Dietary fibres are typically fermented by gut microbes, producing beneficial short-chain fatty acids (SCFAs). In chronic diseases like inflammatory bowel disease (IBD), studies show reduced fibre-fermenting microbiota and SCFAs, alongside worsened symptoms from high-fibre diets, suggesting impaired fibre fermentation may worsen disease outcomes. Our team previously found that select unfermented fibres (e.g., β-fructans) induce gut inflammation and damage in IBD, which was linked to decreased β-fructan consumption. We believe this decrease is a subconscious avoidance of foods associated with worsened symptoms, supporting possible connections between microbiota-driven fibre fermentation and gut-brain axis (GBA) physiology. This further suggests that unfermented fibres' impacts may not be isolated to gut diseases but extend to the nervous system. Given that multiple sclerosis (MS) also shows reduced fibre-fermenting microbiota and SCFA, altered immune pathways, and worsened symptoms on high-fibre diets, I hypothesized that reduced consumption of specific dietary fibres in autoimmune GBA conditions links to lower fibre-fermenting microbiota and worsened symptoms in IBD (gut) and MS (brain). I aimed to: 1) validate our method for examining fibre subtype consumption patterns, 2) assess fibre consumption's association with IBD development and progression, 3) analyze fibre consumption in MS patients, and 4) examine the link between unfermented fibres and CNS damage in experimental autoimmune encephalomyelitis (EAE) mice. I found β-fructan fibre consumption significantly decreased before IBD development (n=3,400) compared to healthy controls, and again during IBD progression from remission to flare (n=155) compared to those in remission. Diet was assessed using a validated food frequency questionnaire (FFQ), with results linked to microbial metabolites. MS patients also consumed significantly less β-fructan than healthy controls. Germ-free EAE MS mice displayed increased spinal demyelination and inflammatory markers in the gut and spine. My findings, described in my thesis, suggest that reduced β-fructan consumption in autoimmune GBA diseases may stem from learned avoidance due to symptoms from reduced β-fructan fermentation. Further research is needed to translate findings clinically for precision nutrition strategies in these diseases.