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Faecal microbiota composition associates with abdominal pain in the general population
  1. Fatemeh Hadizadeh1,2,
  2. Ferdinando Bonfiglio1,3,
  3. Meriem Belheouane4,5,
  4. Marie Vallier4,5,
  5. Sascha Sauer6,
  6. Corinna Bang7,
  7. Luis Bujanda3,8,
  8. Anna Andreasson9,10,
  9. Lars Agreus9,
  10. Lars Engstrand11,12,
  11. Nicholas J Talley9,13,14,15,
  12. Joseph Rafter1,
  13. John F Baines4,5,
  14. Susanna Walter16,
  15. Andre Franke7,
  16. Mauro D’Amato3,17,18
  1. 1 Department of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden
  2. 2 Gastroenterology Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
  3. 3 Department of Gastrointestinal and Liver Diseases, BioDonostia Health Research Institute, San Sebastian, Spain
  4. 4 Institute of Experimental Medicine, Christian-Albrechts-University of Kiel, Kiel, Germany
  5. 5 Evolutionary Genomics, Max Planck Institute for Evolutionary Biology, Plön, Germany
  6. 6 Max Delbrück Center for Molecular Medicine (BIMSB/BIH), Berlin, Germany
  7. 7 Institute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel, Kiel, Germany
  8. 8 Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Universidad del País Vasco UPV/EHU, San Sebastián, Spain
  9. 9 Division of Family Medicine and Primary Care, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden
  10. 10 Stress Research Institute, Stockholm University, Stockholm, Sweden
  11. 11 Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden
  12. 12 Clinical Genomics Facility, Science for Life Laboratory, Solna, Sweden
  13. 13 Faculty of Health and Medicine, University of Newcastle, Newcastle, Australia
  14. 14 Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, USA
  15. 15 Australian GI Research Alliance (AGIRA), Australia
  16. 16 Division of Gastroenterology, Institution of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden
  17. 17 Department of Medicine, Unit of Clinical Epidemiology, Karolinska Institutet, Stockholm, Sweden
  18. 18 IKERBASQUE, Basque Science Foundation, Bilbao, Spain
  1. Correspondence to Professor Mauro D’Amato, Gastrointestinal Genetics Unit, BioDonostia HRI, Paseo Dr Beguiristain s/n, 20014 San Sebastian, Spain; mauro.damato{at}

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We read with great interest the recent communication by Simrén et al,1 reporting a correlation between visceral hypersensitivity and GI symptom severity in functional GI disorders (FGID). Previously, it has been shown that visceral hypersensitivity can be modulated or even induced in animal models, by altering the composition of their gut microbiota with antibiotics or faecal transplantation from IBS donors.2 3 Hence, while a direct link between gut microbiota composition and visceral pain may need to be conclusively established, this holds great potential for translational exploitation in the treatment of IBS and other FGID. Thus far, the potential association between microbiota and abdominal pain in humans has only been investigated in one study that included 15 individuals.4 For this purpose, we studied 159 individuals (average age 59.1, 39.6% men) from the Swedish Population-based Colonoscopy (PopCol) cohort, previously described and with faecal microbiota 16S sequencing data and daily recordings of abdominal pain (number of episodes, duration and intensity) collected over the same period (7.41±7.91 days).5–7 Among these, 52 individuals (assigned to the case group) reported at least one episode …

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