Is White Rice a Yellow-Light or Red-Light Food?

Arsenic is not just considered to be a carcinogen; it’s also designated as a “nonthreshold carcinogen, meaning that any dose, no matter how small, carries some cancer risk”—so there really isn’t a “safe” level of exposure. Given that, it may be reasonable to “use the conservative ALARA” approach, reducing exposure As Low As Reasonably Achievable.

I have a low bar for recommending people avoid foods that aren’t particularly health-promoting in the first place. Remember when that acrylamide story broke, about the chemical found concentrated in french fries and potato chips? (See my video Acrylamide in French Fries for more.) My take was pretty simple: Look, we’re not sure how bad this acrylamide stuff is, but we’re talking about french fries and potato chips, which are not healthy anyway. So, I had no problem provisionally bumping them from my list of yellow-light foods into my red-light list, from “minimize consumption” to “ideally avoid on a day-to-day basis.”

One could apply the same logic here. Junk foods made out of brown rice syrup, rice milk, and white rice are not just processed foods, but also arsenic-contaminated processed foods, so they may belong in the red zone as red-light foods we should avoid. What about something like whole brown rice? That is more difficult, because there are pros to help outweigh the cons. I discuss this in my video Is White Rice a Yellow-Light or Red-Light Food?, where you can see a graphical depiction of my traffic light food system at 0:49.

The rice industry argues that the “many health benefits of rice consumption outweigh any potential risk,” which is the same sentiment you hear coming out of Japan about the arsenic-contaminated seaweed hijiki: Yes, “the cancer risk posed by hijiki consumption exceeds this acceptable [cancer risk] level by a factor of 10,” an order of magnitude, but the Japanese Ministry of Health stresses the “possible health benefits,” such as lots of fiber and minerals, as if hijiki was the only weed in the sea. Why not choose any of the other seaweeds and get all the benefits without the arsenic? So, when the rice industry says the “many health benefits of rice consumption outweigh any potential risk,” it’s as if brown rice was the only whole grain on the planet. Can’t you get the whole grain benefits without the risks by eating oatmeal, barley, or quinoa instead? Or, is there some unique benefit to rice, such that we really should try to keep brown rice in our diet?

Consumer Reports recommended moving rice to the yellow-light zone—in other words, don’t necessarily avoid it completely, but moderate your intake. The rice industry, in a fact sheet entitled “The Consumer Reports Article is Flawed,” criticized Consumer Reports for warning people about the arsenic levels in rice, saying “[t]here is a body of scientific evidence that establishes…the nutritional benefits of rice consumption; any assessment of the arsenic levels in rice that fails to take this information into account is inherently flawed and very misleading.” The rice industry cites two pieces of evidence. First, it asserts that rice-consuming cultures tend to be healthier, but is that because of, or despite, their white rice consumption? And what about the fact that rice-eating Americans tend to be healthier? Perhaps, but they also tend to eat significantly less saturated fat. So, once again, how do we know whether it’s because of—or despite—the white rice?

The rice industry could have cited the study I discuss at 3:12 in my video that showed that brown rice intake of two or more servings a week was associated with a lower risk of diabetes, but presumably, the reason it didn’t is because intake of white rice is associated with an increased risk of diabetes, and white rice represents 95 percent of the U.S. rice industry. Switching out a third of a serving of white rice a day for brown rice might lower diabetes risk by 16 percent, but switching out that same white rice for whole grains in general, like oats or barley, might work even better! So, other grains have about ten times less arsenic and are associated with even lower disease risk. No wonder the rice industry doesn’t cite this study.

It does cite the Adventist studies, though, and some in vitro data. For example, in a petri dish, as you can see at 4:05 in my video, there are rice phytonutrients that, at greater and greater doses, can inhibit the growth of colon cancer cells while apparently leaving normal colon cells alone, which is exciting. And, indeed, those who happened to eat those phytonutrients in the form of brown rice once or more a week between colonoscopies had a 40 percent lower risk of developing polyps. (The consumption of green leafy vegetables, dried fruit, and beans were also associated with lower polyp incidence.) But, the only reason we care about the development of polyps is that polyps can turn into cancer. But, there had never been studies on brown rice consumption and cancer…until now, which I discuss in my video Do the Pros of Brown Rice Outweigh the Cons of Arsenic?.


