The Effects of Too Much Arsenic in the Diet

Even at low-level exposure, arsenic is not just a class I carcinogen, but may also impair our immune function and increase our risk of cardiovascular disease and diabetes.

When people hear about arsenic, they think of it as an acute poison, and, indeed, a tiny amount—a hundred milligrams, about one-tenth the weight of a paperclip—could kill you in an hour. But, there is also chronic arsenic poisoning, where even a dose 10,000 times as small can be harmful if you’re exposed day-after-day for years at a time as I discuss in my video The Effects of Too Much Arsenic in the Diet. Chief among the concerns is cancer.

Arsenic is classified as a class I carcinogen, which is the highest level and includes things known to cause cancer in humans. Other class I carcinogens are asbestos, cigarette smoke, formaldehyde, plutonium, and processed meat (the consumption of bacon, ham, hot dogs, deli meat, and the like). So, arsenic is pretty bad, to say the least, implicated in tens of thousands—or even hundreds of thousands—of cancer cases worldwide every year.

Of course, cancer is our number-two killer. What about heart disease, our leading cause of death? “Long-term exposure to low to moderate arsenic levels was associated with cardiovascular disease incidence and mortality,” meaning heart attacks and strokes.

Arsenic is also considered an immunotoxicant, meaning it’s toxic to our immune system. How do we know that? There’s a virus called varicella, which is what causes chickenpox—the first time we get it. Our immune system is able to stamp it down but not stamp it out. The virus retreats into our nerve cells where it lies in wait for our immune function to dip. And, when it does, the virus re-emerges and causes a disease called shingles. We’ve all been exposed to the virus, but only about one in three of us will get shingles because our immune system is able to keep it at bay. However, the virus can slip its muzzle as we get older or immunosuppressed, for instance, if we’re given arsenic chemotherapy. Shingles is a common side effect, because the arsenic drugs not only kill the cancer but also some of our immune cells, too. That’s at high doses, though. Might even low doses of arsenic, like the kind we’re exposed to in our daily diet, impact our immune function? Researchers tested the levels of arsenic in the urine of thousands of Americans, along with their levels of anti-virus antibodies, and, indeed, they found that the more arsenic the subjects had flowing through their bodies, the lower their defenses.

And, if you’re pregnant, arsenic can pass to your baby, possibly increasing the risk of miscarriage or infant mortality, and “may affect an infant’s immune development and susceptibility to infections early in life.” Indeed, a study out of New Hampshire on infant infections in relation to prenatal arsenic exposure found that the more arsenic the mom was exposed to during pregnancy, the higher the baby’s risk of infection during infancy. However, “it’s unknown whether arsenic-induced epigenetic changes are transgenerational”—that is, whether changes in gene expression can impact the health of not only your own children but your grandchildren as well. Regardless, arsenic exposure isn’t good for mom’s own health, as it is associated with increasing blood pressure.

Hold on. If arsenic suppresses immune system function, then, as a silver lining, would we, for example, have fewer allergies, which is a kind of over-reaction of the immune system? Apparently not. Those with higher arsenic levels tend to have higher rates of food allergies, tend not to sleep as well, and tend not to feel as well. When people were asked how they would rate their health, those reporting “excellent” or “very good” tended to have lower levels of arsenic, compared to those who reported their general health condition as “good,” “fair,” or “poor,” who tended to have higher arsenic levels.

What about diabetes? You can see the results of two dozen population studies on arsenic exposure and confirmed diabetes at 4:07 in my video. Any result above one suggests increased risk for diabetes, and any result below one suggests lower risk. The findings? “Our results support an association between ingested arsenic and DM [diabetes] in humans.” Population studies can’t prove cause and effect, though. “While it would be nice to demonstrate a cause and effect relationship…is it necessary?”

We know arsenic is a carcinogen. We know it causes cancer. What more do we need to take steps to decrease our exposure?

Where is arsenic found in our diet? See my videos Where Does the Arsenic in Chicken Come From?  and Where Does the Arsenic in Rice, Mushrooms, and Wine Come From?.

 Ready for a deep dive into the rice issue? 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:




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:

Updating Our Microbiome Software and Hardware

Good bacteria, those living in symbiosis with us, are nourished by fruits, vegetables, grains, and beans, whereas bad bacteria, those in dysbiosis with us and possibly contributing to disease, are fed by meat, junk food and fast food, seafood, dairy, and eggs, as you can see at 0:12 in my video Microbiome: We Are What They Eat. Typical Western diets can “decimate” our good gut flora.

We live with trillions of symbionts, good bacteria that live in symbiosis with us. We help them, and they help us. A month on a plant-based diet results in an increase in the population of the good guys and a decrease in the bad, the so-called pathobionts, the disease-causing bugs. “Given the disappearance of pathobionts from the intestine, one would expect to observe a reduction in intestinal inflammation in subjects.” So, researchers measured stool concentrations of lipocalin-2, “which is a sensitive biomarker of intestinal inflammation.” As you can see at 1:13 in my video, within a month of eating healthfully, it had “declined significantly…suggesting that promotion of microbial homeostasis”—or balance—“by an SVD [strict vegetarian diet] resulted in reduced intestinal inflammation.” What’s more, this rebalancing may have played a role “in improved metabolic and immunological parameters,” that is, in immune system parameters.

In contrast, on an “animal-based diet,” you get growth of disease-associated species like Bilophila wadsworthia, associated with inflammatory bowel disease, and Alistipes putredinis, found in abscesses and appendicitis, and a decrease in fiber-eating bacteria. When we eat fiber, the fiber-munching bacteria multiply, and we get more anti-inflammatory, anti-cancer short-chain fatty acids. When we eat less fiber, our fiber-eating bacteria starve away.

