https://orcid.org/0000-0002-1647-8151
Abstract
Inflammatory bowel diseases (IBD) are chronic and incurable conditions of the gastro-intestinal tract with an increasing incidence and prevalence worldwide. Common symptoms are abdominal pain, diarrhea, and weight loss. Despite recent advances in medical management, many patients fail to achieve clinical remission and healing of the mucosa of the bowel. The cause is thought to involve an inappropriate reaction of the immune system, the microbiome and the environment in genetically susceptible individuals, leading to chronic bowel inflammation. Evidence is emerging that diet is a key environmental factor that might influence disease onset and course, and therefore may become a therapeutic strategy to mitigate inflammation and symptoms. Since IBD is a heterogeneous disease on a clinical and a molecular level, personalizing dietary advice could be the crucial factor to achieve long-lasting changes in dietary behaviors that could not only improve nutritional status but also tackle gut inflammation and abdominal symptoms on an individual level. In this review, we first discuss different aspects of personalized nutrition, namely the level, focus, and scope of personalized dietary regimens. Then, we provide a framework for the different goals of nutritional therapy in IBD and current evidence for personalized dietary approaches. Lastly, we discuss the need for adequate trial designs, access to the right data types and the bioinformatic tools that are necessary to develop algorithms that will allow us to move from general “healthy eating” advice to truly personalized nutritional plans for the individual IBD patient.
Abbreviations
IBD, inflammatory bowel disease; CD, Crohn’s disease; UC, ulcerative colitis; PUFAs, polyunsaturated fatty acids; UPF, ultra-processed food; TNF, tumor necrosis factor; CMC, carboxymethyl cellulose; GLIM, global clinical nutrition community; BMI, body mass index; QoL, quality of life; CDED, Crohn Disease Exclusion Diet; CD-TREAT, Treatment-with-Eating Diet; IBD-AID, Inflammatory Bowel Disease-Anti-Inflammatory Diet; AIP, Autoimmune Protocol Diet; FODMAP, Fermentable Oligo-, Di-, Monosaccharides and Polyols; GPX4, glutathione peroxidase 4; EEN, Exclusive enteral nutrition; PEN, partial enteral nutrition; TMAO, trimethylamine-N-oxide; CVD, cardiovascular disease; MSCD, modified SCD.
Acknowledgments
The ‘building icon’ was designed by Danil Polshin and downloaded from NounProject.com.
Disclosure
Judith Wellens, Eva Vissers, and Christophe Matthys have no conflicts of interest to declare. Séverine Vermeire has received grants from AbbVie, J&J, Pfizer, Takeda and Galapagos; Séverine Vermeire has received consulting and/or speaking fees from AbbVie, AbolerIS Pharma, AgomAb, Alimentiv, Arena Pharmaceuticals, AstraZeneca, Avaxia, BMS, Boehringer Ingelheim, Celgene, CVasThera, Cytoki Pharma, Dr Falk Pharma, Ferring, Galapagos, Genentech-Roche, Gilead, GSK, Hospira, Imidomics, Janssen, J&J, Lilly, Materia Prima, MiroBio, Morphic, MrMHealth, Mundipharma, MSD, Pfizer, Prodigest, Progenity, Prometheus, Robarts Clinical Trials, Second Genome, Shire, Surrozen, Takeda, Theravance, Tillots Pharma AG, and Zealand Pharma. João Sabino has received Research support from Galapagos and Viatris; has received speaker’s fees from AbbVie, Ferring, Falk, Takeda, Janssen, and Fresenius; and has received consultancy fees from AbbVie, Janssen, Fresenius, Pharmacosmos, and Ferring. João Sabino also reports personal fees from Nestle, grants from The Research Foundation – Flanders and Helmsley Charitable Trust Fund, during the conduct of the study. The authors report no other conflicts of interest in this work.