For those unfamiliar with my traffic light system, I talk about it in my book trailer. Check out How Not to Die: An Animated Summary.

Almost there! This is the corresponding article to the 12th in my 13-video series on arsenic in the food supply. If you missed any of the first 11 videos, see:

Ready for the finale? See Do the Pros of Brown Rice Outweigh the Cons of Arsenic?.

And you may be interested in Benefits of Turmeric for Arsenic Exposure.

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:

What White Blood Cell Count Should We Shoot for?

At the start of my video What Does a Low White Blood Cell Count Mean?, you can see what it looks like when you take a drop of blood, smear it between two pieces of glass, and view at it under a microscope: a whole bunch of little, round, red blood cells and a few big, white blood cells. Red blood cells carry oxygen, while white blood cells are our immune system’s foot soldiers. We may churn out 50 billion new white blood cells a day. In response to inflammation or infection, that number can shoot up to a 100 billion or more. In fact, pus is largely composed of: millions and millions of white blood cells.

Testing to find out how many white blood cells we have at any given time is one of the most common laboratory tests doctors order. It’s ordered it hundreds of millions of times a year. If, for example, you end up in the emergency room with abdominal pain, having a white blood cell count above about 10 billion per quart of blood may be a sign you have appendicitis. Most Americans fall between 4.5 and 10, but most Americans are unhealthy. Just because 4.5 to 10 is typical doesn’t mean it’s ideal. It’s like having a “normal” cholesterol level in a society where it’s normal to die of heart disease, our number-one killer. The average American is overweight, so if your weight is “normal,” that’s actually a bad thing.

In fact, having excess fat itself causes inflammation within the body, so it’s no surprise that those who are obese walk around with two billion more white cells per quart of blood. Given that, perhaps obese individuals should have their own “normal” values. As you can see at 2:06 in my video, if someone with a 47-inch waist walks into the ER with a white blood cell count of 12, 13, or even 14, they may not have appendicitis or an infection. That may just be their normal baseline level, given all the inflammation they have in their body from the excess fat. So, normal levels are not necessarily healthy levels.

It’s like smoking. As you can see at 2:31 in my video, if you test identical twins and one smokes but the other doesn’t, the smoker is going to end up with a significantly higher white cell count. In Japan, for example, as smoking rates have steadily dropped, so has the normal white count range. In fact, it’s dropped such that about 8 percent of men who have never smoked would now be flagged as having abnormally low white counts if you used a cut-off of 4. But, when that cut-off of 4 was set, most people were smoking. So, maybe 3 would be a better lower limit. The inflammation caused by smoking may actually be one of the reasons cigarettes increase the risk of heart attacks, strokes, and other inflammatory diseases. So, do people who have lower white counts have less heart disease, cancer, and overall mortality? Yes, yes, and yes. People with lower white blood cell counts live longer. Even within the normal range, every one point drop may be associated with a 20 percent drop in the risk of premature death.

As you can see at 3:39 in my video, there is an exponential increase in risk in men as white count goes up, even within the so-called normal range, and the same is found for women. The white blood cell count is a “stable, well-standardized, widely available and inexpensive measure of systemic inflammation.” In one study, half of the women around 85 years of age who had started out with white counts under 5.6 were still alive, whereas 80 percent of those who started out over 7 were dead, as you can see at 4:05 in my video—and white blood cell counts of 7, 8, 9, or even 10 would be considered normal. Being at the high end of the normal range may place one at three times the risk of dying from heart disease compared to being at the lower end.

The same link has been found for African-American men and women, found for those in middle age, found at age 75, found at age 85, and found even in our 20s and 30s: a 17 percent increase in coronary artery disease incidence for each single point higher.

