DIETS HIGH IN SALT MAY INCREASE RISK OF AUTOIMMUNE DISEASES

Eating a diet high in sodium 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 conducted on mice and human immune cell cultures, 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).

Significant increases in the incidence of autoimmune diseases, especially multiple sclerosis and type 1 diabetes, suggests that environmental and lifestyle factors, and not just genetics, influence the onset of these diseases. Observational studies have shown that persons who eat more meals out and especially those who frequently eat fast food, have high levels of pathogenic helper T-cells (specifically helper T-cells 17),which are elevated in autoimmune diseases.  Helper T-cells 17 are a type of infection-fighting cell that is likely to become pathogenic, attacking tissues in the body rather than infectious agents. To investigate if high salt intake was possibly increasing these cell levels, Dr. David Hafler and his colleagues as well as researchers at other institutions, fed high salt diets to mice and exposed cultures of human T-cells to elevated levels of sodium.  In both cases, in the presence of sodium, helper T-cells differentiated into the pathogenic helper T-cells 17 at ten times the rate of those not exposed to high levels of sodium.  In fact,  the mice on high salt diets developed a severe form of multiple sclerosis, called autoimmune encephalomyelitis. 

While salt may play a role in autoimmune diseases, the researchers said the picture is most likely complicated. "We don't think salt is the whole story. It's a new, unexplored part of it, but there are hundreds of genetic variants involved in autoimmune disease and environmental factors, too," said Hafler.  In addition to salt, other factors have been shown to influence levels of pathogenic helper T-cells, including microbes, diet, metabolism, environmental factors and cytokines (proteins that help regulate inflammatory responses).

What to do:  While the relationship between salt and autoimmune disease has yet to be conclusively explored, there are plenty of other health benefits to limiting sodium intake.  High salt diets have been shown to raise blood pressure which increases risk for stroke, heart disease, and kidney disease.  High salt intake also is detrimental to bone health.   Daily sodium intake should be less than 2,300 mg of sodium a day (about 1 teaspoon of salt).  Limit your meals out because these are almost always high in sodium.  At home use lemon, herbs, and spices instead of salt to season foods.  Read labels to assess the sodium content of foods as most of our intake comes from salt added by manufacturers.  Deli meats, frozen dinners, boxed noodle and rice dishes, canned soups, canned vegetables, bottled dressings & sauces, bread, and snack foods all tend to be high in sodium. 

Adapted from article available at:

http://www.nlm.nih.gov/medlineplus/news/fullstory_134647.html

http://www.examiner.com/article/can-too-much-dietary-salt-set-families-up-for-developing-autoimmune-diseases

Sources: 

Kleinewietfeld M, Manzel A, Titze J, Kvakan H, Yosef N, et al.  Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells.  Nature (06 March 2013)|doi:10.1038/nature11868.  Available at: http://www.nature.com/nature/journal/vaop/ncurrent/full/nature11868.html?WT.ec_id=NATURE-20130307

Wu C, Yosef N, Thalhamer T, Zhu C, Xiao S et al.  Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1.  Nature (06 March 2013) | doi:10.1038/nature11984. Available at: http://www.nature.com/nature/journal/vaop/ncurrent/full/nature11984.html

Yosef N, Shalek AK, Gaublomme JT, Jin H, Lee Y, et al.  Dynamic regulatory network controlling TH17 cell differentiation.  Nature (06 March 2013) | doi:10.1038/nature11981. Available at: http://www.nature.com/nature/journal/vaop/ncurrent/full/nature11981.html