One Way to Treat Asthma and Autoimmune Diseases with Diet

Cutting two teaspoons of salt’s worth of sodium from one’s daily diet can significantly improve lung function in asthmatics

In the 1960s and 1970s, a mystery was emerging. Why were childhood asthma rates between 2 to 5 percent in the developed world but as low as 0.007 percent in the developing world? For example, in the developing world, instead of 1 in 20 kids affected, or even 1 in 50 kids, it could be more like 1 in 10,000 kids—extremely rare. And, when kids moved from a low-risk area to a high-risk area, their risk went up. What was going on? Were they exposed to something new? Did they leave some protective factor behind?

As I discuss in my video How to Treat Asthma with a Low-Salt Diet, all the way back in 1938, scientists showed they could stop asthma attacks by lowering children’s sodium levels. That was done with a diuretic drug, but subsequent dietary experiments showed that diets high in salt seemed to increase asthmatic symptoms, while “lowering the salt decreased the asthmatic symptoms…” This body of evidence was apparently forgotten…until it was picked up again in the 1980s as a possible explanation for why Western countries had higher asthma rates.

Maybe it was the salt.

As you can see at 1:34 in my video, researchers graphed out childhood death from asthma versus family salt purchases, and it seemed more salt meant more death. Just because a family buys more salt doesn’t necessarily mean the kids are eating more, though. The way to find out how much salt someone is eating is to collect their urine over a 24-hour period and measure the amount of sodium, since how much salt we eat is pretty much how much salt we excrete. The way to test for asthma, called a bronchial challenge test, is to look for an exaggerated response to an inhaled chemical. And, indeed, there was a strong correlation between how their lungs reacted and how much sodium they were taking in. However, there are all sorts of food additives, like preservatives, that can trigger these so-called hypersensitivity reactions, so maybe high sodium intake was just a marker for high processed food intake. Maybe it wasn’t the salt at all.

Or maybe it was other components of the diet. For example, the reason sodium may be a risk factor for another inflammatory disease, rheumatoid arthritis, may be that sodium intake is just a marker for increased fish and other meat intake or decreased fruit and vegetable intake. We needed a study where researchers would take asthmatics, change the amount of salt in their diets, and see what happened—and that’s just what came next.

As you can see at 3:16 in my video, researchers doubled the salt intake of ten asthmatics, and lung sensitivity worsened in nine out of ten. There was no control group, though. Is it possible the subjects would have gotten worse anyway?

In a randomized, double-blind, placebo-controlled trial, researchers put everyone on a low-salt diet, but then gave half of the subjects sustained-release sodium pills to bring their salt intake back up to a more normal level and the other half a placebo. After five weeks, the groups switched regimes for another five weeks. That’s how you can randomize people to a true low-sodium diet without them even realizing it. Genius! So what happened? Asthmatics on the salt got worse. Their lung function got worse, their asthma symptoms got worse, and they had to take more puffs on their inhalers. This study compared asthmatics consuming about three teaspoons’ worth of salt a day to those consuming less than one, so they were effectively able to drop their sodium intake by two teaspoons’ worth of salt, as you can see at 4:04 in my video. If you do a more “pragmatic” trial and only effectively reduce people’s salt intake by a half a teaspoon a day, it doesn’t work.

Even if you are able to cut down your sodium intake enough to get a therapeutic effect, though, it should be considered an adjunct treatment. Do not stop your asthma medications without your doctor’s approval.

Millions suffer from asthma attacks triggered by exercise. Within five minutes of starting to exercise, people can get short of breath and start coughing and wheezing such that lung function significantly drops, as you can see at 0:19 in my video Sodium and Autoimmune Disease: Rubbing Salt in the Wound?. On a high-salt diet, however, the attack is even worse, whereas on a low-salt diet, there’s hardly a significant drop in function at all. To figure out why, researchers had the subjects cough up sputum from their lungs and found that those on the high-salt diet had triple the inflammatory cells and up to double the concentration of inflammatory mediators, as you can see at 0:43 in my video. But why? What does salt intake have to do with inflammation? We didn’t know…until now.

