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Nutrients
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Food Intake and Inflammatory Bowel Disease
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Food Intake and Inflammatory Bowel Disease

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Clinical Nutrition".

Deadline for manuscript submissions: 5 September 2026 | Viewed by 7408

Special Issue Editor

Dr. Won Moon

E-Mail Website
Guest Editor
Department of Internal Medicine, Kosin University College of Medicine, Busan 49267, Republic of Korea
Interests: Crohn's disease; ulcerative colotis; gastrointestinal disease

Special Issue Information

Dear Colleagues,

Inflammatory Bowel Disease (IBD), encompassing Crohn’s disease and ulcerative colitis, is a chronic condition characterized by persistent inflammation of the gastrointestinal tract. Its prevalence has been rising globally, with dietary factors playing a significant role in its pathogenesis and progression.

Dietary patterns, including high-fat, low-fiber, and processed food intake, have been associated with an increased risk of developing IBD. Conversely, diets rich in fiber, fruits, and vegetables may offer protective effects. Additionally, emerging research suggests that specific dietary interventions, such as elimination diets, may influence disease activity and patient outcomes.

This Special Issue aims to explore the intricate relationship between food intake and IBD, highlighting how dietary components affect disease mechanisms, gut microbiota, and clinical outcomes. By compiling diverse research perspectives, we seek to provide comprehensive insights into dietary strategies for IBD management and prevention.

Dr. Won Moon
Guest Editor

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Keywords

  • inflammatory bowel disease (IBD)
  • Crohn’s disease
  • ulcerative colitis
  • nutritional management
  • dietary fiber
  • high-fat diet
  • processed foods
  • saturated fats
  • dietary patterns
  • elimination diets
  • gut microbiota
  • immunomodulation
  • inflammatory response
  • disease relapse prevention
  • clinical outcomes
  • nutritional interventions
  • epidemiological studies
  • dietary guidelines

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Published Papers (5 papers)

