MS Research Update: Salt and Multiple Sclerosis

March 11, 2013 James D. Bowen, M.D.

Increased dietary salt was reported to increase the immune attack on myelin in three studies this week. All three were published in the journal Nature.

  1. A study by Kleinewietfeld, et al, looked at TH17 cells, which is a type of lymphocyte that is highly inflammatory and that causes substantial tissue damage. These cells were grown in cultures in the lab. Some had normal and others high salt levels in their cultures. Those grown in a high salt environment had increased markers for inflammation. This seemed to be due to activation of one particular set of chemical signals in the cell, called the p38/MAPK pathway. They also looked at mice with an MS-like disease called experimental allergic encephalomyelitis (EAE). Mice fed a high salt diet had worse EAE than those fed a normal diet.
  2. A study by Wu, et al, also looked at TH17 cells. An analysis was done on genes associated with activation of TH17 cells, and SGK1 was identified as an important protein in this process. The SGK1 pathway was found to be more active if cells were cultured in a high salt environment. This was then studied in mice with EAE. Mice fed a high salt diet had more severe EAE. Blocking the SGK1 pathway seemed to reverse the effect of the high salt diet on the EAE.
  3. A study by Yosef, et al, also looked a the genes associated with activation of TH17 cells. They identified 22 sets of related genes that increased TH17 cell activity and 5 that decreased activity.

TH17 cells are highly inflammatory and likely contribute to the severe damage done to tissues in a number of diseases. Their precise role in MS is not fully understood, but it is believed that they play a role in the destruction of myelin. These studies add to our understanding of how TH17 cells are regulated. There are many factors that alter the function of these cells as the study by Yosef, et al demonstrates. The finding that salt may be one of these factors is interesting.

However, I believe that it is too early to recommend a decrease in salt intake as a treatment for MS. The studies described above were primarily done in cells that were cultured (in petri dishes). The fact that similar findings were found in mice fed high salt diets suggests that these findings may also apply to living organisms. It is unknown whether these findings apply to humans or whether salt can be reduced in human diets sufficient to alter the behavior of human TH17 cells.

For the past several centuries, humans have had large dietary salt intakes because salt was used extensively as a food preservative; but over the past few decades the dietary salt intake has dramatically fallen with the use of freezing and refrigeration to preserve food. Even though the dietary salt has been decreasing over the past several decades, the incidence of MS seems to be increasing. So it is unknown whether a further decrease in dietary salt would improve MS.

There is another reason to decrease dietary salt though. People with MS do not often die directly from the MS. Most die from the normal diseases of aging. Decreased dietary salt helps decrease the rate of high blood pressure, stroke and heart disease. Thus, decreasing dietary salt may or may not help the MS, but is can help you live longer.

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