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Influence of low FODMAP and gluten-free diets on disease activity and intestinal microbiota in patients with non-coeliac gluten sensitivity.

Dieterich W, Schuppan D, Schink M et al.
Clinical Nutrition. 2018,
https://doi.org/10.1016/j.clnu.2018.03.01
Non-coeliac gluten sensitivity (NCGS) is characterised by gastrointestinal (GI) and extra intestinal (EI) symptoms triggered by ingestion of gluten. Symptoms improve on a gluten-free diet and recur after ingestion of gluten-containing cereals. However, the causative role of gluten is still unclear and there is recognition that non-gluten triggers, for example carbohydrate or amylase trypsin inhibitors (ATIs) may be implicated. A reduced-FODMAP diet has also been shown to partially improve GI symptoms in some individuals with NCGS.
This study looked at the effect of a low FODMAP diet followed by a gluten-free diet (GFD) on the gastrointestinal (GI) and psychological symptoms of NCGS patients, as well as the mucosal inflammation and diet-dependent changes in the microbiota of NCGS patients, compared to healthy controls. Patients were recruited from a specialist hospital outpatient clinic. Exclusion criteria included coeliac disease, other autoimmune conditions, wheat allergy, unclear endoscopic results, doubts over wheat as a trigger, refusal to undergo a wheat challenge or those non-compliant with the diet. In total, 19 patients with NCGS were enrolled in the study. All patients reported experiencing GI symptoms and all but two reported extra intestinal symptoms as well. Eight of the NCGS patients reported intolerance to fructose, lactose or sorbitol. These patients avoided these sugars at baseline but still complained of relevant symptoms which then improved on a gluten (wheat)- free diet and were therefore characterised as NCGS patients. Ten age and sex-matched healthy controls were also included.

Subjects consumed a standard diet with at least two gluten-containing meals per day for at least 4 weeks prior to the start of the study. Dietary advice on a low FODMAP diet and a GFD was provided by a dietitian. A two-week low FODMAP diet was followed by a five-day transition period on a normal, gluten-containing diet, before the subjects went on to a GFD for a period of two weeks. Written information and GF products were provided. The primary outcome measure was improvement of GI symptoms in NCGS under the two diets. Secondary outcome measures included improvement of psychological symptoms, normalisation of intraepithelial lymphocytes (IELs) and goblet cells, and dietary effect on microbiota in NCGS versus healthy controls.

GI and psychological symptoms of all NCGS patients in this study improved after both dietary interventions. Total Global Symptom Relief Scores (GSRS) of NCGS patients improved significantly on a low FODMAP diet, however, the symptom complex notably further improved on a GFD. Abdominal pain, diarrhoea and constipation improved significantly more on a GFD than a low FODMAP diet. A similar scenario was observed for the psychological parameters measured where a significant improvement was observed on a low FODMAP diet and which further improved on a GFD reaching levels comparable to healthy controls.

The NCGS patients were shown to have elevated IELs under the standard, gluten-containing diet, which significantly reduced on a 14-day GFD. This strongly underlines the involvement of the innate immune system in NCGS and points to a nutrient-dependent modification of the immune response in these patients. Histology following the low FODMAP diet was not assessed, however, no prior studies have detected histological changes on a normal versus a low FODMAP diet. A decreased number of mucin-producing Goblet cells was also observed in NCGS patients on a GFD. The increased mucus production under a normal, gluten-containing diet might be an adaptation to microbial dysbalance and/or nutrient stimulation is worthy of further research.

The low FODMAP diet and GFD were found to induce a decrease in Bifidobacteriaceae (Actinobacteria) in both groups although this was only statistically significant in NCGS patients. Interestingly, the effect of diet on the microbial pattern was distinctly more pronounced in the NCGS patients than in the healthy controls. A greater metabolomics variability was noted in NCGS patients suggesting that the microbiota in NCGS patients may be more susceptible to nutrient changes.
In conclusion, this study suggests a multifactorial aetiology for NCGS with functional effects caused by FODMAPs and a mild gluten-triggered immune reaction along with a microbial dysbalance.
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