Multiple sclerosis is an intestinal disease!
The gut regulates inflammation in the body and plays an important role in immunity. Indeed, scientists can observe that fact even in cases of auto-immunity like in Multiple Sclerosis (MS). Multiple Sclerosis is indeed an autoimmune disease related to the abnormal activity of certain antibodies directed against the myelin sheath of nerve fibers, which could have several triggers. Some triggers would be after a viral or bacterial event, in a subject genetically predisposed to the disease.
For Multiple Sclerosis, a diet improves intestinal health and preserves the intestinal lining. According to science, it is possible that vitamin D has an important role to play in MS. This diet is low in carbohydrates, high in healthy fats and contains a lot of prebiotic fiber that multiplies short chain fatty acids.
Research on Short Chain Fatty Acids and MS
Research suggests that nutrition and bacterial metabolites may affect immunity for MS and autoimmunity. We have noted in the scientific literature that long chain fatty acids (CLFA) improve the differentiation and proliferation of certain immune cells that negatively modify the intestinal bacterial population.
As for short-chain dietary fatty acids (SCFA), they positively modify the intestinal bacterial population. Researchers artificially created a form of MS in the laboratory to show that CLFAs decreased the concentration of SCFA in the intestine and worsened the disease by increasing pathogenic cell populations in the small intestine.
The CLFA-based treatment has improved brain cells and reduced damage through a lasting footprint on certain immune cells. In other words, short-chain fatty acids increase the population of good bacteria, which in turn exerts a positive influence on the brain in the case of MS.
This data shows a direct dietary impact on the immune response of the gut and then the central nervous system in autoimmunity. This could therefore have therapeutic implications for autoimmune diseases such as Multiple Sclerosis. (1)
We produce short-chain fatty acids through the use of prebiotics, such as inulin from Jerusalem artichokes, chicory or beetroot or other fibers such as guar gum.
Vitamin D and MS
It has since been shown that vitamin D has a strong and consistent positive influence in decreasing the risk of MS and its clinical evolution. Cases of more active MS have much lower levels of vitamin D compared to healthy controls.
The results of these case-control and cross-sectional studies paved the way for cohort studies indicating significant inverse associations between serum (OH) D and clinical activity in MS. Evidence of observation and ongoing research into vitamin D supplementation would confirm its use as an intervention for the onset and clinical evolution of MS. In addition to being a distinct factor in the etiology of MS, vitamin D has been shown to interact with a variety of other risk factors, ranging from genetic predictors such as the HLA-DR1 genotype to behavioral factors such as smoking.
Gut microbiota and MS
An intestinal microbiota transplant from an individual with Multiple Sclerosis in mice triggers autoimmune neurodegeneration, confirming the role of intestinal flora in this disease.
Thus, the role of the gut microbiota in the emergence of MS is confirmed. A link between intestinal commensal bacteria and autoimmune pathologies has been demonstrated in animal models of MS.
The intestinal microbiota of each individual was transferred to rodents predisposed to autoimmune encephalomyelitis, the animal model of MS. Disease was triggered in more than 60% of animals that received flora from MS subjects against 30% among those who received the flora of healthy subjects.
An analysis of the intestinal microbiota of the grafted animals reveals a decrease of a bacterial strain (Sutterella) in the animals that received the subject microbiota SEP. However, the presence of this bacterium is associated with a better defense against inflammatory diseases. (2)
References:
(1) https://www.drperlmutter.com/wp-content/uploads/2015/10/Fatty-Acids-MS2.pdf
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