Article in Nature genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
27 authors.
Marta Riise MoksnesDepartment of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Osteoporosis Centre, Centre for Bone and Arthritis Research at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. marta.r.moksnes@ntnu.no.ORCID http://orcid.org/0000-0002-2690-5153
Eivind CowardHUNT Center for Molecular and Clinical Epidemiology, Department of Public Health and Nursing, Norwegian University of Science and Technology, Trondheim, Norway.
Maria NethanderDepartment of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Osteoporosis Centre, Centre for Bone and Arthritis Research at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0003-3688-906X
Louise GrahnemoDepartment of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Osteoporosis Centre, Centre for Bone and Arthritis Research at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0001-5276-6612
Anna E TörnqvistDepartment of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Osteoporosis Centre, Centre for Bone and Arthritis Research at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Lei LiDepartment of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Osteoporosis Centre, Centre for Bone and Arthritis Research at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Johan SvenssonDepartment of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Osteoporosis Centre, Centre for Bone and Arthritis Research at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0002-4487-6405
Arnulf LanghammerHUNT Research Centre, Department of Public Health and Nursing, NTNU, Norwegian University of Science and Technology, Levanger, Norway.ORCID http://orcid.org/0000-0001-5296-6673
Guro F GiskeødegårdHUNT Center for Molecular and Clinical Epidemiology, Department of Public Health and Nursing, Norwegian University of Science and Technology, Trondheim, Norway.ORCID http://orcid.org/0000-0003-2157-8824
Ben BrumptonHUNT Center for Molecular and Clinical Epidemiology, Department of Public Health and Nursing, Norwegian University of Science and Technology, Trondheim, Norway.ORCID http://orcid.org/0000-0002-3058-1059
Rebecka HjortHUNT Center for Molecular and Clinical Epidemiology, Department of Public Health and Nursing, Norwegian University of Science and Technology, Trondheim, Norway.
Eivind Ness-JensenHUNT Center for Molecular and Clinical Epidemiology, Department of Public Health and Nursing, Norwegian University of Science and Technology, Trondheim, Norway.ORCID http://orcid.org/0000-0001-6005-0729
Gunnar EngströmDepartment of Clinical Sciences in Malmö, Lund University, Malmö, Sweden.
Thaher PelaseyedDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0002-6434-3913
Kristian Hveem *HUNT Center for Molecular and Clinical Epidemiology, Department of Public Health and Nursing, Norwegian University of Science and Technology, Trondheim, Norway.
Claes Ohlsson *Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Osteoporosis Centre, Centre for Bone and Arthritis Research at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. claes.ohlsson@medic.gu.se.ORCID http://orcid.org/0000-0002-9633-2805
Funding
Hjärt-Lungfonden (Swedish Heart-Lung Foundation) 2019-0505Hjärt-Lungfonden (Swedish Heart-Lung Foundation) 20200173Knut och Alice Wallenbergs Stiftelse (Knut and Alice Wallenberg Foundation) KAW 2015.0317 and KAW 2020.0230Novo Nordisk NNF20OC0063886Novo Nordisk Fonden (Novo Nordisk Foundation) NNF 190C0055250 and 22OC0078421Svenska Sällskapet för Medicinsk Forskning (Swedish Society for Medical Research) S17-0005Vetenskapsrådet (Swedish Research Council) 2018-02784Vetenskapsrådet (Swedish Research Council) 2018-02837Vetenskapsrådet (Swedish Research Council) 2019-01236Vetenskapsrådet (Swedish Research Council) 2019-01471Vetenskapsrådet (Swedish Research Council) 2020-01392 and 2024-02412
6 · The paper itself
Abstract
The gut microbiota is associated with human health and disease. Here we conducted a genome-wide association study of host genetic factors influencing gut microbiota composition in 12,652 individuals from the Trøndelag Health Study (HUNT), with replication in Nordic cohorts (n = 16,017-21,976). We identified 12 reproducible SNP-species associations across six genomic loci, including known (LCT, ABO) and novel (HLA-DQB1, MUC12, SLC37A2, FUT2) regions. Additionally, we detected genetic signals associated with gut microbiota functional modules at three loci (LCT, ABO, FUT2). Follow-up analyses suggest that these host-microbiota associations are linked to the pathogenesis of celiac disease and hemorrhoidal disease. Mendelian randomization analyses provided evidence supporting a causal effect of body mass index on gut microbiota composition. These findings highlight the interplay between host genetics and gut microbiota for human health and disease.
Indexed as
Gastrointestinal MicrobiomeABO Blood-Group SystemBody Mass IndexCeliac DiseaseCohort StudiesFemaleFucosyltransferasesGalactoside 2-alpha-L-fucosyltransferaseGenetic Predisposition to DiseaseGenome-Wide Association StudyHLA-DQ beta-ChainsHumansLactaseMaleMendelian Randomization AnalysisPolymorphism, Single NucleotideABO Blood-Group SystemFucosyltransferasesGalactoside 2-alpha-L-fucosyltransferaseHLA-DQB1 antigenHLA-DQ beta-ChainsLactase
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
The HUNT study identifies host genetic factors reproducibly associated with human gut microbiota composition. · full record | OpenQuestion