject><subject>Epidemiology</subject><subject>Fatty acids</subject><subject>Fatty Acids, Omega-3 - blood</subject><subject>Genetic analysis</subject><subject>Genetic diversity</subject><subject>Genetic variance</subject><subject>Genomes</subject><subject>Human and Clinical Nutrition</subject><subject>Humans</subject><subject>Impact analysis</subject><subject>Leukocytes</subject><subject>Linolenic acid</subject><subject>Mendelian Randomization Analysis</subject><subject>Observational studies</subject><subject>Older people</subject><subject>Peptic Ulcer - blood</subject><subject>Peptic Ulcer - genetics</subject><subject>Peptic Ulcer - prevention & control</subject><subject>Peptic ulcers</subject><subject>Plants</subject><subject>Plasma</subject><subject>Plasma levels</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Randomization</subject><subject>Risk</subject><subject>Ulcers</subject><subject>United Kingdom</subject><issn>0007-1145</issn><issn>1475-2662</issn><issn>1475-2662</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kcFO3DAQhq2KqrvQPkAvyBIXLqH2OE5sbmgFBYmqldo9R5PYAUMSBzsR2revV7uAVNSTNZpvPv-aIeQrZ2ec8fLbb8ZYyXkuIWeplvCBLHleygyKAg7IctvOtv0FOYzxIZWKM_2JLISWIJRkS_K4wjliRzFG3zicnB-ob-nYYeyRDpmgv9ZXF_TZTfd0tOPkGjp3jQ3UuGgx2nOKdHr2WcR-7Cz9YQdjO4cDDTgY37u4U8ZpNpvP5GOLXbRf9u8RWV9d_lldZ7c_v9-sLm6zBrSaMiO0AcMKBilkyVkrykJq2wDUtUbUjWYK8lYaNIqVtZS2LRCYahW0UBshjsjpzjsG_zTbOFUpR2O7Dgfr51gJDqrMlch1Qk_-QR_8HIaULlECyrQjYIniO6oJPsZg22oMrsewqTirtpeo3l0izRzvzXPdW_M68bL6BIi9FPs6OHNn3_7-v_Yv2geRUA</recordid><startdate>20241028</startdate><enddate>20241028</enddate><creator>Dai, Zebin</creator><creator>Wang, Qinjian</creator><creator>He, Bingbing</creator><creator>Shi, Fang</creator><creator>Chen, Wei</creator><creator>Jiang, Qingxi</creator><creator>Zhou, Dan</creator><creator>Xue, Zhanxiong</creator><creator>Yang, Bo</creator><general>Cambridge University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><orcidid>https://orcid.org/0009-0004-3645-6824</orcidid></search><sort><creationdate>20241028</creationdate><title>Causal association of plasma n-3 PUFA with peptic ulcer disease: a two-sample Mendelian randomisation study</title><author>Dai, Zebin ; Wang, Qinjian ; He, Bingbing ; Shi, Fang ; Chen, Wei ; Jiang, Qingxi ; Zhou, Dan ; Xue, Zhanxiong ; Yang, Bo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c298t-d39d2d0602523710f37659ec22bb9aa9c90824f5dad807b55ef6a208f82f2bd33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>alpha-Linolenic Acid - blood</topic><topic>Anti-inflammatory agents</topic><topic>Biobanks</topic><topic>Biomarkers</topic><topic>Confounding (Statistics)</topic><topic>Diet</topic><topic>Disease</topic><topic>Disease prevention</topic><topic>Eicosapentaenoic Acid - blood</topic><topic>Epidemiology</topic><topic>Fatty acids</topic><topic>Fatty Acids, Omega-3 - blood</topic><topic>Genetic analysis</topic><topic>Genetic diversity</topic><topic>Genetic variance</topic><topic>Genomes</topic><topic>Human and Clinical Nutrition</topic><topic>Humans</topic><topic>Impact analysis</topic><topic>Leukocytes</topic><topic>Linolenic acid</topic><topic>Mendelian Randomization Analysis</topic><topic>Observational studies</topic><topic>Older people</topic><topic>Peptic Ulcer - blood</topic><topic>Peptic Ulcer - genetics</topic><topic>Peptic Ulcer - prevention & control</topic><topic>Peptic ulcers</topic><topic>Plants</topic><topic>Plasma</topic><topic>Plasma levels</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Randomization</topic><topic>Risk</topic><topic>Ulcers</topic><topic>United