In multiple sclerosis (MS), a person’s immune system wrongly attacks the myelin cells that sheath and protect the nerves, which results in an array of neurological symptoms that can be permanent when the disease advances.

MS is an important healthcare issue because it is the most common autoimmune disease affecting working-age adults (15–60 years of age), but we do not yet have a good understanding of how MS develops and progresses. Several recent studies, however, have found that high salt intake could be a potential new risk factor for MS development and inflammation.

Researchers are interested in improving our understanding of MS development, which can help in disease prevention and halting the progression of the disease. Currently, a history of infectious mononucleosis, smoking, obesity, being female, and vitamin deficiency has been linked to an increase in MS risk.

The development of MS is also strongly affected by a person’s genetics, as there are certain populations like the Inuit, Yakutes, Australian Aborigines, and New Zealanders that see nearly no MS cases. Studies of immigrants have found that after living in a new environment for some time, people may take on the risk of developing MS in the new environment, which underlines the fact that the interaction of external and genetic factors plays a role in MS development.

Studies investigating MS risk factors

In 2015, Krementsov and colleagues published a mice study in the Federation of American Societies for Experimental Biology (FASEB), which found that a high salt diet in C57BL6/J mice resulted in worse clinical signs of the mouse version of MS. They also tested a high salt diet in mice with various other genetic profiles, and found that MS in mice is mediated by salt intake, sex, and genetic profile.

In October, Yale researchers Sumida and colleagues illuminated the biochemical pathways of this interaction between salt and MS inflammation. In MS, faulty regulatory T cells (Treg cells) have been implicated in the MS disease state by causing irregularities in T-cells, IFN-γ, and cytokine IL-10, which are all key players in how the body fights infections. Sumida and colleagues found that high salt environment triggers the beta-catenin/Wnt signalling pathway, which disrupts the normal function of Treg cells.

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These studies have further solidified the relationship between high salt intake, genetic factors, and MS development. Since the modern day diet is increasingly high in salt content, this may partially explain the increase in autoimmune diseases seen in recent years. However, further epidemiological studies are necessary to clarify the impact of salt intake on MS risk, such as demonstrating a dose-dependent relationship.

The clinical impact of further research can be significant; clinicians may utilize this information to instruct MS patients to partake in low-salt diets to prevent inflammation, and pharmaceutical companies may look for drugs that target the salt-mediated MS pathways.