Evidence map›Paper›PMID 42319657›Full record

ArticleDigestive diseases and sciences2026

Habitual Ultra-processed Food Intake Is Associated with Gut Dysbiosis and Pro-inflammatory Metabolite Profiles in Korean Patients with IBD.

Woo-Jeong Shon, Kyung A Kim, Joo Sung Kim, Byeong Gwan Kim, Jong Pil Im, Hyun Jung Lee, Si Hyun Kim, Ji Won Kim, Hyoun Woo Kang, Kwang Woo Kim and 6 more

Abstract read
In one paragraph

Article in Digestive diseases and sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Frontiers in microbiology · 2026
    Review
4 · The record

Corrections and comments

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

16 authors.

Woo-Jeong Shon *Department of Biopharmaceutical Sciences, Cheongju University, Cheongju, Republic of Korea.
Kyung A Kim *Department of Internal Medicine, Seoul National University College of Medicine, 101 Daehak-Ro, Jongno-Gu, Seoul, 03080, Korea.
Joo Sung KimDepartment of Internal Medicine, Seoul National University College of Medicine, 101 Daehak-Ro, Jongno-Gu, Seoul, 03080, Korea.
Byeong Gwan KimDepartment of Internal Medicine, Seoul National University College of Medicine, 101 Daehak-Ro, Jongno-Gu, Seoul, 03080, Korea.
Jong Pil ImDepartment of Internal Medicine, Seoul National University College of Medicine, 101 Daehak-Ro, Jongno-Gu, Seoul, 03080, Korea.
Hyun Jung LeeDepartment of Internal Medicine, Seoul National University College of Medicine, 101 Daehak-Ro, Jongno-Gu, Seoul, 03080, Korea.
Si Hyun KimDepartment of Internal Medicine and Liver Research Institute, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Republic of Korea.
Ji Won KimDepartment of Internal Medicine, Seoul National University College of Medicine, 101 Daehak-Ro, Jongno-Gu, Seoul, 03080, Korea.
Hyoun Woo KangDivision of Gastroenterology, Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, Seoul National University College of Medicine, Seoul, Republic of Korea.
Kwang Woo KimDivision of Gastroenterology, Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, Seoul National University College of Medicine, Seoul, Republic of Korea.
Jung-Won ChoiDepartment of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, Republic of Korea.
Dae Hee CheonDepartment of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, Republic of Korea.
Donghyun KimDepartment of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, Republic of Korea.
Jaehoon ChoiDepartment of Laboratory Medicine, EONE Laboratories, Incheon, 22014, Republic of Korea.
Eun Soo KimDivision of Gastroenterology and Hepatology, Department of Internal Medicine, School of Medicine, Kyungpook National University, Daegu, Republic of Korea.
Seong-Joon KohDepartment of Internal Medicine, Seoul National University College of Medicine, 101 Daehak-Ro, Jongno-Gu, Seoul, 03080, Korea. jel1206@snu.ac.kr.ORCID https://orcid.org/0000-0001-8001-8777

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsUltra-processed food (UPF) is increasingly consumed worldwide and may influence gut microbial ecology relevant to inflammatory bowel disease (IBD). However, patient-level multi-omics data remains scarce. We investigated whether habitual UPF intake is associated with specific microbiota and metabolite profiles in Korean patients with IBD.

methodsDietary intake was assessed using a validated food frequency questionnaire, and food was categorized by the NOVA system. UPF intake was expressed as percent of energy, and 313 patients were stratified into UPF low (Q1-Q2) and UPF high (Q3-Q4). Fecal samples of 174 patients underwent 16S rRNA sequencing and untargeted metabolomics. Microbiome differences were tested using PERMANOVA for beta-diversity and Mann-Whitney U tests for taxa. Differential metabolites were defined by p < 0.05 and |fold change|≥ 1.5, followed by Reactome enrichment with FDR correction. Correlations among microbiota, metabolites, and UPF subgroups were examined using Spearman tests with Benjamini-Hochberg adjustment. Associations between UPF intake and clinical characteristics were analyzed using Spearman tests, η

resultsMicrobial beta-diversity differed significantly between UPF low and UPF high participants. UPF high participants showed expansion of pro-inflammatory pathobionts (Escherichia-Shigella, Proteus, Parasutterella, Enterococcus, Fusobacterium, and Clostridium innocuum group) and depletion of anti-inflammatory commensals (Faecalibacterium, Butyricicoccus, Lachnospiraceae ND3007 group, and Bifidobacterium). Metabolomic profiling revealed enrichment of inflammatory pathways (phospholipid metabolism, eNOS/NO signaling, mitochondrial β-oxidation, FMO3-mediated TMA to TMAO, tryptophan catabolism) and reduction of anti-inflammatory metabolites (AHR ligands, BAAT-conjugated bile acids). Integrated analyses demonstrated significant correlations between dysbiotic taxa and inflammatory metabolites. Among NOVA-defined UPF subgroups, sugar-sweetened beverages, ready-to-eat dishes, and packaged snacks and confectioneries showed the strongest associations with these adverse signatures. Analysis of clinical characteristics showed trends between total UPF intake and inflammatory markers (WBC, CRP, fecal calprotectin), and association with upper gastrointestinal tract involvement in patients with CD. Subgroup analysis showed that sugar-sweetened beverage intake was significantly associated with CRP elevation and upper gastrointestinal involvement in patients with CD.

conclusionsIn IBD, higher UPF intake, particularly from specific NOVA-defined subgroups, is associated with gut dysbiosis and a pro-inflammatory metabolome, which in turn correlates with unfavorable clinical characteristics. These findings provide patient-based multi-omics evidence and underscore clinically relevant dietary targets for IBD management.

Indexed as

DysbiosisFast FoodsGastrointestinal MicrobiomeInflammatory Bowel DiseasesAdultFecesFemaleHumansMaleMetabolomeMetabolomicsMiddle AgedRepublic of KoreaYoung AdultGut microbiotaInflammatory bowel diseaseMetabolomicsMulti-omicsNOVA classificationUltra-processed foods

Identifiers

PMID42319657
PMCPMC13558304

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Registered trials

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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 Socratic graph.