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Research

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25 pages, 7141 KB  
Article
Preventive Effect of Chenopodium formosanum Koidz. on Dextran Sulfate Sodium-Induced Chronic Colitis in Mice
by Hsing-Jung Yeh, Hung-Ming Chao, Chun-Chao Chang, Wei-Yu Kao, Suh-Ching Yang, Jane C.-J. Chao and Chun-Kuang Shih
Nutrients 2026, 18(6), 959; https://doi.org/10.3390/nu18060959 - 18 Mar 2026
Viewed by 352
Abstract
Background: Chenopodium formosanum Koidz. (djulis) is an indigenous cereal crop native to Taiwan, and its effects on patients with inflammatory bowel disease (IBD) warrant exploration. The present study investigated whether the consumption of djulis can alleviate chronic colitis induced by dextran sulfate [...] Read more.
Background: Chenopodium formosanum Koidz. (djulis) is an indigenous cereal crop native to Taiwan, and its effects on patients with inflammatory bowel disease (IBD) warrant exploration. The present study investigated whether the consumption of djulis can alleviate chronic colitis induced by dextran sulfate sodium (DSS) in mice. Methods: Forty mice were randomly divided into five groups: blank group (B), control group (C), low-dose group (L), medium-dose group (M), and high-dose group (H). Body weight and disease activity index (DAI) were recorded throughout this study. Groups C, L, M, and H were administered 2% DSS water on days 1–5 and 10–15 to induce chronic colitis. Groups L, M, and H were administered 5%, 10%, and 15% djulis, respectively. Serum and colon samples were collected for further analysis. Results: The DAI scores of groups L, M, and H were significantly lower than those of group C (p < 0.05), and the DAI scores of group H on day 18 were significantly lower than those of group L (p < 0.05). Colon length analysis revealed that DSS intervention significantly shortened colon length in group C (p < 0.05), whereas mice consuming djulis (groups L, M, and H) exhibited a restoration of colon length, with the effect being most pronounced in group H. DSS significantly increased the secretion of certain pro-inflammatory cytokines in the serum, such as interleukin (IL)-1β (p < 0.05), and the expression of some pro-inflammatory proteins in the colon, such as the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) (p < 0.05); however, djulis reversed these effects (especially in group H). In addition, mice in group H exhibited beneficial gut microbiota. Conclusions: Djulis alleviated chronic colitis in mice by reducing inflammation and modulating the gut microbiota. Further research is required to confirm these potential benefits in humans and elucidate the mechanisms involved. Full article
(This article belongs to the Special Issue Food Intake and Inflammatory Bowel Disease)
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21 pages, 6800 KB  
Article
Short Chain Fatty Acids Lower Inflammation and Restore Intestinal Integrity and Function Markers in Mycobacterium paratuberculosis—Infection In Vitro Model
by Piotr P. Lagod, Ahmad Qasem and Saleh A. Naser
Nutrients 2025, 17(23), 3663; https://doi.org/10.3390/nu17233663 - 23 Nov 2025
Viewed by 1031
Abstract
Background: Infection with Mycobacterium avium paratuberculosis (MAP) is closely associated with Crohn’s disease (CD) development, where excessive inflammation and marked intestinal damage are observed. Objectives: In this study, the role of short chain fatty acids, including propionic acid (PPA) and butyric acid [...] Read more.
Background: Infection with Mycobacterium avium paratuberculosis (MAP) is closely associated with Crohn’s disease (CD) development, where excessive inflammation and marked intestinal damage are observed. Objectives: In this study, the role of short chain fatty acids, including propionic acid (PPA) and butyric acid (BA), was evaluated in an in vitro model, mimicking CD characteristics. Methods: MAP-infected THP-1 macrophages were treated with 1 mM and 10 mM of PPA or BA, and the conditioned media was co-cultured in Caco-2 cells. Results: Both PPA and BA caused an M2 shift with significant downregulation (p-value < 0.0001) in pro-inflammatory markers at both the RNA and protein levels. The downregulation is most likely due to the antimicrobial properties of PPA and BA. MAP growth was inhibited by several folds in MGIT (Mycobacteria Growth Indicator Tube) culture media supplemented with PPA or BA. Dysfunctional Caco-2 intestinal epithelial cells’ integrity and function, due to MAP infection, were restored with PPA and BA treatment. Specifically, NOX1 expression was significantly decreased in 10 mM of PPA or BA-treated cells (p < 0.001), as validated by RT-PCR and microscopy. PPA and BA restored tight junction integrity by decreasing Claudin-2 expression in the MAP group. Conclusions: The data clearly demonstrated that short chain fatty acids contain anti-inflammatory and antimicrobial properties with downstream beneficial effects on damaged intestinal epithelial cells, suggesting potential benefits as a dietary supplement for CD patients, particularly those who are not pregnant, due to a possible increased risk of autism spectrum disorder (ASD) development in offspring associated with propionic acid exposure. Full article
(This article belongs to the Special Issue Food Intake and Inflammatory Bowel Disease)
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12 pages, 785 KB  
Article
Ultra-Processed Food Intake in Children with Inflammatory Bowel Disease: A Pilot Case–Control Study
by Emese Kasznár, Dorina Bajzát, Anna Karoliny, Judit Szentannay, András Szabó, Eszter Gombos, Vivien Regián, Anikó Havasi, Erzsébet Pálfi and Katalin Eszter Müller
Nutrients 2025, 17(22), 3532; https://doi.org/10.3390/nu17223532 - 12 Nov 2025
Cited by 1 | Viewed by 1055
Abstract
Background: The consumption of ultra-processed foods (UPFs) has increased globally, particularly in developed countries. UPFs are energy-dense and nutrient-poor, and they often contain additives that can disrupt gut flora and increase intestinal permeability. There is evidence to suggest that processed foods may [...] Read more.
Background: The consumption of ultra-processed foods (UPFs) has increased globally, particularly in developed countries. UPFs are energy-dense and nutrient-poor, and they often contain additives that can disrupt gut flora and increase intestinal permeability. There is evidence to suggest that processed foods may contribute to the onset of IBD and also impact its progression and response to treatment. This study investigated whether children with IBD consume more UPFs than healthy controls and examined the association between UPF intake and disease activity. Methods: This pilot cross-sectional case–control study recruited children with IBD from the Gastroenterology Outpatient Clinic at the Heim Pál National Pediatric Institute in Budapest, Hungary, between December 2023 and February 2025. Age- and sex-matched healthy controls (HCs) were also enrolled. Dietary intake was assessed using two days of 24 h recalls. UPF intake was categorized using the NOVA system and expressed as a percentage of total daily energy intake. Results: A total of 47 children with IBD were matched with HCs. There was no difference in total energy intake between the two groups. Children with UC had a significantly higher intake of UPFs than HCs (MD: 10.5%, p = 0.02), whereas no difference was observed in children with CD after excluding oral nutritional support. No difference in UPF intake was observed between children with active or inactive disease. However, children receiving biological therapy consumed significantly fewer UPFs than those receiving other treatments (MD: 8%, p = 0.04). Conclusions: Children with IBD consume more UPFs compared to HC. The UPF intake of children with CD was not lower than healthy children despite the recommended Crohn’s Disease Exclusion Diet (CDED). Full article
(This article belongs to the Special Issue Food Intake and Inflammatory Bowel Disease)
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Review

