Eating too much salt could mess with your immune cells

A tipped-over salt shaker with spilled salt.
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Eating too much salt may reduce the amount of energy that immune system cells can make, preventing them from working normally, according to a new study.

Eating an excess of sodium has previously been linked to many different problems in the body, including high blood pressure and higher risk of stroke, heart failure, osteoporosis, stomach cancer and kidney disease, Live Science previously reported.

"Of course the first thing you think of is the cardiovascular risk," co-author Markus Kleinewietfeld, an associate professor at Hasselt University in Belgium, said in a statement. "But multiple studies have shown that salt can affect immune cells in a variety of ways." If salt disrupts immune functioning for a long period of time, it could potentially drive inflammatory or autoimmune diseases in the body, he added.

Related: 6 easy ways to eat more fruits and vegetables

A few years ago, a group of researchers in Germany discovered that high salt concentrations in the blood can directly impact the functioning of a group of immune system cells known as monocytes, which are the precursors of Pac Man-like cells called phagocytes that identify and devour pathogens and infected or dead cells in the body. 

In the new study, Kleinewietfeld and his colleagues conducted a series of experiments to figure out how. First, they zoomed in on that link in the lab using mouse and human monocytes. They found that within three hours of exposure to high salt concentrations, the immune cells produced less energy, or adenosine triphosphate (ATP).

Mitochondria, the cells' power plants, produce ATP from energy found in  food using a series of biochemical reactions, according to the statement. ATP then fuels many different cellular processes, such as powering muscles or regulating metabolism, according to the statement. 

Specifically, the researchers discovered that high salt concentrations inhibit a group of enzymes known as complex II in the chain reaction that produces ATP, which leads the mitochondria to produce less ATP. With less ATP (less energy), the monocytes matured into abnormal-looking phagocytes. 

The researchers found that these unusual phagocytes were more effective at fighting off infections. Still, that's not necessarily a good thing, the researchers say, as an increased immune response can lead to more inflammation in the body, which in turn, can increase the risk of heart disease

The researchers then conducted multiple experiments in people; in one, healthy male participants took daily salt supplement tablets of 6,000 milligrams — nearly three times the recommended amount — for two weeks. In another experiment, a group of participants ate a whole pizza from an Italian restaurant.

They found that after eating the pizza, which contained 10,000 mg of salt, participants' mitochondria produced less energy. But this effect wasn't long-lasting; eight hours after the participants ate the pizza, blood tests showed that their mitochondria were functioning normally again.

"That's a good thing," Dominik Müller, a professor at the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and the Experimental and Clinical Research Center in Berlin, said in the statement. "If it had been a prolonged disturbance, we'd be worried about the cells not getting enough energy for a long time."

Still, it's not clear whether mitochondria are affected in the long-term if a person consistently eats a high-salt diet, according to the statement. The researchers hope to understand whether salt can impact other cells, because mitochondria exist in almost every cell in the body, according to the statement.

The findings were published on April 28 in the journal Circulation.

Originally published on Live Science.

Yasemin Saplakoglu
Staff Writer

Yasemin is a staff writer at Live Science, covering health, neuroscience and biology. Her work has appeared in Scientific American, Science and the San Jose Mercury News. She has a bachelor's degree in biomedical engineering from the University of Connecticut and a graduate certificate in science communication from the University of California, Santa Cruz.