Short Oral Presentation Nutrition Society of Australia 50th Annual Scientific Meeting 2026

The effects of low FODMAP on the vaginal and gut microbiota in women with endometriosis may help stratify dietary response (146963)

Yenkai Lim 1 , Rebecca Burgell 2 , Yuet Sang Jimmy Lee 2 , Dakota Rhys-Jones 2 , Roni Ratner 3 , Daniel So 2 , Peter Gibson 2 , Jane Varney 2 , Jane Muir 2 , Mark Morrison 1 4 5
  1. Frazer Institute, Faculty of Health, Medicine, and Behavioural Sciences, University of Queensland, Brisbane, QLD, Australia
  2. Department of Gastroenterology, Monash University, Melbourne, Australia
  3. Department of Obstetrics and Gynaecology, Monash University, Melbourne, Australia
  4. Department of Medicine, University of Melbourne, Melbourne, Australia
  5. Department of Gastroenterology and Hepatology, Princess Alexandra Hospital, Brisbane, Australia

Endometriosis affects around 10% of women globally (1) and painful gastrointestinal (GI) symptoms occur in up to 90% of cases, irrespective of bowel infiltration of the disease (2).  A recent randomised, controlled crossover feeding trial (EndoFOD) showed that GI symptom response rate was 60% on a low fermentable oligo-, di-, monosaccharides and polyols (FODMAP) diet compared to only 26% on the control diet (3). However, mechanisms driving GI symptom response remain unclear. Our study aims to determine microbiomal predictors of GI symptom response in the EndoFOD study via faecal and vaginal swabs. Women with endometriosis and poorly controlled GI symptoms completed a 7-day baseline (habitual diet) before randomisation to a 28-day low FODMAP or control diet, both modelled on the Australian Dietary Guidelines. Participants then washout for ≥28‐days, before crossover to the alternate dietary intervention. Response was defined as a >20 mm reduction in VAS‐IBS from baseline to the end of intervention, or a VAS‐IBS<30 mm if the baseline score was ≤50 mm. Stool and vaginal microbiota samples were collected using DNA Genotek collection kits on the final day of baseline and each dietary intervention. Microbial DNA was extracted from samples and subjected to 16S rRNA gene amplicon profiling (vaginal) or metagenomic sequencing (stool). Data were processed using standard quality control and taxonomy annotation (16S:QIIME2;MGS:MetaPhlAn4), with bioinformatic analysis performed using RStudio. Compared to baseline, Shannon diversity metrics of stool microbiota were not affected by either dietary intervention. However, at baseline, responders to the low FODMAP diet exhibited greater relative abundance of the genus Akkermansia than non-responders (p=0.009, q=0.25). Post diet, the low FODMAP responders showed a significant reduction in the relative abundances of Anaerostipes (p=0.002, q=0.04) as well as reductions relative abundances of Blautia (p=0.03, q=0.34), Roseburia (p=0.04, q=0.34) and Ruminococcus (p=0.04, q=0.34) compared to the non-responders. For vaginal microbiota, Shannon diversity was reduced relative to baseline only in those women with a positive response to the low FODMAP diet (p=0.002). Data integration of vaginal and stool microbiomes for all women after the low FODMAP diet was performed using “DIABLO” (4). There appears to be a strong positive correlation between the relative abundances of stool Anaerostipes and vaginal Murdochiella, and with Anaerostipes forming an additional network comprised vaginal Atopobium, Clostridia_UCG, Sutterella, and Ureaplasma; and with Murdochiella forming a network with stool Blautia, Ruminococcus, Roseburia and Bifidobacterium. These preliminary analyses suggest there are both pre-diet and post-diet stool biomarkers in women with endometriosis for the positive response in GI symptoms to a low FODMAP diet. Our preliminary results also suggest the taxonomic features of the vaginal microbiome can be linked with these coordinate changes in the stool microbiome, and thereby vaginal microbiome dynamics and composition can also be affected by diet.

  1. DeCorte P et al. (2025) BJOG, 132(2):118-30
  2. Maroun P et al. (2009) Aust NZJ Obstet Gynaecol, 49(4):411-4
  3. Varney JE et al. (2025) Aliment Pharmacol Ther, 61(12):1889-903
  4. Singh A et al. (2019) Bioinformatics, 35(17):3055-62