Abstract
Studies on the role of nutritional factors and physical activity (PA) in the pathogenesis of multiple sclerosis (MS) go back a long time. Despite the intrinsic difficulty of studying their positive or negative role in MS, the interest of researchers on these topics increased during the last few decades, since the role of diet has been investigated with the perspective of the association with disease-modifying drugs (DMD). The association of DMD, diets, and PA might have an additive effect in modifying disease severity. Among the various diets investigated (low-carbohydrate, gluten-free, Mediterranean, low-fat, fasting-mimicking, and Western diets) only low-carbohydrate, Mediterranean, and fast-mimicking diets have shown both in animal models and in humans a positive effect on MS course and in patient-reported outcomes (PROs). However, the Mediterranean diet is easier to be maintained compared to fast-mimicking and low-carbohydrate diets, which may lead to detrimental side effects requiring careful clinical monitoring. Conversely, the Western diet, which is characterized by a high intake of highly saturated fats and carbohydrates, may lead to the activation of pro-inflammatory immune pathways and is therefore not recommended. PA showed a positive effect both in animal models as well as on disease course and PROs in humans. Training with combined exercises is considered the more effective approach.
Highlights
Multiple sclerosis (MS) is a chronic, neuroinflammatory disease of the central nervous system (CNS) characterized by immune-mediated damage to oligodendrocytes with myelin and axonal damage [1]
disease-modifying drugs (DMD) available at the present time are effective in specific subtypes and phases of MS as well as their use may be limited by lack of tolerance, side effects, or the presence of comorbidities with a large number of patients with unsatisfied needs
The dysbiosis sustained by detrimental dietary habits (e.g., Western diet, low vitamin D intake, etc.) with increasing of phylum Firmicutes (e.g., Blautia, Dorea), some Bacterioides genera (Pedobacteria and Flavobacteria), Streptococcus oralis, Streptococcus mitis, Methanobrevibacter, Akkermansia, Proteobacteria, and decreasing of other Bacterioides genera (Prevotella, Bacterioides, Parabacterioides), Clostridium, Adlercreutzia, and Butyricinimonas might be associated to reduced anti-inflammatory cytokines production (e.g., IL-10). The results of these mechanisms would cause a reduction of anti-inflammatory metabolites such as propionate and butyrate, determining effects on Treg cells reduction, Th17 cells expansion, upregulation of genes involved in antigen presentation to B and T cells, and activation of the complement and coagulation cascade with intestinal barrier dysfunction [7]
Summary
Multiple sclerosis (MS) is a chronic, neuroinflammatory disease of the central nervous system (CNS) characterized by immune-mediated damage to oligodendrocytes with myelin and axonal damage [1]. The dysbiosis sustained by detrimental dietary habits (e.g., Western diet, low vitamin D intake, etc.) with increasing of phylum Firmicutes (e.g., Blautia, Dorea), some Bacterioides genera (Pedobacteria and Flavobacteria), Streptococcus oralis, Streptococcus mitis, Methanobrevibacter, Akkermansia, Proteobacteria, and decreasing of other Bacterioides genera (Prevotella, Bacterioides, Parabacterioides), Clostridium, Adlercreutzia, and Butyricinimonas might be associated to reduced anti-inflammatory cytokines production (e.g., IL-10) The results of these mechanisms would cause a reduction of anti-inflammatory metabolites such as propionate and butyrate, determining effects on Treg cells reduction, Th17 cells expansion ( at intestinal levels), upregulation of genes involved in antigen presentation to B and T cells, and activation of the complement and coagulation cascade with intestinal barrier dysfunction [7]. The nutritional lifestyle leading to high BMI, abdominal obesity, or dysbiosis might induce a systemic pro-inflammatory state contributing to disease pathogenesis and severity
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