As you can see at 5:00 in my video, the higher your white count, the worse your arterial function may be and the stiffer your arteries may be, so it’s no wonder white blood cell count is a useful predictor of high blood pressure and artery disease in your heart, brain, legs, and neck. Even diabetes? Yes, even diabetes, based on a compilation of 20 different studies. In fact, it may be associated with everything from fatty liver disease to having an enlarged prostate. And, having a higher white blood cell count is also associated with an increased risk of dying from cancer. So, what would the ideal range be? I cover that in my video What Is the Ideal White Blood Cell Count?.

A higher white blood cell count may be an important predictor for cardiovascular disease incidence and mortality, decline in lung function, cancer mortality, all-cause mortality, heart attacks, strokes, and premature death in general. This is no surprise, as the number of white blood cells we have circulating in our bloodstreams are a marker of systemic inflammation. Our bodies produce more white blood cells day to day in response to inflammatory insults.

We’ve known about this link between higher white counts and heart attacks since the 1970s, when we found that higher heart attack risk was associated with higher white blood cell counts, higher cholesterol levels, and higher blood pressures, as you can see at 0:53 in my video What Is the Ideal White Blood Cell Count?. This has been found in nearly every study done since then. There are decades of studies involving hundreds of thousands of patients showing dramatically higher mortality rates in those with higher white counts. But why? Why does white blood cell count predict mortality? It may be because it’s a marker of inflammation and oxidation in the body. In fact, it may even be a biomarker for how fast we are aging. It may be more than just an indicator of inflammation—it may also be an active player, contributing directly to disease via a variety of mechanisms, including the actual obstruction of blood flow.

The average diameter of a white blood cell is about seven and a half micrometers, whereas our tiniest vessels are only about five micrometers wide, so the white blood cell has to squish down into a sausage shape in order to squeeze through. When there’s inflammation present, these cells can get sticky. As you can see at 2:20 in my video, a white blood cell may plug up a vessel as it exits a small artery and tries to squeeze into a capillary, slowing down or even momentarily stopping blood flow. And, if it gets stuck there, it can end up releasing all of its internal weaponry, which is normally reserved for microbial invaders, and damage our blood vessels. This may be why in the days leading up to a stroke or heart attack, you may find a spike in the white cell count.

Whether white count is just a marker of inflammation or an active participant, it’s better to be on the low side. How can we reduce the level of inflammation in our body? Staying away from even second-hand smoke can help drop your white count about half of a point. Those who exercise also appear to have an advantage, but you don’t know if it’s cause and effect unless you put it to the test. In one study, two months of Zumba classes—just one or two hours a week—led to about a point and a half drop in white count. In fact, that may be one of the reasons exercise is so protective. But is that just because they lost weight?

Fitness and fatness both appear to play a role. More than half of obese persons with low fitness—51.5 percent—have white counts above 6.6, but those who are more fit or who have less fat are less likely to have counts that high, as you can see at 3:47 in my video. Of course, that could just be because exercisers and leaner individuals are eating healthier, less inflammatory diets. How do we know excess body fat itself increases inflammation, increases the white count? You’d have to find some way to get people to lose weight without changing their diet or exercise habit. How’s that possible? Liposuction. If you suck about a quart of fat out of people, you can significantly drop their white count by about a point. Perhaps this should get us to rethink the so-called normal reference range for white blood cell counts. Indeed, maybe we should revise it downward, like we’ve done for cholesterol and triglycerides.

Until now, we’ve based normal values on people who might be harboring significant background inflammatory disease. But, if we restrict it to those with normal C-reactive protein, another indicator of inflammation, then instead of “normal” being 4.5 to 10, perhaps we should revise it closer to 3 to 9.

Where do the healthiest populations fall, those not suffering from the ravages of chronic inflammatory diseases, like heart disease and common cancers? Populations eating diets centered around whole plant foods average about 5, whereas it was closer to 7 or 8 in the United States at the time. How do we know it isn’t just genetic? As you can see at 5:38 in my video, if you take those living on traditional rural African diets, who have white blood cell counts down around 4 or 5, and move them to Britain, they end up closer to 6, 7, or even 8. Ironically, the researchers thought this was a good thing, referring to the lower white counts on the “uncivilized” diet as neutropenic, meaning having too few white blood cells. They noted that during an infection or pregnancy, when more white cells are needed, the white count came right up to wherever was necessary. So, the bone marrow of those eating traditional plant-based diets had the capacity to create as many white cells as needed but “suffers from understimulation.”

