{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,28]],"date-time":"2026-05-28T03:37:37Z","timestamp":1779939457491,"version":"3.53.1"},"reference-count":45,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2023,4,4]],"date-time":"2023-04-04T00:00:00Z","timestamp":1680566400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100014188","name":"Ministry of Science and ICT, South Korea","doi-asserted-by":"publisher","award":["2022R1A2C2009998"],"award-info":[{"award-number":["2022R1A2C2009998"]}],"id":[{"id":"10.13039\/501100014188","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["R01\u2010HL139865"],"award-info":[{"award-number":["R01\u2010HL139865"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["R01\u2010HL155915"],"award-info":[{"award-number":["R01\u2010HL155915"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000057","name":"National Institute of General Medical Sciences","doi-asserted-by":"publisher","award":["R35\u2010GM124836"],"award-info":[{"award-number":["R35\u2010GM124836"]}],"id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Obesity"],"published-print":{"date-parts":[[2023,5]]},"abstract":"Abstract<\/jats:title>\n \n Objective<\/jats:title>\n Although the association between adiposity and gastrointestinal (GI) diseases has been explored, the causal effects of adiposity on GI diseases are largely unknown.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n Mendelian randomization was conducted using single\u2010nucleotide polymorphisms associated with BMI and waist circumference (WC) as instrumental variables, and the causal associations of BMI or WC with GI conditions were estimated among >400,000 UK Biobank participants, >170,000 Finnish\u2010descent participants, and numerous consortia participants of predominantly European ancestry.<\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Genetically predicted BMI was robustly associated with increased risk of nonalcoholic fatty liver disease (NAFLD), cholecystitis, cholelithiasis, and primary biliary cholangitis. For the diseases, the odds ratio per 1\u2010SD increase in genetically predicted BMI (4.77\u2009kg\/m\n 2<\/jats:sup>\n ) ranged from 1.22 (95% CI: 1.12\u20131.34;\n p<\/jats:italic>\n \u2009<\u20090.0001) for NAFLD to 1.65 (95% CI: 1.31\u20132.06;\n p<\/jats:italic>\n \u2009<\u20090.0001) for cholecystitis. Genetically predicted WC was robustly associated with increased risk of NAFLD, alcoholic liver disease, cholecystitis, cholelithiasis, colon cancer, and gastric cancer. Alcoholic liver disease was consistently associated with WC even after adjusting for alcohol consumption in a multivariable Mendelian randomization analysis. The odds ratio per 1\u2010SD increase in genetically predicted WC (12.52\u2009cm) for such associations ranged from 1.41 (95% CI: 1.17\u20131.70;\n p<\/jats:italic>\n \u00a0=\u00a00.0015) for gastric cancer to 1.74 (95% CI: 1.21\u20131.78;\n p<\/jats:italic>\n \u2009<\u20090.0001) for cholelithiasis.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n High genetically predicted adiposity was causally associated with an increased risk of GI abnormalities, particularly of hepatobiliary organs (liver, biliary tract, and gallbladder) that are functionally related to fat metabolism.<\/jats:p>\n \n \n \n image<\/jats:alt-text>\n <\/jats:graphic>\n <\/jats:boxed-text>\n <\/jats:p>\n 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