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Multiple sclerosis, more commonly termed MS, is a fickle condition that tends to remit and relapse over time. For this reason, it is hard to evaluate the effectiveness of diet in controlling it. But solid new evidence suggests sodium restriction may help.

Researchers have serious challenges in evaluating the effectiveness of dietary changes in the management of multiple sclerosis, also known as MS.

MS is a condition of natural remissions and relapses. Symptoms sometimes get better no matter what MS patients do, and symptoms sometimes get worse no matter what MS patients do. For that reason, it is a good thing to be cautious about intepreting the benefits or problems associated with a medication, a medical therapy, a nutritional supplement, or a change in diet. New basic research into the biology of the MS-affected brain, however, suggests that sodium restriction may be very useful in controlling the symptoms of MS.

MS-Affected Brain Soaks Up Sodium, Brain Scans Reveal

Scientists at the Aix-Marseille Université in France conducted brain scans (MRI) in 20 patients who had primary progressive MS, 9 patients who had secondary progressive MS, and 15 controls for comparison. The scans measured total sodium content in gray matter, white matter, and lesions in the brain, the lesions caused by the disease.

The brain scans found higher sodium levels in the brains of patients who had active disease.

Sodium levels were not as high in the brains of patients whose MS was in remission, or in the brains of people who did not have the disease. The MRI scans revealed that sodium levels increased in regions of the brain most clearly associated with MS, the premotor, primary motor, and Somatosensory cortices, the cingulate, prefrontal, and visual cortices, and the corpus callosum, thalamis, cerebellum, and brainstem. Higher sodium levels in the anterior prefrontal cortex and premotor cortex were associated with greater disability from the disease.

Indicator of Disease, or Cause of Disease?

The French researchers concluded that higher sodium levels in the brain were a clear indicator of the progression of MS, but correlation is not the same as causation. It is not possible to conclude from the findings that the brain accumulates sodium during MS that sodium is a cause of MS. However, other research suggests that the relationship is causative, and that is not "sodium" that drives MS and other autoimmune diseases, but rather "sodium chloride," or table salt, in the diet.

Publishing their findings in the prestigious journal Nature, scientists in the departments of neurology and immunobiology at the Yale University School of Medicine found that high salt levels (that is, high levels of sodium chloride) increased the production of a highly specialized kind of white blood cell known as the Th17 cell. These white blood cells are helper T cells that produce an inflammatory chemical known as interleukin-17, or IL-17. This chemical interacts with brain cells to "turn on" a gene that tells the brain cell it is time to die. 

High salt levels, however, increase the numbers of Th17 cells. More and more Th17 cells release the inflammatory chemicals that tell more and more brain cells that their life cycle is over, and more and more brain tissue dies.

Sodium accumulates in parts of the brain most affected by MS, and salt stimulates the immune system to destroy cells in the parts of the brain most affected by MS. But does eliminating salt from the diet reduce symptoms of MS?

Continue reading after recommendations

  • Kleinewietfeld M1, Manzel A, Titze J, Kvakan H, Yosef N, Linker RA, Muller DN, Hafler DA. Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. Nature. 2013 Apr 25.496(7446):518-22. doi: 10.1038/nature11868. Epub 2013 Mar 6.
  • Maarouf A, Audoin B, Konstandin S, Rico A, Soulier E, Reuter F, Le Troter A, Confort-Gouny S, Cozzone PJ, Guye M, Schad LR, Pelletier J, Ranjeva JP, Zaaraoui W. Topography of brain sodium accumulation in progressive multiple sclerosis. MAGMA. 2014 Feb
  • 27(1):53-62. doi: 10.1007/s10334-013-0396-1. Epub 2013 Aug 3.PMID: 23907269.
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