“The ‘Western diet,’ high in saturated fatty acids and salt, has long been postulated as one potential…cause for the increasing incidence of autoimmune diseases in developed countries…” The rapidly increasing incidence of autoimmune diseases may be due to an overactivation of immune cells called T helper 17 (Th17) cells. “The development of…multiple sclerosis, psoriasis, type I diabetes, Sjögren’s syndrome, asthma, and rheumatoid arthritis are all shown to involve Th17-driven inflammation,” and one trigger for the activation of those Th17 cells may be elevated levels of salt in our bloodstream. “The sodium content of processed foods and ‘fast foods’…can be more than 100 times higher in comparison to similar homemade meals.”

And, sodium chloride—salt—appears to drive autoimmune disease by the induction of these disease-causing Th17 cells. It turns out there is a salt-sensing enzyme responsible for triggering the formation of these Th17 cells, as you can see at 2:07 in my video.

Organ damage caused by high-salt diets may also activate another type of inflammatory immune cell. A high-salt diet can overwork the kidneys, starving them of oxygen and triggering inflammation, as you can see at 2:17 in my video. The more salt researchers gave people, the more activation of inflammatory monocyte cells, associated with high-salt intake induced kidney oxygen deficiency. But that study only lasted two weeks. What happens over the long term?

One of the difficulties in doing sodium experiments is that it’s hard to get free-living folks to maintain a specific salt intake. You can do so-called metabolic ward studies, where people are essentially locked in a hospital ward for a few days and their food intake is controlled, but you can’t do that long term—unless you can lock people in a space capsule. Mars520 was a 520-day space flight simulation to see how people might do on the way to Mars and back. As you can see at 3:17 in my video, the researchers found that those on a high-salt diet “displayed a markedly higher number of monocytes,” which are a type of immune cell you often see increased in settings of chronic inflammation and autoimmune disorders. This may “reveal one of the consequences of excess salt consumption in our everyday lives,” since that so-called high-salt intake may actually just be the average-salt intake. Furthermore, there was an increase in the levels of pro-inflammatory mediators and a decrease in the level of anti-inflammatory mediators, suggesting that a “high-salt diet had a potential to bring about an excessive immune response,” which may damage the immune balance, “resulting in either difficulties on getting rid of inflammation or even an increased risk of autoimmune disease.”

What if you already have an autoimmune disease? In the study titled “Sodium intake is associated with increased disease activity in multiple sclerosis,” researchers followed MS patients for a few years and found that those patients eating more salt had three to four times the exacerbation rate, were three times more likely to develop new MS lesions in their brains, and, on average, had 8 more lesions in their brain—14 lesions compared to 6 in the low-salt group. The next step is to try treating patients with salt reduction to see if they get better. But, since reducing our salt intake is a healthy thing to do anyway, I don’t see why we have to wait.


What else can we do for asthma? See:

Have you heard that salt reduction was controversial? That’s what the processed food industry wants you to think. Check out the science in:

What are some of the most powerful dietary interventions we have for autoimmune disease? See, for example:

In health,

Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations:

How to Prevent the Infection that May Trigger Type 1 Diabetes

The compelling finding of Mycobacterium avium paratuberculosis (MAP) circulating disproportionately within the bloodstream of type 1 diabetics was subsequently confirmed by culturing it straight out of their blood. MAP infection and type 1 diabetes appear to go together, but we didn’t know which came first. Does the infection make kids more susceptible to diabetes? Might diabetes make kids more susceptible to infection? Maybe this MAP bug just likes hanging out in sugary blood. In that case, we might expect to also see it in type 2 diabetics, but, no: Paratuberculosis infection is not associated with type 2 diabetes, which makes sense since type 2 is not an autoimmune disease.

In order for the idea of MAP infection triggering type 1 diabetes to be sound, there would have to be an immune response mounted to the bug, and, indeed, there is. Researchers in Sardinia found an “extremely significant” antibody response against paratuberculosis (paraTB) bacteria in type 1 diabetics. But do the antibodies attacking the bug cross-react with our own insulin-producing cells to generate that autoimmune reaction? Apparently so. Antibodies recognizing the molecular signatures of MAP cross-react with the molecular signatures present on our insulin-producing beta cells in the pancreas, as you can see at 1:09 in my video Does Paratuberculosis in Meat Trigger Type 1 Diabetes?.

