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Exclusive Enteral Nutrition (EEN) is a primary and effective treatment for children with Crohn's disease. It creates varying microbiome profiles and helps induce remission in these patients. Medium-chain fatty acids are part of EEN. They include lauric acid, decanoic acid, and octanoic acid. These acids lead to protective microbiota changes in Crohn's disease patients. Lachnospiraceae are protective. They increase significantly with medium-chain fatty acids and triglycerides. Microbial species, strains, and functions change a lot after stopping EEN.
Following Exclusive Enteral Nutrition (EEN) treatment, 8 out of 11 patients showed a >50% reduction in fecal calprotectin (FC). They were labeled FC responders. Tumor Necrosis Factor alfa (TNF-alfa) production from their blood cells decreased during EEN (P = .008). It reached levels similar to healthy controls. Fecal concentrations of acetate, butyrate, propionate, choline, and uracil decreased significantly in FC responders. Meanwhile, p-cresol increased significantly. At EEN completion, TNFα production correlated positively with butyrate (rho = 0.70; P = .016). EEN treatment influenced microbiota structure (beta diversity). A total of 28 microbial taxa changed significantly in FC responders. At EEN completion, TNFα production correlated positively with fiber fermenters from Lachnospiraceae_UCG-004 and Faecalibacterium prausnitzii. It correlated negatively with Hungatella and Eisenbergiella tayi.
Exclusive Enteral Nutrition (EEN) is the first choice for children and adolescents with active luminal Crohn’s Disease (CD) to induce remission and promote mucosal healing, according to the current guidelines of European specialist societies (ECCO/ESPGHAN)
Rheenen et al. 2021 doi:10.1093/ecco-jcc/jjaa161 Advance Access publication October 7, 2020 ECCO Guideline/Consensus Paper
Although EEN is extremely effective in promoting disease remission, several patients’ related factors may adversely impact EEN adherence and response. Personalized treatments should be proposed that weigh benefits and risks based on the patient’s disease location, phenotype, and disease activity and aim to promote a rapid control of inflammation to reduce long-term bowel damage
The databases PUBMED (MEDLINE), SCOPUS, and WEB OF SCIENCE showed 232 studies with patients with Crohn’s Disease (CD), from which 9 met inclusion criteria. The combined analyzed population consists of 118 patients with Crohn’s Disease (CD) and treated with Exclusive Enteral Nutrition (EEN) with a time of intervention of 2–12 weeks. Studies were conducted in children, except for one study. All applied feeding formulas had similar energy values and composition. In all studies, Exclusive Enteral Nutrition (EEN) treatment decreases inflammatory markers (i.e., high sensitivity C-reactive protein (hs-CRP), and Fecal calprotectin (FCal)). A change in the abundance of numerous bacterial families (Clostridiaceae, Eubacteriaceae, Bacteroidaceae) was noticed, especially in Bacteroidaceae, measured by 16S rRNA gene sequencing of fecal samples. An increase in families connected to the more severe clinical course (Fusobacteria, Prevotella, Lachnospiraceae) was observed in only 2.5% of Crohn’s Disease (CD) patients. Our analyses suggest Exclusive Enteral Nutrition (EEN) has a beneficial influence on the gut microbiome in patients with Crohn’s Disease (CD), which is interrelated with clinical patient improvement and time of disease remission
After 6–8 weeks of EEN, reintroducing a regular diet often leads to a recurrence of inflammation and disease activity.
Exclusive Enteral Nutrition (EEN) influences gut microbiota composition, but high relapse rates post-EEN suggest a Crohn's Disease (CD)-conditioned microbiome can re-establish after treatment.
Crohn's disease (CD) is linked to reduced bacterial diversity and disrupted microbiome-host metabolic circuits.
Exclusive Enteral Nutrition (EEN) shows protective effects in colitis models. Human studies indicate incomplete microbiome recovery post-antibiotics. Functional evidence for EEN-induced microbiome changes is still insufficient as a therapeutic mechanism.
see also:
Crohn’s disease (CD) & Fecal calprotectin (FCal)
Dysbiosis & Inflammatory Bowel Disease (IBD)
Emulsifiers / Emulsion & Inflammatory Bowel Disease (IBD)
Exclusive Enteral Nutrition (EEN) & Inflammatory Bowel Disease (IBD)
Gut microbiota & Inflammatory Bowel Disease (IBD)
Modulen IBD & Crohn’s Disease (CD)
Nutritonal Therapy & Crohn’s disease (CD)
Pediatric Inflammatory Bowel Disease (IBD)
Pediatric Inflammatory Bowel Disease (IBD) & Drugs/Treatments