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17 pages, 799 KB  
Review
Ultra-Processed Foods and Inflammatory Bowel Disease: A Narrative Review of Epidemiology, Mechanisms, and Dietary Implications
by So Yoon Choi and Won Moon
Nutrients 2025, 17(24), 3852; https://doi.org/10.3390/nu17243852 - 10 Dec 2025
Cited by 1 | Viewed by 4001
Abstract
Ultra-processed foods (UPFs), industrial formulations rich in refined substrates and additives, have been increasingly examined as plausible contributors to gut dysbiosis and mucosal inflammation relevant to inflammatory bowel disease (IBD). This narrative review synthesizes epidemiological, mechanistic, and interventional evidence on UPF intake and [...] Read more.
Ultra-processed foods (UPFs), industrial formulations rich in refined substrates and additives, have been increasingly examined as plausible contributors to gut dysbiosis and mucosal inflammation relevant to inflammatory bowel disease (IBD). This narrative review synthesizes epidemiological, mechanistic, and interventional evidence on UPF intake and IBD based on a structured literature search from 2010 to 2025. Large-scale prospective cohorts consistently associate higher UPF intake with increased risk of Crohn’s disease (CD), whereas findings for ulcerative colitis (UC) remain weaker or inconsistent. Among individuals with established IBD, observational data suggest that greater UPF consumption correlates with higher disease activity and relapse, although potential confounding and reverse causation must be considered. Preclinical studies demonstrate that specific UPF constituents—including emulsifiers, carrageenan, maltodextrin, microparticles, and excess dietary salt—can disrupt epithelial barrier integrity, alter the gut microbiota, and activate immune pathways, providing biological plausibility while underscoring translational gaps. Interventional evidence, particularly for exclusive enteral nutrition and the Crohn’s Disease Exclusion Diet, suggests clinical benefit from reducing UPFs or selected additives, mainly in CD, though data in adults and UC remain limited. Overall, current evidence indicates that dietary strategies to limit UPF exposure may represent a promising and modifiable component of IBD management. Future research should prioritize standardized exposure assessment, mechanism-based human trials, and personalized nutrition approaches to refine clinical applicability. Full article
(This article belongs to the Special Issue Food Intake and Inflammatory Bowel Disease)
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Other

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14 pages, 3771 KB  
Brief Report
PPAR-γ Activation Alleviates Intestinal Dysfunction and Lactose Malabsorption in Experimental Food Allergy Rats
by Yuyang Hao, Lu Yao, Yuxin Jin, Sheng Yin, Zhiwei He and Huilian Che
Nutrients 2026, 18(4), 653; https://doi.org/10.3390/nu18040653 - 16 Feb 2026
Viewed by 542
Abstract
Background/Objectives: Food allergy-induced intestinal inflammation can impair lactose digestion and absorption by damaging the epithelium, leading to secondary lactase deficiency with no effective treatments. The immunometabolism nuclear receptor PPAR-γ regulates gut epithelial function and nutrient absorption. This study aimed to determine whether PPAR-γ [...] Read more.
Background/Objectives: Food allergy-induced intestinal inflammation can impair lactose digestion and absorption by damaging the epithelium, leading to secondary lactase deficiency with no effective treatments. The immunometabolism nuclear receptor PPAR-γ regulates gut epithelial function and nutrient absorption. This study aimed to determine whether PPAR-γ activation can preserve lactose digestion and absorption during allergic inflammation and to elucidate the underlying mechanisms. Methods: In an ovalbumin-sensitized Brown Norway rat model of food allergy, animals were treated with either the PPAR-γ agonist rosiglitazone or the antagonist GW9662. Lactose absorption was assessed by in vivo lactose tolerance tests (blood glucose monitoring) and intestinal transit measurements. Jejunal tissues were analyzed for lactase gene expression, lactase enzyme activity, and SGLT1/GLUT2 transporter levels. Results: Allergic rats exhibited reduced weight gain, delayed intestinal transit, and lactose malabsorption (lower blood glucose after lactose challenge), accompanied by sharply decreased jejunal lactase mRNA, enzyme activity, and SGLT1/GLUT2 levels. Rosiglitazone treatment restored intestinal PPAR-γ expression and markedly improved lactose absorption, normalizing the lactose tolerance curve. Rosiglitazone also increased lactase gene expression and enzyme activity, and upregulated SGLT1 levels. In contrast, PPAR-γ inhibition with GW9662 further reduced lactase and transporter levels and failed to improve absorption. Conclusions: PPAR-γ signaling maintains intestinal lactose digestive capacity of rats during allergic inflammation by sustaining lactase production and monosaccharide transporter expression. Our findings verify an immunometabolism mechanism linking nuclear receptor activation to enhanced nutrient absorption and highlight PPAR-γ agonism as a promising therapeutic strategy to alleviate food allergy-associated lactose malabsorption. Full article
(This article belongs to the Special Issue Food Intake and Inflammatory Bowel Disease)
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