Is this just in Sardinia, or might we find these same results elsewhere? The same results were in fact found on mainland Italy with a group of type 1 diabetics “with a genetic background different from Sardinians”—a strong association between paraTB bacteria exposure and type 1 diabetes. The findings were confirmed in further studies, confirmed once more in other pediatric populations, and confirmed in a group of type 1 diabetic adults, as well.

The paratuberculosis bacterium may also explain why type 1 diabetes risk is associated with a specific gene on chromosome 2 called SLC11A1. What does that gene do? SLC11A1 activates the immune cell that eats mycobacteria for breakfast. This could explain how a mutation in that gene could increase the susceptibility to type 1 diabetes—namely, by increasing the susceptibility to mycobacterial infections, like Mycobacterium avium paratuberculosis. Indeed, an “[a]ccumulating line of evidence points…[to] MAP in the development of T1DM [type 1 diabetes] as an environmental trigger.” It’s likely no coincidence. These types of bacteria have evolved to disguise themselves to look like human proteins for the express purpose of avoiding detection by our immune system. These are not the droids you’re looking for. If, however, our immune system sees through the disguise and starts attacking the bacteria, our similar-looking proteins can become a victim of friendly fire, which is what nearly all of these studies have been pointing to. Nearly, but not all.

A 2015 review found that seven out of seven human studies found an association between type 1 diabetes and paratuberculosis exposure, but it’s actually seven out of eight. Since that review came out, a study in India was published finding no link. A few possible explanations were offered. Maybe it’s because vaccination for regular TB is compulsory in India, which might offer “cross protection from MAP as in case of leprosy,” or because they eat so much less meat due to “certain cultural and culinary practices such as widespread vegetarianism,” or because of their “compulsory boiling of milk before consumption…” If we measure the heat inactivation of milk with high concentrations of naturally infected feces, which is probably the main source of milk contamination, pasteurization may not completely inactivate the bacteria, but sterilization at boiling temperatures should (as you can see at 3:40 in my video). This may depend on the degree of fecal clumping, though. MAP bacteria may be able to ride out pasteurization by hiding in tiny fecal clumps in milk, but only rarely should MAP survive over 100 degrees Celsius, perhaps explaining the disparate India findings. 

Bottom line: “To reduce human exposure to MAP via consumption of dairy and meat products…[more] studies are needed for estimating the amount of MAP” in milk, meat, and feces, as well as “the amount of faecal contamination of milk and carcasses [meat]” to figure out what we need to do to kill it. In the meanwhile, what’s the potential public health impact of Mycobacterium avium paratuberculosis? The majority of specialists in the field agree that it “is likely a risk to human health” and should be “a high- or medium-priority…public health issue.” 


I started speaking out about the link between human disease and paratuberculosis infection in milk and meat 15 years ago. As cynical as I can be at times, even I am shocked that the industry hasn’t done more to clean up its act. It reminds me of the bovine leukemia virus story. See:

If you missed the first two installments in this series, check out Does Paratuberculosis in Milk Trigger Type 1 Diabetes? and Meat Consumption and the Development of Type 1 Diabetes.

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations:

The Role of Meat and Dairy in Triggering Type 1 Diabetes

Type 1 diabetes “arises following the autoimmune destruction of the insulin-producing pancreatic β [beta] cells…[and] is most often diagnosed in children and adolescents, usually presenting with a classic trio of symptoms” as their blood sugars spike: excessive thirst, hunger, and urination. They need to go on insulin for the rest of their lives, since their own immune systems attacked and destroyed their ability to produce it. What would cause our body to do such a thing? I examine this in my video, Does Paratuberculosis in Milk Trigger Type 1 Diabetes?