As you can see at 6:26 in my video, similar findings were reported in Western plant eaters, with an apparent stepwise drop in white count as diets got more and more plant based, but could there be non-dietary factors, such as lower smoking rates, in those eating more healthfully? What we need is an interventional trial to put it to the test, and we got one: Just 21 days of removing meat, eggs, dairy, alcohol, and junk affected a significant drop in white count, even in people who started out down at 5.7.

What about patients with rheumatoid arthritis who started out even higher, up around 7? As you can see at 7:03 in my video, there was no change in the control group who didn’t change their diet, but there was a 1.5 point drop within one month on whole food plant-based nutrition. That’s a 20 percent drop. That’s more than the drop-in inflammation one might get quitting a 28-year pack-a-day smoking habit. The most extraordinary drop I’ve seen was in a study of 35 asthmatics. After four months of a whole food plant-based diet, their average white count dropped nearly 60 percent, from around 12 down to 5, though there was no control group nor enough patients to achieve statistical significance.

If white blood cell count is such a clear predictor of mortality and is so inexpensive, reliable, and available, why isn’t it used more often for diagnosis and prognosis? Maybe it’s a little too inexpensive. The industry seems more interested in fancy new risk factors it can bill for.

I touch on the health of the rural Africans I discussed in How Not to Die from Heart Disease.


For more on fighting inflammation, see:

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:

What Exercise Authorities Don’t Tell You About Optimal Duration

Physical fitness authorities seem to have fallen into the same trap as the nutrition authorities, recommending what they think may be achievable, rather than simply informing us of what the science says and letting us make up our own minds.

Researchers who accept grants from The Coca-Cola Company may call physical inactivity “the biggest public health problem of the 21st century,” but, in actually, physical inactivity ranks down at number five in terms of risk factors for death in the United States and even lower in terms of risk factors for disability, as you can see at 0:17 in my video How Much Should You Exercise? What’s more, inactivity barely makes the top ten globally. As we’ve learned, diet is our greatest killer by far, followed by smoking.

Of course, that doesn’t mean you can just sit on the couch all day. Exercise can help with mental health, cognitive health, sleep quality, cancer prevention, immune function, high blood pressure, and life span extension, topics I cover in some of my other videos. If the U.S. population collectively exercised enough to shave just 1 percent off the national body mass index, 2 million cases of diabetes, one and a half million cases of heart disease and stroke, and 100,000 cases of cancer might be prevented.

Ideally, how much should we exercise? The latest official “Physical Activity Guidelines for Americans” recommends adults get at least 150 minutes a week of moderate aerobic exercise, which comes out to be a little more than 20 minutes a day. That is actually down from previous recommendations from the Surgeon General, as well as from the Centers for Disease Control and Prevention (CDC) and the American College of Sports Medicine, which jointly recommend at least 30 minutes each day. The exercise authorities seem to have fallen into the same trap as the nutrition authorities, recommending what they think may be achievable, rather than simply informing us what the science says and letting us make up our own minds. They already emphasize that “some” physical activity “is better than none,” so why not stop patronizing the public and just tell everyone the truth?

As you can see at 2:16 in my video, walking 150 minutes a week is better than walking 60 minutes a week, and following the current recommendations for 150 minutes appears to reduce your overall mortality rate by 7 percent compared with being sedentary. Walking for just 60 minutes a week only drops your mortality rate about 3 percent, but walking 300 minutes weekly lowers overall mortality by 14 percent. So, walking twice as long—40 minutes a day compared with the recommended 20 daily minutes—yields twice the benefit. And, an hour-long walk each day may reduce mortality by 24 percent. I use walking as an example because it’s an exercise nearly everyone can do, but the same applies to other moderate-intensity activities, such as gardening or cycling.

