Williams Turpin1, Mei Dong2, Gila Sasson1, Juan Antonio Raygoza Garay3, Osvaldo Espin-Garcia4, Sun-Ho Lee3, Anna Neustaeter1, Michelle I Smith1, Haim Leibovitzh1, David S Guttman5, Ashleigh Goethel1, Anne M Griffiths6, Hien Q Huynh7, Levinus A Dieleman8, Remo Panaccione9, A Hillary Steinhart10, Mark S Silverberg1, Guy Aumais11, Kevan Jacobson12, David Mack13, Sanjay K Murthy14, John K Marshall15, Charles N Bernstein16, Maria T Abreu17, Paul Moayyedi15, Andrew D Paterson18, Wei Xu4, Kenneth Croitoru19. 1. Zane Cohen Centre for Digestive Diseases, Mount Sinai Hospital, Toronto, Ontario, Canada. 2. Department of Biostatistics, Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada. 3. Zane Cohen Centre for Digestive Diseases, Mount Sinai Hospital, Toronto, Ontario, Canada; Department of Medicine, University of Toronto, Toronto, Ontario, Canada. 4. Division of Biostatistics, Dalla Lana School of Public Health, University of Toronto, and Department of Biostatistics, Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada. 5. Department of Cell & Systems Biology, University of Toronto, Toronto, Ontario, Canada; Centre for the Analysis of Genome Evolution & Function, University of Toronto, Toronto, Ontario, Canada. 6. Division of Gastroenterology, The Hospital for Sick Children, Toronto, Ontario, Canada. 7. Division of Gastroenterology and Nutrition, Department of Pediatrics, University of Alberta, Edmonton, Alberta, Canada. 8. Division of Gastroenterology and the Centre of Excellence for Gastrointestinal Inflammation and Immunity Research (CEGIIR), Department of Medicine, University of Alberta, Edmonton, Alberta, Canada. 9. Inflammatory Bowel Disease Clinic, Division of Gastroenterology and Hepatology, University of Calgary, Calgary, Alberta, Canada. 10. Zane Cohen Centre for Digestive Diseases, Mount Sinai Hospital, Toronto, Ontario, Canada; Division of Biostatistics, Dalla Lana School of Public Health, University of Toronto, and Department of Biostatistics, Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada. 11. Department of Medicine, Hôpital Maisonneuve-Rosemont, Montreal University, Montreal, Quebec, Canada. 12. Canadian Gastro-Intestinal Epidemiology Consortium (CanGIEC); British Columbia Children's Hospital Research Institute, University of British Columbia, Vancouver, British Columbia, Canada. 13. Division of Gastroenterology, Hepatology & Nutrition, Children's Hospital of Eastern Ontario and University of Ottawa, Ottawa, Ontario, Canada. 14. The Ottawa Hospital Inflammatory Bowel Disease Centre, Department of Medicine, University of Ottawa, Ottawa, Ontario, Canada. 15. Department of Medicine, McMaster University, Farncombe Family Digestive Health Research Institute, Hamilton, Ontario, Canada. 16. Inflammatory Bowel Disease Clinical and Research Centre, and Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada. 17. Department of Medicine, Crohn's and Colitis Center, University of Miami Miller School of Medicine, Miami, Florida. 18. Department of Biostatistics, Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada; Genetics and Genome Biology, The Hospital for Sick Children Research Institute, The Hospital for Sick Children, Toronto, Ontario, Canada. 19. Zane Cohen Centre for Digestive Diseases, Mount Sinai Hospital, Toronto, Ontario, Canada. Electronic address: ken.croitoru@sinaihealth.ca.