Whatever it is, it has been on the rise around the world, starting after World War 2. “Understanding why and how this produced the current pandemic of childhood diabetes would be an important step toward reversing it.” A plausible guess is “molecular mimicry, whereby a foreign antigen (bacterial or viral) provokes an immune response, which cross-reacts” with a similar-looking protein on our pancreas such that when we attack the bug, our own organ gets caught in the cross-fire. Given this, what pancreatic proteins are type 1 diabetics self-attacking? In the 1980s, a protein was identified that we came to realize in the 1990s looked an awful lot like a certain mycobacterial protein. Mycobacteria are a family of bacteria that cause diseases like tuberculosis and leprosy, and, in one study, all newly diagnosed type 1 diabetic children were found to have immune responses to this mycobacterial protein. This didn’t make any sense as incidence of type 1 diabetes has been going up in the industrialized world, whereas TB and leprosy rates have gone down. However, there is one mycobacterial infection in farm animals that has shot up with the industrialization and globalization of animal agriculture: paratuberculosis (paraTB), which causes Johne’s disease in animals. Paratuberculosis is now recognized as a global problem for the livestock industry.

Weren’t there a dozen or so studies suggesting that “cow’s milk exposure may be an important determinant of subsequent type 1 diabetes” in childhood? Indeed. After putting two and two together, an idea was put forward in 2006: Could mycobacterium paratuberculosis from cattle be a trigger for type 1 diabetes? The idea was compelling enough for researchers put it to the test.

They attempted to test the association of Mycobacterium avium paratuberculosis (MAP), the full name for the bug, with type 1 diabetes by testing diabetics for the presence of the bacteria in their blood. Lo and behold, most of the diabetic patients tested positive for the bug, compared to only a minority of the healthy control subjects. This evidence of MAP bacteria in the blood of patients with type 1 diabetes “might provide an important foundation in establishing an infectious etiology,” or cause, for type 1 diabetes. “These results also might possibly have implications for countries that have the greatest livestock populations and high incidence of MAP concurrent with the highest numbers of patients with” diabetes, like the United States.

Johne’s is the name of the disease when farm animals get infected by MAP. The reason diabetes researchers chose to look at Sardinia, an island off the coast of Italy, is because paratuberculosis is present in more than 50 percent of Sardinian herds. Surpassing that, though, is the U.S. dairy herd. According to a recent national survey, 68 percent of the U.S. dairy herd are infected with MAP, especially those cattle at big, industrial dairies, as you can see at 3:33 in my video. Ninety-five percent of operations with more than 500 cows came up positive. It’s estimated the disease costs the U.S. industry more than a billion dollars a year.

How do people become exposed? “The most important routes of access of MAP to the [human] food chain appear to be contaminated milk, milk products and meat” from infected cattle, sheep, and goats. MAP or MAP DNA has been detected in raw milk, pasteurized milk, infant formula, cheese, ice cream, muscle and organ tissues, and retail meat. We know paraTB bacteria survive pasteurization because Wisconsin researchers bought hundreds of pints of retail milk off store shelves from three of the top U.S. milk-producing states and tested for the presence of viable, meaning living, MAP bacteria. They found that 2.8 percent of the retail milk tested came back positive for live paraTB bacteria, with most brands yielding at least one positive sample. If paraTB does end up being a diabetes trigger, then “these findings indicate that retail milk [in the United States] would need to be considered as a transmission vector.” Why hasn’t the public heard about this research? Perhaps because the industry is not too keen on sharing it. Indeed, according to an article in the Journal of Dairy Science: “Fear of consumer reaction…can impede rational, open discussion of scientific studies.”

Not only is MAP a serious problem for the global livestock industry, but it also may trigger type 1 diabetes, given that paraTB bacteria have been found in the bloodstream of the majority of type 1 diabetics tested who presumably are exposed through the retail milk supply as the bacteria can survive pasteurization. But what about the meat supply? MAP has been found in beef, pork, and chicken. It’s an intestinal bug, and unfortunately, “[f]aecal contamination of the carcass in the abattoir [slaughter plant] is unavoidable…” Then, unless the meat is cooked well-done, it could harbor living MAP.