A meta-analysis of physical activity dose and longevity found that the equivalent of about an hour a day of brisk walking at four miles per hour was good, but 90 minutes was even better. What about more than 90 minutes? Unfortunately, so few people exercise that much every day that there weren’t enough studies to compile a higher category. If we know 90 minutes of exercise a day is better than 60 minutes, which is better than 30 minutes, why is the recommendation only 20 minutes? I understand that only about half of Americans even make the recommended 20 daily minutes, so the authorities are just hoping to nudge people in the right direction. It’s like the Dietary Guidelines for Americans advising us to “eat less…candy.” If only they’d just give it to us straight. That’s what I try to do with NutritionFacts.org.

Most of the content in my book How Not to Die came from my video research, but this particular video actually sprung from the book. I wanted to include exercise in my Daily Dozen list, but needed to do this research to see what was the best “serving size.”

I wish someone would start some kind of FitnessFacts.org website to review the exercise literature. I’ve got my brain full with the nutrition stuff—though there’s so much good information I don’t have time to review that there could be ten more sites just covering nutritional science!


For more on all that exercise can do for our bodies and minds, see

Some tips for maximizing the benefits:

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:

What Happens if You Have Red Wine or Avocados with a Meal?

Whole plant sources of sugar and fat can ameliorate some of the postprandial (after meal) inflammation caused by the consumption of refined carbohydrates and meat.

Studies have shown how adding even steamed skinless chicken breast can exacerbate the insulin spike from white rice, but fish may be worse. At 0:18 in my video The Effects of Avocados and Red Wine on Meal-Induced Inflammation, you can see how the insulin scores of a low-carbohydrate plant food, peanuts, is lower compared to common low-carb animal foods—eggs, cheese, and beef. Fish was even worse, with an insulin score closer to doughnut territory.

At 0:36 in my video, you can see the insulin spike when people are fed mashed white potatoes. What do you think happens when they’re also given tuna fish? Twice the insulin spike. The same is seen with white flour spaghetti versus white flour spaghetti with meat. The addition of animal protein may make the pancreas work twice as hard.

You can do it with straight sugar water, too. If you perform a glucose challenge to test for diabetes, drinking a certain amount of sugar, at 1:10 in my video, you can see the kind of spike in insulin you get. But, if you take in the exact same amount of sugar but with some meat added, you get a higher spike. And, as you can see at 1:25 in my video, the more meat you add, the worse it gets. Just adding a little meat to carbs doesn’t seem to do much, but once you get up to around a third of a chicken’s breast worth, you can elicit a significantly increased surge of insulin.

So, a chicken sandwich may aggravate the metabolic harm of the refined carb white bread it’s on, but what about a PB&J? At 1:49 in my video, you can see that adding nuts to Wonder Bread actually calms the insulin and blood sugar response. What if, instead of nuts, you smeared on an all fruit strawberry jam? Berries, which have even more antioxidants than nuts, can squelch the oxidation of cholesterol in response to a typical American breakfast and even reduce the amount of fat in your blood after the meal. And, with less oxidation, there is less inflammation when berries are added to a meal.

So, a whole plant food source of sugar can decrease inflammation in response to an “inflammatory stressor” meal, but what about a whole plant food source of fat? As you can see at 2:38 in my video, within hours of eating a burger topped with half an avocado, the level of an inflammatory biomarker goes up in your blood, but not as high as eating the burger without the avocado. This may be because all whole plant foods contain antioxidants, which decrease inflammation, and also contain fiber, which is one reason even high fat whole plant foods like nuts can lower cholesterol. And, the same could be said for avocados. At 3:12 in my video, you can see avocado causing a significant drop in cholesterol levels, especially in those with high cholesterol, with even a drop in triglycerides.

