Evidence map›Paper›PMID 41585377›Full record

ArticleeGastroenterology2026

Reduced fibre-fermenting capacity of gut microbes in multiple sclerosis may result in prebiotic dietary fibre β-fructan promoting inflammation and CNS damage.

Stephanie L Tollenaar, Reihane Khorasaniha, Juan Jovel, Ismaila Ba, Athalia Voisin, Richard Miller, Hana Olof, Ramsha Mahmood, Ruth Ann Marrie, Erin Strachan and 21 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in eGastroenterology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

31 authors.

Stephanie L Tollenaar *Agriculture, Food and Nutrition Sciences Department, University of Alberta, Edmonton, Alberta, Canada.
Reihane Khorasaniha *Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
Juan JovelFaculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada.
Ismaila BaDepartment of Statistical Sciences, University of Toronto, Toronto, Ontario, Canada.
Athalia VoisinDepartment of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
Richard MillerDepartment of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
Hana OlofDepartment of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
Ramsha MahmoodDepartment of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
Ruth Ann MarrieDepartment of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.ORCID https://orcid.org/0000-0002-1855-5595
Erin StrachanDepartment of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada.
Luisa P SoaresDepartment of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada.
Christopher ChengDepartment of Medicine, University of Alberta, Edmonton, Alberta, Canada.
Jonathan JanveauxDepartment of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
Deenaz ZaidiDepartment of Medicine, University of Alberta, Edmonton, Alberta, Canada.
Charles N BernsteinDepartment of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
Christine BonnerPublic Health Agency of Canada, Winnipeg, Manitoba, Canada.
Amit Bar-OrCenter for NeuroInflammation and Experimental Therapeutics and Children's Hospital of Philadelphia, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Emmanuelle WaubantWeill Institute for Neurosciences, University of California San Francisco, San Francisco, California, USA.
E Ann YehInstitute of Medical Science, University of Toronto, Toronto, Ontario, Canada.
Morag GrahamPublic Health Agency of Canada, Winnipeg, Manitoba, Canada.
Douglas L ArnoldDepartment of Neurology and Neurosurgery, McGill University, Montreal, Quebec, Canada.
Julia O'MahonyCleveland Clinic, Cleveland, Ohio, USA.
Brenda L BanwellDepartment of Pediatrics, Johns Hopkins University, Baltimore, Maryland, USA.
Feng ZhuDepartment of Neurology, The University of British Columbia, Vancouver, British Columbia, Canada.
Ali I MirzaDepartment of Medicine, The University of British Columbia, Vancouver, British Columbia, Canada.
Soheila Karimi-AbdolrezaeeDepartment of Physiology and Pathophysiology, University of Manitoba, Winnipeg, Manitoba, Canada.
Sue TsaiDepartment of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada.
Helen TremlettDepartment of Medicine, The University of British Columbia, Vancouver, British Columbia, Canada.
Kevin McGregorDepartment of Statistics, University of Manitoba, Winnipeg, Manitoba, Canada.
Benjamin P WillingAgriculture, Food and Nutrition Sciences Department, University of Alberta, Edmonton, Alberta, Canada.
Heather ArmstrongDepartment of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.ORCID https://orcid.org/0000-0003-3991-9201

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Some people with multiple sclerosis display changes in their gut microbiota with separate evidence suggesting that symptoms may worsen following a high-fibre diet. We hypothesised that in people with multiple sclerosis whose gut microbiota are less able to efficiently ferment dietary fibres, unfermented β-fructans induce inflammation. Methods: Diet data (n=48 individuals with multiple sclerosis, n=78 unaffected controls) and stool microbiome data (n=31 individuals with multiple sclerosis, n=61 unaffected controls) were previously collected from participants. Daily fibre subtype intakes were calculated and compared with faecal shotgun metagenomic sequencing in paediatric onset multiple sclerosis and unaffected persons. Response to unfermented β-fructans was examined in a germ-free experimental autoimmune encephalomyelitis (EAE) mouse model (unable to ferment fibres). Mice were fed β-fructans or control fibre diet beginning at symptom onset (day 14). EAE 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: Individuals with 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 individuals with paediatric-onset multiple sclerosis showed reduced fibre fermenting properties, and our animal findings suggest that unfermented β-fructans can worsen demyelination and promote gut-brain axis immune activation. Lower β-fructan consumption was observed among participants with paediatric-onset multiple sclerosis. Future longitudinal studies are warranted to confirm the findings uncovered in this manuscript.

Indexed as

Brain-Gut AxisDietary FibreEncephalomyelitis, Autoimmune, ExperimentalGastrointestinal MicrobiomeMultiple Sclerosis

Identifiers

PMID41585377
PMCPMC12829359

What Socratic holds

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LicenceCC BY-NC
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.