For many years, it has been recognised that a high-salt diet is bad for you. Eating too much sodium increases the risk of high blood pressure, heart disease, stroke, stomach cancer, kidney stones and osteoporosis. A reduction in salt intake could prevents thousands of deaths each year in England and Wales from cardiovascular disease alone.
Recently, though, salt (also known as sodium chloride) has become implicated in a new group of ailments. Research from Yale, Harvard and other leading institutions has found that a high-salt diet worsens symptoms in autoimmune diseases such as multiple sclerosis and rheumatoid arthritis. The connection has come as a surprise, even to the scientists who first identified the link. “I would never have thought that this link existed,” said Vijay Kuchroo, a scientist at Harvard University who is studying the effect of salt on multiple sclerosis. “It just never occurred to me.”
Over the past 30 years, autoimmune disease has overall risen by between 5% and 7% a year. The increase can’t be explained by genetics – our DNA hasn’t changed that rapidly. Researchers have suggested several possible explanations, including environmental toxins, smoking, low levels of vitamin D, and certain infections. But none of these theories has provided an adequate answer.
“Salt could explain a lot of this mystery,” says David Hafler, professor of neurology and immunobiology at Yale University, and one of the first to make the connection. He notes that autoimmune diseases have increased most in developed countries, where salt consumption is highest.
The effect of salt on the immune system may be even more widespread. In recent years, scientists have found evidence that hypertension is caused by an immune overreaction; scientists had previously thought that it developed as a result of the chronic water retention that occurs with high salt consumption.
The first clue to the link between salt and autoimmunity came from a burger and fries. In 2011, interested in how intestinal bacteria might alter the course of autoimmune disease, Hafler examined the eating habits of a group of more than 80 subjects over a year. The bacteria research is ongoing, but in the meantime, he and his colleagues noticed something else.
“To my surprise, it turned out that if you ate fast food more frequently, you had more inflammatory immune cells [known as TH17 cells] in your blood,” he said. “What do these restaurants have in their food? Lots of salt.”
Intrigued, Hafler began a study of how salt affects rats with an animal version of MS, a disease that damages the brain and nervous system. The results were striking: animals on a high-salt diet had 10 times more TH17 cells than those on a regular diet. More importantly, they got much sicker. Most of the animals on the high-salt regimen became paralysed, while those that ate less salt tended to remain much more mobile. Hafler then moved on to human immune cells, and found that exposing them to high levels of salt led to major increases in the inflammatory cells.
Last year, scientists from Harvard Medical School and the Raúl Carrea Institute for Neurological Research in Argentina studied salt consumption among 122 patients with multiple sclerosis. They found that those who ate a lot of salt were four times more likely to develop more serious symptoms than those who ate little. The high-salt group also had a threefold greater chance of developing new brain lesions related to the disease.
Further evidence of the role of salt in autoimmune disease came in the form of a Swedish study published last year, which found that smokers who consumed a lot of salt had double the risk of developing rheumatoid arthritis.
The link between salt and overactive immune cells appears to be a gene known as SGK1, which plays a key role in allowing the body to absorb salt. The more salt you ingest, the more active SGK1 becomes. Kuchroo, along with Aviv Regev, a computational biologist at the Broad Institute in Boston, has found that the gene also has another function: it controls TH17 cells. They theorise that high levels of SGK1 can lead to a flood of TH17, causing the immune system to spin out of control.
Overconsumption of salt is a recent development; for most of the 2m years our species has existed, humans have probably ingested very small amounts. But in the past few hundred years, trade and manufacturing advances have made salt inexpensive and plentiful. Today, most people eat far more than they need. A study published last year in the New England Journal of Medicine looked at salt consumption in 187 countries; in all but six, people ate too much. According to the NHS, the average adult in the UK eats about 8g salt a day, 2g more than the agency’s recommended upper limit. Kuchroo goes further: “We get 10 times as much salt as we need. We have not evolved for high salt consumption.”
At the same time, he and others note that it is likely that not everyone risks immune overdrive from a diet heavy on pickles, bacon and crisps. It may be that certain people are more vulnerable, perhaps those with a higher sensitivity to salt, or a predisposition to autoimmune diseases. They also emphasise that salt is probably just one of several factors that play a role in rising rates of autoimmune disease.
At the same time, if salt does prove to be key trigger in autoimmunity, it could open up a new and relatively simple way to prevent or treat these diseases. Hafler already recommends that his MS patients reduce their intake of salt. “If I had an autoimmune disease, I would definitely cut down on salt,” he says. “There’s really no downside. It’s hard to argue against a low-salt diet.”
