Item type:Article, Open Access

Unveiling the Important Role of Gut Microbiota and Diet in Multiple Sclerosis

Abstract

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS), characterized by neurodegeneration, axonal damage, demyelination, and inflammation. Recently, gut dysbiosis has been linked to MS and other autoimmune conditions. Namely, gut microbiota has a vital role in regulating immune function by influencing immune cell development, cytokine production, and intestinal barrier integrity. While balanced microbiota fosters immune tolerance, dysbiosis disrupts immune regulation, damages intestinal permeability, and heightens the risk of autoimmune diseases. The critical factor in shaping the gut microbiota and modulating immune response is diet. Research shows that high-fat diets rich in saturated fats are associated with disease progression. Conversely, diets rich in fruits, yogurt, and legumes may lower the risk of MS onset and progression. Specific dietary interventions, such as the Mediterranean diet (MD) and ketogenic diet, have shown potential to reduce inflammation, support neuroprotection, and promote CNS repair. Probiotics, by restoring microbial balance, may also help mitigate immune dysfunction noted in MS. Personalized dietary strategies targeting the gut microbiota hold promise for managing MS by modulating immune responses and slowing disease progression. Optimizing nutrient intake and adopting anti-inflammatory diets could improve disease control and quality of life. Understanding gut-immune interactions is essential for developing tailored nutritional therapies for MS patients.

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Džidić Krivić, Amina; Begagić, Emir; Hadžić, Semir; Bećirović, Amir; Bećirović, Emir; Hibić, Harisa; Tandir Lihić, Lejla; Kadić Vukas, Samra; Bečulić, Hakija; Kasapović, Tarik; Pojskic, Mirza: Unveiling the Important Role of Gut Microbiota and Diet in Multiple Sclerosis. In: Brain Scieces. 2025, 15, 253, Jg. (), S. 1-23. DOI: https://doi.org/10.17192/openumr/1038.

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Except where otherwise noted, this item's license is described as Attribution 4.0 International

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