You may want to think twice before adding salt to whatever it is you’re eating. Three new studies published in the journal Nature suggest too much salt may be linked to several autoimmune diseases including multiple sclerosis, psoriasis, rheumatoid arthritis and arthritis of the spine.
“The diet does affect the autoimmune system in ways that have not been previously recognized,” said senior author Dr. David Hafler, a professor of neurology and immunobiology at the Yale School of Medicine, in New Haven, Connecticut.
Yale researchers first began looking into salt when they noticed that people who ate fast food seemed to have higher levels of inflammatory cells than those who don’t.
After putting mice on a high salt diet, Hafler and his team discovered an increase in the rodents’ production of a type of infection-fighting cell that is closely associated with autoimmune diseases. The mice also developed autoimmune encephalomyelitis, a severe form of multiple sclerosis.
In addition to Hafler’s research, scientists from the Broad Institute in Boston examined how genes regulate the immune response, and researchers from Harvard Medical School and Brigham and Women’s Hospital in Boston explored how autoimmunity is controlled by a network of genes.
In all three studies, salt appeared to play a part in the development of the molecular pathways that can lead to autoimmune disease by over-stimulating what are known as helper T-cells into creating unhealthy inflammation.
Inflammatory cells are normally used by the immune system to protect against bacterial, viral, fungal and parasitic infections. In the case of autoimmune diseases, too many inflammatory cells are produced and they begin attacking healthy tissue.
Finding the molecular switches that cause the body to overproduce T-cells has been difficult because conventional methods of activating immune cells in the laboratory often harm the cells or alter the course of their development.
A physicist at Harvard University was able to solve that problem by using silicone nanowires to disarm single genes in cells. Once that was accomplished, scientists were able to piece together a functional model of how T-cells are controlled.
Researchers then observed immune cell production over 72 hours. One protein kept cropping up: serum glucocorticoid kinase 1 (SGK1), which is known to regulate salt levels in other types of cells. They found that mouse cells cultured in high-salt conditions had higher SGK1 levels and produced more T-cells than those grown in normal conditions.
“If you incrementally increase salt, you get generation after generation of these T-cells,” said study co-author Vijay Kuchroo, an immunologist at Brigham and Women’s Hospital in Boston, Massachusetts.
“We think of helper T-cells as sort of the orchestra leaders, helping the immune system know what the cells should be doing in response to different microbial pathogens,” Dr. John O’Shea, director of intramural research at the U.S. National Institute of Arthritis and Musculoskeletal and Skin Diseases told Health Day.
The importance of these studies, he added, is that they appear to indicate that salt is another factor driving helper T-cell differentiation.
Although two of the studies found that a high-salt diet accelerated the progression of multiple sclerosis in mice, researchers say that the evidence so far cannot predict the effect of salt on human autoimmunity.
Despite that lack of evidence, Hafler recommends that for general health concerns alone, “people should probably already be on a low-salt diet.”
“If I had an autoimmune disease, I would put myself on a low-salt diet now. It’s not a bad thing to do. But we have to do more studies to prove it.”