Ceballos D, Hernández-Camba A, Ramos L. Diet and microbiome in the beginning of the sequence of gut inflammation. World J Clin Cases 2021; 9(36): 11122-11147 [PMID: 35071544 DOI: 10.12998/wjcc.v9.i36.11122]
Corresponding Author of This Article
Daniel Ceballos, MD, PhD, Assistant Professor, Chief Physician, Department of Gastroenterology, Hospital Universitario de Gran Canaria Doctor Negrin, Barranco de La Ballena s/n - 35019, Las Palmas 35019, Canarias, Spain. dcebsan@gobiernodecanarias.org
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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: http://creativecommons.org/licenses/by-nc/4.0/
World J Clin Cases. Dec 26, 2021; 9(36): 11122-11147 Published online Dec 26, 2021. doi: 10.12998/wjcc.v9.i36.11122
Diet and microbiome in the beginning of the sequence of gut inflammation
Daniel Ceballos, A Hernández-Camba, Laura Ramos
Daniel Ceballos, Department of Gastroenterology, Hospital Universitario de Gran Canaria Doctor Negrin, Las Palmas 35019, Canarias, Spain
A Hernández-Camba, Department of Gastroenterology, Hospital Universitario Nuestra Señora de La Candelaria, Santa Cruz de Tenerife 38010, Canarias, Spain
Laura Ramos, Department of Gastroenterology, Hospital Universitario de Canarias, San Cristóbal de La Laguna 38320, Canarias, Spain
Author contributions: All authors wrote, reviewed the manuscript for important intellectual content, agree to the version published, and declare not having any conflict of interest in this manuscript.
Conflict-of-interest statement: The authors declare no conflicts of interests.
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: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Daniel Ceballos, MD, PhD, Assistant Professor, Chief Physician, Department of Gastroenterology, Hospital Universitario de Gran Canaria Doctor Negrin, Barranco de La Ballena s/n - 35019, Las Palmas 35019, Canarias, Spain. dcebsan@gobiernodecanarias.org
Received: April 18, 2021 Peer-review started: April 18, 2021 First decision: July 27, 2021 Revised: August 26, 2021 Accepted: November 18, 2021 Article in press: November 18, 2021 Published online: December 26, 2021 Processing time: 248 Days and 19.5 Hours
Abstract
Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the gastrointestinal tract due, at least partially, to an aberrant and excessive mucosal immune response to gut bacteria in genetically-predisposed individuals under certain environmental factors. The incidence of IBD is rising in western and newly industrialized countries, paralleling the increase of westernized dietary patterns, through new antigens, epithelial function and permeability, epigenetic mechanisms (e.g., DNA methylation), and alteration of the gut microbiome. Alteration in the composition and functionality of the gut microbiome (including bacteria, viruses and fungi) seems to be a nuclear pathogenic factor. The microbiome itself is dynamic, and the changes in food quality, dietary habits, living conditions and hygiene of these western societies, could interact in a complex manner as modulators of dysbiosis, thereby influencing the activation of immune cells’ promoting inflammation. The microbiome produces diverse small molecules via several metabolic ways, with the fiber-derived short-chain fatty acids (i.e., butyrate) as main elements and having anti-inflammatory effects. These metabolites and some micronutrients of the diet (i.e., vitamins, folic acid, beta carotene and trace elements) are regulators of innate and adaptive intestinal immune homeostasis. An excessive and unhealthy consumption of sugar, animal fat and a low-vegetable and -fiber diet are risk factors for IBD appearance. Furthermore, metabolism of nutrients in intestinal epithelium and in gut microbiota is altered by inflammation, changing the demand for nutrients needed for homeostasis. This role of food and a reduced gut microbial diversity in causing IBD might also have a prophylactic or therapeutic role for IBD. The relationship between dietary intake, symptoms, and bowel inflammation could lead to dietary and lifestyle recommendations, including diets with abundant fruits, vegetables, olive oil and oily fish, which have anti-inflammatory effects and could prevent dysbiosis and IBD. Dietary modulation and appropriate exclusion diets might be a new complementary management for treatment at disease flares and in refractory patients, even reducing complications, hospitalizations and surgery, through modifying the luminal intestinal environment.
Core Tip: Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the gastrointestinal tract. The incidence of IBD is rising in western and newly industrialized countries, paralleling the increase of westernized dietary patterns. Microbiome is changing in western societies and can influence the activation of immune cells promoting inflammation. Change in the composition and functionality of the gut microbiome seems to be a nuclear pathogenic factor. An excessive and unhealthy consumption of sugar, animal fat and a low vegetables and fiber diet are risk factor for IBD appearance. This role of food and a reduced gut microbial diversity in cause of IBD might have also a prophylactic or therapeutic role for IBD. Dietary modulation and appropriate exclusion diets might be a new complementary management for treatment at disease flares and in refractory patients.