In terms of meat, “ground beef represents the greatest potential risk for harboring MAP…[as] a significant proportion originates from culled dairy cattle,” who may be culled because they have paratuberculosis. These animals may go straight into the human food chain. There also exists greater prevalence of fecal contamination and lymph nodes in ground meat, and the grinding can force the bacteria deep inside the ground beef burger. As such, “given the weight of evidence and the severity and magnitude of potential human health problems, the precautionary principle suggests that it is time to take actions to limit…human exposure to MAP.” At the very least, we should stop funneling animals known to be infected into the human food supply.

We know that milk exposure is associated with type 1 diabetes, but what about meat? As I discuss in my video Meat Consumption and the Development of Types 1 Diabetes, researchers attempted to tease out the nutritional factors that could help account for the 350-fold variation in type 1 diabetes rates around the world. Why do some parts of the world have rates hundreds of times higher than others? Yes, the more dairy populations ate, the higher their rates of childhood type 1 diabetes, but the same was found for meat, as you can see at 2:07 in my video. This gave “credibility to the speculation that the increasing dietary supply of animal protein after World War II may have contributed to the reported increasing incidence of type 1 diabetes…” Additionally, there was a negative correlation—that is, a protective correlation that you can see at 2:26 in my video—between the intake of grains and type 1 diabetes, which “may fit within the more general context of a lower prevalence of chronic diseases” among those eating more plant-based diets.

What’s more, the increase in meat consumption over time appeared to parallel the increasing incidence of type 1 diabetes. Now, we always need to be cautious about the interpretation of country-by-country comparisons. Just because a country eats a particular way doesn’t mean the individuals who get the disease ate that way. For example, a similar study looking specifically at the diets of children and adolescents between different countries “support[ed] previous research about the importance of cow’s milk and [other] animal products” in causing type 1 diabetes. But, the researchers also found that in countries where they tended to eat the most sugar, kids tended to have lower rates of the disease, as you can see at 3:18 in my video. This finding didn’t reach statistical significance since there were so few countries examined in the study, but, even if it had and even if there were other studies to back it up, there are countless factors that could be going on. Maybe in countries where people ate the least sugar, they also ate the most high fructose corn syrup or something. That’s why you always need to put it to the test. When the diets of people who actually got the disease were analyzed, increased risk of type 1 diabetes was associated with milk, sugar, bread, soda, eggs, and meat consumption.

In Sardinia, where the original link was made between paraTB and type 1 diabetes, a highly “statistically significant dose-response relationship” was found, meaning more meat meant more risk, especially during the first two years of children’s lives. So, “[h]igh meat consumption seems to be an important early in life cofactor for type 1 diabetes development,” although we needed more data.

The latest such study, which followed thousands of mother-child pairs, found that mothers eating meat during breastfeeding was associated with an increased risk of both preclinical and full-blown, clinical type 1 diabetes by the time their children reached age eight. The researchers thought it might be the glycotoxins, the AGEs found in cooked meat, which can be transferred from mother to child through breastfeeding, but they have learned that paratuberculosis bacteria can also be transferred through human breast milk. These bacteria have even been grown from the breast milk of women with Crohn’s disease, another autoimmune disease linked to paraTB bacteria exposure.


For a deeper discussion of other possibilities as to why cow’s milk consumption is linked to this autoimmune destruction of insulin production, see Does Casein in Milk Trigger Type 1 Diabetes? and Does Bovine Insulin in Milk Trigger Type 1 Diabetes?.

If we don’t drink milk, though, what about our bone health? See my videos Long-Term Vegan Bone Health and Is Milk Good for Our Bones?.

The vast majority of cases of diabetes in the United States are type 2, though. Ironically, meat may also play a role there. See my videos Why Is Meat a Risk Factor for Diabetes? and How May Plants Protect Against Diabetes? for more information.

For more on the links between milk and diabetes, see my videos Does Casein in Milk Trigger Type 1 Diabetes? and Does Bovine Insulin in Milk Trigger Diabetes?. What about treating and preventing diabetes through diet? Check out How Not to Die from Diabetes and How to Prevent Prediabetes from Turning Into Diabetes.

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations: