Winter is the season for hats, heavy coats — and hand lotion. The cold, dry air can irritate your skin and flare up conditions like eczema, one of the most common inflammatory diseases, characterized by itchy hands, scalps, knees and elbows.
You likely know someone who suffers from eczema — though they may not be willing to show it. With an estimated 31.6 million cases in the U.S. alone, eczema rivals diabetes in the category of inflammatory ailments and acne when it comes to skin diseases.
Now, a new German study suggests eczema may be so prevalent because of too much table salt in our diets.
The report, published Wednesday in Science Translational Medicine, outlines a connection between consuming table salt and the aggravation of T-helper cells — members of our immune system that sometimes run amok. When they do, T-helper cells can cause hyperactive inflammation and breed allergy-based illnesses, such as arthritis, asthma and eczema.
The scientists discovered that the level of salt we eat as part of a Western diet causes T-helper cells to launch the renegade inflammatory responses that occur with chronic allergies. With eczema, this mayhem appears to happen directly in the skin; the team found salt accumulation was 30 times higher in the skin of eczema patients versus normal people.
Allergies have steadily increased in human populations over the last 50 years, and past research has pointed the finger at changes in human habits and our environment. But because our diets also became unhealthier over this timeframe, now these scientists are thinking, maybe it was just salt all along.
Here’s what you need to know.
A quick primer on T-helper cells
T-helper cells, as their name suggests, help against infections. Think of them as the snitches of the immune system.
Normally, T-helper cells can spot a nasty microbe — be it a virus, bacterium, fungus or parasite — when it has invaded the body. Then the “Th” cells, as they’re branded, call in the cavalry, recruiting other members of the immune system to take the suckers out.
These battalions, made up of different types of Th cells, divide up the labor when it comes to fighting infections.
For more than 20 years, it was thought that there were just two types: Th1 and Th2 cells, said Christina Zielinski, an immunologist at the Technical University of Munich, who co-led the study. “People called it the paradigm of Th1-Th2 dualism.”
The Th1 squad detects intracellular threats — bacteria like tuberculosis or viruses that hide inside of our cells. The Th2 troops help destroy parasitic worms — such as tapeworms — by dictating the production of mucus. The buggers slide right out.
In 2005, however, scientists uncovered a third squad — Th17 cells — that had been hiding the whole time among the ranks.
“Th17 cells are critical for fighting extracellular pathogens — yeast and certain bacterial infections — that largely live outside our cells, particularly on mucosal surfaces like in the mouth or GI tract,” said Dr. Jay Kolls, a professor of medicine and pediatrics at Tulane University, who wasn’t involved in the study.
What the scientists found
T-helper cells start contributing to disease when they become overactivated, which can be triggered by things like stress or natural substances like pollen and peanuts. This hyperactivity is ultimately how T-helper cells contribute to unnecessary inflammation and our allergies.
Overzealous T-helper cells become desperate to snitch on anything they can find — and they turn against other cells or proteins living in our bodies. That’s called autoimmunity.
Zielinski began wondering if salt might be a trigger for eczema after reading a famous German medical book written 100 years ago by pediatrician Heinrich Finkelstein. It was titled Lehrbuch der Sauglingskrankheiten or “The Textbook of Sickling Diseases.”
“According to [Finkelstein’s] personal observations, a salt-restricted diet leads to improvement of atopic dermatitis in children,” Zielinski said. “Atopic dermatitis” is the technical term for the chronic, allergy-version of eczema — which makes up nearly 60 percent of all eczema cases.
Zielinski’s lab began probing the link between salt and atopic dermatitis by extracting T-helper cells from the blood of healthy humans. T-helper cells circulate in the bloodstream as naive foot soldiers, until they encounter a trigger and join the appropriate squad — either Th1, Th2 or Th17.
When Zielinkski’s team exposed naive Th cells in a petri dish to high doses of sodium, the cells dove strongly toward a Th2 response. That’s important because Th2 responses “have been primarily implicated in allergic diseases, such as asthma and atopic dermatitis,” Kolls said.
But the salt doesn’t stop there — it continues to enhance inflammatory reactions even after the Th2 cells have matured. That may explain why researchers found patches of skin with high salt corresponded with eczema. Biopsies of eczema lesions contained 30 times the amount of salt relative to skin tissue removed from healthy subjects.
To a lesser degree, a portion of the naive T-helper cells also veered toward becoming Th17 — raising the specter of a Yale University study published six years ago on salt and another autoimmune disease: multiple sclerosis. That study found mice who were fed high-salt diets developed more severe brain inflammation in a model of multiple sclerosis. An overabundant Th17 response has also been implicated in psoriasis, another autoimmune disease.
Both Zielinski’s study on eczema and the Yale study on multiple sclerosis isolated one particular enzyme — called SGK1 — as being involved, which Kolls described as “interesting.” SGK1 is known to be a sensor for sodium levels inside of kidney cells, which keep tabs on salt levels pumping through our arteries and veins.
Zielinski said T-helper cells may be relying on SGK1 to monitor salt in organs like the skin or lymph nodes, because sodium levels there can be much higher than what passes through the mainstream blood circulation.
Why it matters
Dr. Emma Guttman-Yassky, director of the Center for Excellence in Eczema at the Icahn School of Medicine at Mount Sinai, said these new findings may matter the most for children.
“In atopic dermatitis [the allergy version of eczema], we’re mostly dealing with Th2,” Guttman-Yassky said. “But children have increased Th17 too,” or what she calls “Th2/Th17 skewed.”
That children have an increase in both types is noteworthy, not only because eczema tends to develop first in childhood, but because a leading and recently approved eczema drug — dupilumab — focuses primarily on preventing a Th2 response.
“It is a great drug, but it will only fully clear eczema in 40 percent of patients,” said Guttman-Yassky, who helped develop dupilumab. She said additional remedies will be needed to cover the full spectrum of T-helper responses involved with atopic eczema, which can also vary in adults. African adults with the skin disease skew toward Th2, while Asians have more Th17.
What does all of this mean for your diet? Zielinski, Kolls and Guttman-Yassky all said more evidence in living animals is needed to confirm this link between salt and autoimmune diseases, including eczema. Human cells, skin biopsies and rodent models are good proxies in the beginning, but future studies would need to put eczema patients on various diets to pinpoint how much salt is too much salt for our skin.
However, for an eczema patient who has run out of options, Kolls said a doctor could try recommending a low-sodium diet without much fear of bad consequences.
“If a patient had significant atopic dermatitis that’s been difficult to manage, a trial on a lower sodium diet is certainly not going to hurt,” Kolls said, citing how low sodium helps with conditions like hypertension and cardiovascular risks. “And it may benefit.”