| Autor: |
Herfindal AM; Department of Chemistry, Biotechnology and Food Sciences, Norwegian University of Life Sciences, Ås, Norway., van Megen F; KG Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway.; Unit for Clinical Nutrition, Division of Cancer Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.; Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway., Gilde MKO; Department of Chemistry, Biotechnology and Food Sciences, Norwegian University of Life Sciences, Ås, Norway., Valeur J; Unger-Vetlesen Institute, Lovisenberg Diaconal Hospital, Oslo, Norway., Rudi K; Department of Chemistry, Biotechnology and Food Sciences, Norwegian University of Life Sciences, Ås, Norway., Skodje GI; Healthy Life Centre, Municipality of Nes, Nes, Norway., Lundin KEA; KG Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway.; Department of Gastroenterology, Oslo University Hospital Rikshospitalet, Oslo, Norway., Henriksen C; Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway., Bøhn SK; Department of Chemistry, Biotechnology and Food Sciences, Norwegian University of Life Sciences, Ås, Norway. |
| Abstrakt: |
Individuals with coeliac disease (CeD) often experience gastrointestinal symptoms despite adherence to a gluten-free diet (GFD). While we recently showed that a diet low in fermentable oligo-, di-, monosaccharides and polyols (FODMAP) successfully provided symptom relief in GFD-treated CeD patients, there have been concerns that the low FODMAP diet (LFD) could adversely affect the gut microbiota. Our main objective was therefore to investigate whether the LFD affects the faecal microbiota and related variables of gut health. In a randomised controlled trial GFD-treated CeD adults, having persistent gastrointestinal symptoms, were randomised to either consume a combined LFD and GFD ( n 39) for 4 weeks or continue with GFD (controls, n 36). Compared with the control group, the LFD group displayed greater changes in the overall faecal microbiota profile (16S rRNA gene sequencing) from baseline to follow-up (within-subject β -diversity, P < 0·001), characterised by lower and higher follow-up abundances (%) of genus Anaerostipes ( P group < 0·001) and class Erysipelotrichia ( P group = 0·02), respectively. Compared with the control group, the LFD led to lower follow-up concentrations of faecal propionic and valeric acid (GC-FID) in participants with high concentrations at baseline ( P interaction ≤ 0·009). No differences were found in faecal bacterial α -diversity ( P group ≥ 0·20) or in faecal neutrophil gelatinase-associated lipocalin (ELISA), a biomarker of gut integrity and inflammation ( P group = 0·74), between the groups at follow-up. The modest effects of the LFD on the gut microbiota and related variables in the CeD patients of the present study are encouraging given the beneficial effects of the LFD strategy to treat functional GI symptoms (Registered at clinicaltrials.gov as NCT03678935). |
