Outcome of a FODMAP restriction diet with subsequent blinded reintroduction in functional dyspepsia/postprandial distress syndrome

Recent studies have shown increased duodenal mucosal permeability as a possible key player in the pathophysiology of functional dyspepsia (FD). Adverse reaction to nutrients is an important candidate underlying mechanism. Intragastric infusion of fermentable oligo-, di-, monosaccharides and polyols (FODMAPs) induced symptoms reminiscent of FD with a rapid onset. We evaluated the effect of a low FODMAP diet (LFD) and individual FODMAP-triggers on symptom severity and duodenal mucosal permeability in FD. Patients with FD followed a 6-week LFD and filled out the validated Leuven Postprandial Distress Syndrome (LPDS) daily diary, Short Form-Nepean Dyspepsia Index (SF-NDI) Questionnaire, patient assessment of upper gastrointestinal symptoms (PAGI-SYM) and Patient Health Questionnaire (PHQ). Patients underwent an endoscopy with duodenal biopsies to define mucosal integrity by quantifying transepithelial electrical resistance (TEER) and dextran flux. LFD was followed by a blinded reintroduction during which patients were challenged by 7 powders (fructans, fructose, galacto-oligosaccharides (GOS), lactose, mannitol, sorbitol, glucose). 36 FD patients entered the study. LPDS improved significantly at the end of the LFD in 73%. In addition, SF-NDI, PAGI-SYM and PHQ improved significantly. Dextran flux and TEER were not significantly different, but delta TEER correlated positively with delta LPDS. A large variety of FODMAP powders was able to induce recurrence with mannitol as the most prevalent triggering FODMAP (23%). Surprisingly, 27% showed higher LPDS scores during intake of glucose. A LFD significantly improved PDS symptoms, but this was not associated with altered mucosal integrity. Powder reintroduction identified a large variety in individual FODMAPs and glucose as triggers.