Kingdom</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dai, Zebin</creatorcontrib><creatorcontrib>Wang, Qinjian</creatorcontrib><creatorcontrib>He, Bingbing</creatorcontrib><creatorcontrib>Shi, Fang</creatorcontrib><creatorcontrib>Chen, Wei</creatorcontrib><creatorcontrib>Jiang, Qingxi</creatorcontrib><creatorcontrib>Zhou, Dan</creatorcontrib><creatorcontrib>Xue, Zhanxiong</creatorcontrib><creatorcontrib>Yang, Bo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>British journal of nutrition</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dai, Zebin</au><au>Wang, Qinjian</au><au>He, Bingbing</au><au>Shi, Fang</au><au>Chen, Wei</au><au>Jiang, Qingxi</au><au>Zhou, Dan</au><au>Xue, Zhanxiong</au><au>Yang, Bo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Causal association of plasma n-3 PUFA with peptic ulcer disease: a two-sample Mendelian randomisation study</atitle><jtitle>British journal of nutrition</jtitle><addtitle>Br J Nutr</addtitle><date>2024-10-28</date><risdate>2024</risdate><volume>132</volume><issue>8</issue><spage>1014</spage><epage>1021</epage><pages>1014-1021</pages><issn>0007-1145</issn><issn>1475-2662</issn><eissn>1475-2662</eissn><abstract>Dietary n-3 PUFA may have potential benefits in preventing peptic ulcer disease (PUD). However, data from observational epidemiological studies are limited. Thus, we conducted a Mendelian randomisation analysis to reveal the causal impact of n-3 PUFA on PUD. Genetic variants strongly associated with plasma levels of total or individual n-3 PUFA including plant-derived α-linolenic acid and marine-derived EPA, DPA and DHA were enrolled as instrumental variables. Effect size estimates of the n-3 PUFA-associated genetic variants with PUD were evaluated using data from the UK biobank. Per one sd increase in the level of total n-3 PUFA in plasma was significantly associated with a lower risk of PUD (OR = 0·91; 95 % CI 0·85, 0·99; P = 0·020). The OR were 0·81 (95 % CI 0·67, 0·97) for EPA, 0·72 (95 % CI 0·58, 0·91) for DPA and 0·87 (95 % CI 0·80, 0·94) for DHA. Genetically predicted α-linolenic acid levels in plasma had no significant association with the risk of PUD (OR = 5·41; 95 % CI 0·70, 41·7). Genetically predicted plasma levels of n-3 PUFA were inversely associated with the risk of PUD, especially marine-based n-3 PUFA. Such findings may have offered an effective and feasible strategy for the primary prevention of PUD.</abstract><cop>Cambridge, UK</cop><pub>Cambridge University Press</pub><pmid>39523850</pmid><doi>10.1017/S0007114524001752</doi><tpages>8</tpages><orcidid>https://orcid.org/0009-0004-3645-6824</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | alpha-Linolenic Acid - blood Anti-inflammatory agents Biobanks Biomarkers Confounding (Statistics) Diet Disease Disease prevention Eicosapentaenoic Acid - blood Epidemiology Fatty acids Fatty Acids, Omega-3 - blood Genetic analysis Genetic diversity Genetic variance Genomes Human and Clinical Nutrition Humans Impact analysis Leukocytes Linolenic acid Mendelian Randomization Analysis Observational studies Older people Peptic Ulcer - blood Peptic Ulcer - genetics Peptic Ulcer - prevention & control Peptic ulcers Plants Plasma Plasma levels Polymorphism, Single Nucleotide Randomization Risk Ulcers United Kingdom |
| title | Causal association of plasma n-3 PUFA with peptic ulcer disease: a two-sample Mendelian randomisation study |
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