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World J Gastroenterol. Nov 7, 2023; 29(41): 5618-5629
Published online Nov 7, 2023. doi: 10.3748/wjg.v29.i41.5618
Diet as an epigenetic factor in inflammatory bowel disease
Karina Marangoni, Gilson Dorneles, Daniella Miranda da Silva, Letícia Pereira Pinto, Carina Rossoni, Sabrina Alves Fernandes
Karina Marangoni, Egas Moniz School of Health and Science, Caparica - Almada, Portugal, Caparica 2820-062, Portugal
Karina Marangoni, National Institute of Sciences and Technology - Theranostics and Nanobiotechnology, Federal University of Uberlandia - MG, Brazil, Uberlândia 38400-902, Brazil
Gilson Dorneles, Corporate Social Responsibility, Hospital Moinhos de Vento, Porto Alegre 90035-004, Brazil
Daniella Miranda da Silva, Postgraduate Program in Gastroenterology, Universidade Federal do Rio Grande do Sul, Porto Alegre 91540-000, Brazil
Daniella Miranda da Silva, Department of Nutrition, Uniasselvi - Group Vitru, Santa Catarina 89082-262, Brazil
Letícia Pereira Pinto, Sabrina Alves Fernandes, Postgraduate Program in Hepatology, Universidade Federal de Ciências da Saúde de Porto Alegre, Porto Alegre 90050-170, Brazil
Carina Rossoni, Faculty of Medicine, Institute of Environmental Health, University of Lisbon, Lisboa 1649-026, Portugal
Carina Rossoni, Master in Physical Activity and Health, Polytechnic Institute of Beja, Beja 7800-000, Portugal
Carina Rossoni, Degree in Nutrition Sciences, Lusófona University, Lisboa 1749-024, Portugal
Author contributions: All authors contributed to the literature review and writing of the article; Fernandes SA conceived the research project and critically reviewed the manuscript; and all authors read and approved the final manuscript.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Sabrina Alves Fernandes, PhD, Associate Research Scientist, Postdoc, Research Scientist, Researcher, Senior Researcher, Postgraduate Program in Hepatology, Universidade Federal de Ciências da Saúde de Porto Alegre, Sarmento Leite 245, Porto Alegre 90050-170, Brazil. sabrinaafernandes@gmail.com
Received: July 29, 2023
Peer-review started: July 29, 2023
First decision: September 11, 2023
Revised: September 24, 2023
Accepted: October 25, 2023
Article in press: October 25, 2023
Published online: November 7, 2023
Processing time: 101 Days and 5 Hours
Abstract

Inflammatory bowel disease (IBD) has as a main characteristic the exacerbation of the immune system against enterocytes, compromising the individual’s intestinal microbiota. This inflammatory cascade causes several nutritional deficiencies, which further compromise immunological functioning and, as a result, worsen the prognosis. This vicious cycle can be interrupted as the patient’s dietary pattern meets their needs according to their clinical condition, acting directly on the inflammatory process of IBD through the interaction of food, intestinal microbiota, and epigenome. Specific nutritional intervention for IBD has a crucial role in preventing and managing disease activity. This review addresses epigenetic modifications through dietary compounds as a mechanism for modulating the intestinal microbiota of patients with IBD.

Keywords: Inflammatory bowel disease; Epigenetics; Nutrition; Nutrigenetics

Core Tip: Inflammatory bowel disease is an autoimmune disease that oscillates between phases of active disease and remission. In any of these situations there are epigenetic mechanisms involved, which are modified by lifestyle, with diet being one of the factors of epigenetic modulation.