If eating berries with a meal decreases inflammation, what about drinking berries? Sipping wine with your white bread significantly blunts the blood sugar spike from the bread, but the alcohol increases the fat in the blood by about the same amount. As you can see at 3:40 in my video, you’ll get a triglycerides bump when you eat some cheese and crackers, but if you sip some wine with the same snack, triglycerides shoot through the roof. How do we know it was the alcohol? Because if you use dealcoholized red wine, the same wine but with the alcohol removed, you don’t get the same reaction. This has been shown in about a half dozen other studies, along with an increase in inflammatory markers. So, the dealcoholized red wine helps in some ways but not others.

A similar paradoxical effect was found with exercise. If people cycle at high intensity for about an hour a half-day before drinking a milkshake, the triglycerides response is less than without the prior exercise, yet the inflammatory response to the meal appeared worse, as you can see at 4:18 in my video. The bottom line is not to avoid exercise but to avoid milkshakes.

The healthiest approach is a whole food, plant-based diet, but there are “promising pharmacologic approaches to the normalization” of high blood sugars and fat by taking medications. “However, resorting to drug therapy for an epidemic caused by a maladaptive diet is less rational than simply realigning our eating habits with our physiological needs.”

Protein from meat can cause more of an insulin spike than pure table sugar. See the comparisons in my video Paleo Diets May Negate Benefits of Exercise.

Interested in more information on the almond butter study I mentioned? I discuss it further in How to Prevent Blood Sugar and Triglyceride Spikes After Meals.

Berries have their own sugar, so how can eating berries lower the blood sugar spike after a meal? Find out in If Fructose Is Bad, What About Fruit?


For more on avocados, check out:

And here are more videos on red wine:

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:

Are the BPA-Free Plastics Like Tritan Safe?

Do BPA-free plastics such as Tritan, have human hormone-disrupting effects? And what about BPS and BPF?

Recent human studies indicate that exposure to the plastics chemical BPA may be associated with infertility, miscarriage, premature delivery, reduced male sexual function, polycystic ovaries, altered thyroid and immune function, diabetes, heart disease, and more. Yet, “[a]s recently as March 2012, FDA stated that low levels of BPA in food are considered safe.” However, just months later, to its credit, the agency banned the use of BPA plastics in baby bottles and sippy cups. Regulators standing up to industry? Maybe I shouldn’t be so cynical! But, wait. The ban was at the behest of the plastics industry. It had already stopped using BPA in baby bottles so it was their idea to ban it.

The industry had switched from BPA to similar compounds like BPF and BPS. So, our diets now contain everything from BPA to BPZ, and the majority of us have these new chemicals in our bodies as well. Are they any safer?

As I discuss in my video Are the BPA-Free Alternatives Safe?, based on the similarities of their chemical structures, they are all predicted to affect testosterone production and estrogen receptor activity, as you can see at 1:40 in my video. However, they were only recently put to the test.

As you can see at 1:50 in my video, we’ve known BPA significantly suppresses testosterone production, and, from “the first report describing BPS and BPF adverse effects on physiologic function in humans,” we know those compounds do, too. Well, kind of. The experiments were performed on the testicles of aborted human fetuses. But, the bottom line is that BPS and BPF seem to have “antiandrogenic anti-male hormone effects that are similar to those of BPA.” So when you’re assured you shouldn’t worry because your sales slip is BPA-free, the thermal paper may just contain BPS instead. What’s more, BPS receipts may contain up to 40 percent more BPS than they would have contained BPA. So BPA-free could be even worse. In fact, all BPA-replacement products tested to date released “chemicals having reliably detectable EA,” estrogenic activity.

This includes Tritan, which is specifically marketed as being estrogen-activity-free. As you can see at 3:06 in my video, however, researchers dripped an extract of Tritan on human breast cancer cells in a petri dish, and it accelerated their growth. This estrogenic effect was successfully abolished by an estrogen blocker, reinforcing it was an estrogen effect. Now, the accelerated growth of the cancer cells from the Tritan extract occurred after the plastic was exposed to the stressed state of simulated sunlight. Only one out of three Tritan products showed estrogen activity in an unstressed state, for instance when they weren’t exposed to microwaving, heat, or UV rays. “Because there would be no value in trading one health hazard for another, we should urgently focus on the human health risk assessment of BPA substitutes.”