Abstract
BACKGROUND & AIMS: Case-control studies have shown that patients with Crohn's disease (CD) have a microbial composition different from healthy individuals. Although the causes of CD are unknown, epidemiologic studies suggest that diet is an important contributor to CD risk, potentially via modulation of bacterial composition and gut inflammation. We hypothesized that long-term dietary clusters (DCs) are associated with gut microbiome compositions and gut inflammation. Our objectives were to identify dietary patterns and assess whether they are associated with alterations in specific gut microbial compositions and subclinical levels of gut inflammation in a cohort of healthy first-degree relatives (FDRs) of patients with CD. METHODS: As part of the Genetic, Environmental, Microbial (GEM) Project, we recruited a cohort of 2289 healthy FDRs of patients with CD. Individuals provided stool samples and answered a validated food frequency questionnaire reflecting their habitual diet during the year before sample collection. Unsupervised analysis identified 3 dietary and 3 microbial composition clusters. RESULTS: DC3, resembling the Mediterranean diet, was strongly associated with a defined microbial composition, with an increased abundance of fiber-degrading bacteria, such as Ruminococcus, as well as taxa such as Faecalibacterium. The DC3 diet was also significantly associated with lower levels of subclinical gut inflammation, defined by fecal calprotectin, compared with other dietary patterns. No significant associations were found between individual food items and fecal calprotectin, suggesting that long-term dietary patterns rather than individual food items contribute to subclinical gut inflammation. Additionally, mediation analysis demonstrated that DC3 had a direct effect on subclinical inflammation that was partially mediated by the microbiota. CONCLUSIONS: Overall, these results indicated that Mediterranean-like dietary patterns are associated with microbiome and lower intestinal inflammation. This study will help guide future dietary strategies that affect microbial composition and host gut inflammation to prevent diseases.
BACKGROUND & AIMS: Case-control studies have shown that patients with Crohn's disease (CD) have a microbial composition different from healthy individuals. Although the causes of CD are unknown, epidemiologic studies suggest that diet is an important contributor to CD risk, potentially via modulation of bacterial composition and gut inflammation. We hypothesized that long-term dietary clusters (DCs) are associated with gut microbiome compositions and gut inflammation. Our objectives were to identify dietary patterns and assess whether they are associated with alterations in specific gut microbial compositions and subclinical levels of gut inflammation in a cohort of healthy first-degree relatives (FDRs) of patients with CD. METHODS: As part of the Genetic, Environmental, Microbial (GEM) Project, we recruited a cohort of 2289 healthy FDRs of patients with CD. Individuals provided stool samples and answered a validated food frequency questionnaire reflecting their habitual diet during the year before sample collection. Unsupervised analysis identified 3 dietary and 3 microbial composition clusters. RESULTS: DC3, resembling the Mediterranean diet, was strongly associated with a defined microbial composition, with an increased abundance of fiber-degrading bacteria, such as Ruminococcus, as well as taxa such as Faecalibacterium. The DC3 diet was also significantly associated with lower levels of subclinical gut inflammation, defined by fecal calprotectin, compared with other dietary patterns. No significant associations were found between individual food items and fecal calprotectin, suggesting that long-term dietary patterns rather than individual food items contribute to subclinical gut inflammation. Additionally, mediation analysis demonstrated that DC3 had a direct effect on subclinical inflammation that was partially mediated by the microbiota. CONCLUSIONS: Overall, these results indicated that Mediterranean-like dietary patterns are associated with microbiome and lower intestinal inflammation. This study will help guide future dietary strategies that affect microbial composition and host gut inflammation to prevent diseases.
Authors: María A Núñez-Sánchez; Silvia Melgar; Keith O'Donoghue; María A Martínez-Sánchez; Virgina E Fernández-Ruiz; Mercedes Ferrer-Gómez; Antonio J Ruiz-Alcaraz; Bruno Ramos-Molina Journal: Int J Mol Sci Date: 2022-07-28 Impact factor: 6.208
Authors: L Godny; L Reshef; T Sharar Fischler; S Elial-Fatal; T Pfeffer-Gik; B Raykhel; K Rabinowitz; A Levi-Barda; T T Perets; R Barkan; I Goren; J E Ollech; H Yanai; U Gophna; I Dotan Journal: Gut Microbes Date: 2022 Jan-Dec