Publications // 2026

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Bernstein CN, Nugent Z, Panaccione R, Marshall DA, Kaplan GG, Vanner S, Dieleman LA, Graff LA, Otley A, Jones J, Buresi M, Murthy S, Bargaonkar M, Bressler B, Bitton A, Croitoru KC, Sidani S, Fernandes A, Moayyedi P. Patient reported symptoms are independent of extent of disease in longstanding ulcerative colitis: MAGIC in IMAGINE. Journal of Clinical Gastroenterology 2026; in press.

 

Background: The Inflammation, Microbiome, and Alimentation: Gastro-Intestinal and Neuropsychiatric Effects Strategy for Patient Oriented Research Network (IMAGINE) has conducted a five-year multicenter prospective observational cohort study, Mind And Gut Interactions Cohort (MAGIC) in 14 centres across Canada from 2018-2022. Herein, we investigated the relationship between ulcerative colitis (UC) phenotypes; demographics and other relevant outcomes and symptom reporting.

Methods:  At baseline, participants answered surveys assessing disease activity, medications and complementary therapies, lifestyle factors, psychological status, and comorbidities. UC phenotypes were classified by the Montreal Classification. Herein, we describe the association between phenotypes and demographics, medications used, comorbidities and symptoms experienced in adults with UC. The Inflammatory Bowel Disease Symptom Inventory (IBDSI) was used to assess symptoms

Results: The maximal extent phenotypic distribution based on chart review was E1 (proctitis) n=261 (14.5%), E2 (left sided colitis) n=671 (37.2%), E3 subtotal or pancolitis n=794 (44.0%). More males had E3. Different phenotypes did not lead to differences in the use of complementary therapies. There was greater likelihood of primary sclerosing cholangitis but a lower likelihood of hypertension in E3. Among the 25 different symptoms queried in the IBDSI there was no difference across phenotypes, except among persons with overall active IBDSI there was more waking for urges for bowel movements in persons with E3.

Conclusions Overall, there was no difference in symptom reporting based on extent of UC except for cohort with overall active IBDSI there were some differences in nocturnal waking based on disease extent.

 

 

O’Mahony SL, Tollenaar SI, Khorasaniha R, Jovel J, Ba I,  Voisin A, Miller R, Olof H, Mahmood R, Marrie RA, Strachan E, Soares LP, Cheng C, Janveaux J, Azaidi D, Bernstein CN, Bonner C, Bar-Or A, Waubant E, Yeh A, Graham M. Arnold DL, Banwell BL, Zhu F, Mirza AI, Karimi-Abdolrezaee S, Tsai S, Tremlett H, McGregor K, Willing BP, Armstrong HK. Reduced fibre-fermenting capacity of gut microbes in multiple sclerosis may result in prebiotic dietary fibre β-fructan promoting inflammation and CNS damage. Gastroenterology 2026; e100296 in press.

 

Background Some people with multiple sclerosis display changes in their gut microbiota with separate evidence suggesting worsened symptoms following a high-fibre diet. We hypothesised that in people with multiple sclerosis whose gut microbiota are less able to adequately ferment fibres, unfermented β-fructans induce inflammation.

Methods Diet data (n=48 multiple sclerosis, n=78 unaffected controls) and stool microbiome data (n=31 multiple sclerosis, n=61 unaffected controls) were previously collected from participants. Daily fibre subtype intakes were calculated and compared with fecal shotgun metagenomic sequencing in pediatric onset multiple sclerosis and unaffected persons. Response to unfermented β-fructans was examined in a germ-free experimental autoimmune encephalomyelitis mouse model (unable to ferment fibres). Mice were fed β-fructans or control fibre diet beginning at symptom onset (day 14). Experimental autoimmune encephalomyelitis scores and weights were recorded daily. Intestinal and central nervous system tissues were collected at two endpoints to examine inflammatory responses and demyelinating lesions.

Results Paediatric onset multiple sclerosis consumed less β-fructans (2.4 g/day±0.3 SD; p<0.05) than unaffected participants (3.6 g/day±0.4), which coincided with differences in the gut microbiota including lower fibre fermenting enzymes. Mice exposed to unfermented β-fructans sustained worsened EAE symptoms (day 20–28; p<0.05), immune activation in the gut and immune activation plus demyelinating lesions in the spinal cord compared with mice on control diet.

Conclusions  The gut microbiota of pediatric-onset multiple sclerosis had lower fibre fermenting properties, and our animal findings suggest that β-fructans induce worsened demyelination and gut–brain axis immune activation. Lower β-fructan consumption was observed among participants with pediatric-onset multiple sclerosis. Future longitudinal studies are warranted to confirm the findings uncovered in this manuscript.

 

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