In the meanwhile, there are steps we can take to limit our exposure. We can reduce our use of polycarbonate plastics, which are usually labeled with recycle codes three or seven, and we can opt for fresh and frozen foods over canned goods, especially when it comes to tuna and condensed soups. Canned fruit consumption doesn’t seem to matter, but weekly canned vegetable consumption has been associated with increased BPA exposure. If you do use plastics, don’t microwave them, put them in the dishwasher, leave them in the sun or a hot car, or use once they’re scratched. But using glass, ceramic, or stainless steel containers is probably best.


For more on BPA, check out my videos:

Unfortunately, BPA isn’t the only plastics chemical that may have adverse health effects. See:

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:

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 Foster a Healthy Gut Flora

What’s more important: probiotics or prebiotics? And where can we best get them?

“Virtually every day we are all confronted with the activity of our intestine, and it is no surprise that at least some of us have developed a fascination for our intestinal condition and its relation to health and disease.”

“Over the last years the intestinal microbiota [our gut flora] has been identified as a fascinating ‘new organ’” with all sorts of functions. Well, if the bacteria in our gut make up an entire, separate organ inside our body, what about doing an organ transplant? I discuss this in my video How to Become a Fecal Transplant Super Donor.

What would happen if you transferred intestinal bacteria from lean donors into obese subjects? Researchers figured that rebalancing the obesity-causing bacteria with an infusion of gut bacteria from a lean donor might help. They had wanted the study to be placebo-controlled, which, for drugs is easy, because the control subjects can just be given a sugar pill. But, when you’re inserting a tube down people’s throats and transplanting feces, what do you use as the placebo—or poocebo, if you will? Both the donors and the subjects brought in fresh stools, and the subjects were randomized to either get a donor’s stool or their own collected feces. So, the placebo was simply getting their own stool back.

What happened? As you can see at 1:32 in my video, the insulin sensitivity of the skinny donors was up around 50, which is a good thing. High insulin sensitivity means a low level of insulin resistance, which is the cause of both type 2 diabetes and prediabetes. The obese subjects started out around 20 and, after an infusion of their own feces, stayed around 20. The group of obese donors getting the skinny fecal infusion similarly started out low but then shot up near to where the slim folks were.

It’s interesting that not all lean donors’ stools conveyed the same effect on insulin sensitivity. Some donors, the so-called super-fecal donors, had very significant effects, whereas others had little or no effect, as you can see at 2:02 in my video. It turns out this super-donor effect is most probably conveyed by the amounts of short-chain fatty acid-producing intestinal bacteria in their feces. These are the food bacteria that thrive off of the fiber we eat. The short-chain fatty acids produced by fiber-eating bacteria may contribute to the release of gut hormones that may be the cause of this beneficial, improved insulin sensitivity.

“The use of fecal transplantation has recently attracted considerable attention because of its success in treatments as well as its capacity to provide cause–effect relations,” that is, cause-and-effect evidence that the bacteria we have in our gut can affect our metabolism. Within a few months, however, the bacterial composition returned back to baseline, so the effects on the obese subjects were temporary.

We can get similar benefits by just feeding what few good gut bacteria we may already have. If you have a house full of rabbits and feed them pork rinds, all the bunnies will die. Yes, you can repopulate your house by infusing new bunnies, but if you keep feeding them pork rinds, they’ll eventually die off as well. Instead, even if you start off with just a few rabbits but if you feed them what they’re meant to eat, they’ll grow and multiply, and your house will soon be full of fiber-eating bunnies. Fecal transplants and probiotics are only temporary fixes if we keep putting the wrong fuel into our guts. But, by eating prebiotics, such as fiber, which means “increasing whole plant food consumption,” we may select for—and foster the growth of—our own good bacteria.

However, such effects may abate once the high-fiber intake ceases. Therefore, our dietary habits should include a continuous consumption of large quantities of high-fiber foods to improve our health. Otherwise, we may be starving our microbial selves.


The microbiome is one of the most exciting research areas in medicine these days. For more information, see, for example:

For more on health sources of prebiotics, check out:

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: