Salty Diet Might Help Trigger MS, Rheumatoid Arthritis

By Barbara Bronson Gray

HealthDay Reporter

WEDNESDAY, March 6 (HealthDay News) -- Eating lots of foods loaded with salt may do more than raise your blood pressure: Researchers report that it could also contribute to the development of autoimmune diseases, where the body's immune system mistakenly mounts an attack upon some part of the body.

Three new studies suggest salt may be a prime suspect in a wide range of autoimmune diseases, including multiple sclerosis (MS), psoriasis, rheumatoid arthritis and ankylosing spondylitis (arthritis of the spine).

A significant increase in the incidence of autoimmune diseases, especially multiple sclerosis and type 1 diabetes, suggests that environmental factors, and not genetics, may explain the trend, the researchers noted.

"The diet does affect the autoimmune system in ways that have not been previously recognized," said senior study author Dr. David Hafler, a professor of neurology and immunobiology at the Yale School of Medicine, in New Haven, Conn.

It was an accidental discovery that triggered the researchers' interest in salt; they stumbled upon the fact that people who ate at fast food restaurants seemed to have higher levels of inflammatory cells than others, Hafler explained.

In the study, Hafler and his team found that giving mice a high-salt diet caused the rodents to produce a type of infection-fighting cell that is closely associated with autoimmune diseases. The mice on salt diets developed a severe form of multiple sclerosis, called autoimmune encephalomyelitis. Findings from animal studies are not always mirrored in human trials, however.

Inflammatory cells are normally used by the immune system to protect people from bacterial, viral, fungal and parasitic infections. But, in the case of autoimmune diseases, they attack healthy tissue.

Hafler's study is one of three papers, published in the March 6 issue of the journal Nature, that show how salt may overstimulate the immune system. In addition to Hafler's research, scientists from the Broad Institute in Boston explored how genes regulate the immune response, and researchers from Harvard Medical School and Brigham and Women's Hospital in Boston zeroed in on how autoimmunity is controlled by a network of genes.

All three studies help explain, each from a different angle, how "helper" T-cells can drive autoimmune diseases by creating inflammation. Salt seems to cause enzymes to stimulate the creation of the helper T-cells, escalating the immune response.

"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," explained Dr. John O'Shea, director of intramural research at the U.S. National Institute of Arthritis and Musculoskeletal and Skin Diseases, in Bethesda, Md. "The strength of these papers is that they have found another factor that drives [helper T-cell] differentiation -- salt."

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