They are what we eat.

Eat a lot of phytates, and our gut flora get really good at breaking down phytates. We assumed this was just because we were naturally selecting for those populations of bacteria able to do that, but it turns out our diet can teach old bugs new tricks. There’s one type of fiber in nori seaweed that our gut bacteria can’t normally breakdown, but the bacteria in the ocean that eat seaweed have the enzyme to do so. When it was discovered that that enzyme was present in the guts of Japanese people, it presented a mystery. Sure, sushi is eaten raw, so some seaweed bacteria may have made it to their colons, but how could some marine bacteria thrive in the human gut? It didn’t need to. It transferred the nori-eating enzyme to our own gut bacteria.

“Consequently, the consumption of food with associated environmental bacteria is the most likely mechanism that promoted this CAZyme [enzyme] update into the human gut microbe”—almost like a software update. We have the same hardware, the same gut bacteria, but the bacteria just updated their software to enable them to chew on something new.

Hardware can change, too. A study titled “The way to a man’s heart is through his gut microbiota” was so named because the researchers were talking about TMAO, trimethylamine N-oxide. As you can see at 3:33 in my video, certain gut flora can take carnitine from the red meat we eat or the choline concentrated in dairy, seafood, and eggs, and convert it into a toxic compound, which may lead to an increase in our risk of heart attack, stroke, and death.

This explains why those eating more plant-based diets have lower blood concentrations of TMAO. However, they also produce less of the toxin even if you feed them a steak. You don’t see the same “conversion of dietary L-carnitine to TMAO…suggesting an adoptive response of the gut microbiota in omnivores.” They are what we feed them.

As you can see at 4:17 in my video, if you give people cyclamate, a synthetic artificial sweetener, most of their bacteria don’t know what to do with it. But, if you feed it to people for ten days and select for the few bacteria that were hip to the new synthetic chemical, eventually three quarters of the cyclamate consumed is metabolized by the bacteria into another new compound called cyclohexylamine. Stop eating it, however, and those bacteria die back. Unfortunately, cyclohexylamine may be toxic and so was banned by the FDA in 1969. In a vintage Kool-Aid ad from 1969, Pre-Sweetened Kool-Aid was taken “off your grocer’s shelves,” but Regular Kool-Aid “has no cyclamates” and “is completely safe for your entire family.”

But, if you just ate cyclamate once in a while, it wouldn’t turn into cyclohexylamine because you wouldn’t have fed and fostered the gut flora specialized to do so. The same thing happens with TMAO. Those who just eat red meat, eggs, or seafood once in a while would presumably make very little of the toxin because they hadn’t been cultivating the bacteria that produce it.

Here’s the link to my video on TMAO: Carnitine, Choline, Cancer, and Cholesterol: The TMAO Connection. For an update on TMAO, see How Our Gut Bacteria Can Use Eggs to Accelerate Cancer, Egg Industry Response to Choline and TMAO, and How to Reduce Your TMAO Levels.

Interested in more on keeping our gut bugs happy? 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

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 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:

Combating Air Pollution Effects with Food

There is a food that offers the best of both worlds—significantly improving our ability to detox carcinogens like diesel fumes and decreasing inflammation in our airways—all while improving our respiratory defenses against infections.

Outdoor air pollution may be the ninth leading cause of death and disability in the world, responsible for millions of deaths from lung cancer, emphysema, heart disease, stroke, and respiratory infection. In the United States, living in a polluted city was associated with 16, 27, and 28 percent increases in total, cardiovascular, and lung cancer deaths, compared to living in a city with cleaner air. As well, living in a city with polluted air may lead to up to a 75 percent increase in the risk of a heart attack. “Additionally, the possibility of dying in a traffic jam is two and a half times greater in a polluted city.” No one wants to be living in a traffic jam, but it’s better than dying in one.

In addition to causing deaths, air pollution is also the cause of a number of health problems. It may not only exacerbate asthma but also increase the risk of developing asthma in the first place. These pollutants may trigger liver disease and even increase the risk of diabetes. Indeed, “even when atmospheric pollutants are within legally established limits, they can be harmful to health.” So, what can we do about it?

Paper after paper have described all the terrible things air pollution can do to us, but “most…failed to mention public policy. Therefore, while science is making great strides in demonstrating the harmful effects of atmospheric pollution on human health, public authorities are not using these data” to reduce emissions, as such measures might inconvenience the population “and, therefore, might not be politically acceptable.” We need better vehicle inspections, efficient public transport, bus lanes, bicycle lanes, and even urban tolls to help clean up the air, but, while we’re waiting for all of that, is there anything we can do to protect ourselves?

As I discuss in my video Best Food to Counter the Effects of Air Pollution, our body naturally has detoxifying enzymes, not only in our liver, but also lining our airways. Studies show that people born with less effective detox enzymes have an exaggerated allergic response to diesel exhaust, suggesting that these enzymes actively combat the inflammation caused by pollutants in the air. A significant part of the population has these substandard forms of the enzyme, but, either way, what can we do to boost the activity of whichever detoxification enzymes we do have?

One of my previous videos Prolonged Liver Function Enhancement from Broccoli investigated how broccoli can dramatically boost the activity of the detox enzymes in our liver, but what about our lungs? Researchers fed some smokers a large stalk of broccoli every day for ten days to see if it would affect the level of inflammation within their bodies. Why smokers? Smoking is so inflammatory that you can have elevated C-reactive protein (CRP) levels for up to 30 years after quitting, and that inflammation can start almost immediately after you start smoking, so it’s critical to never start in the first place. If you do, though, you can cut your level of that inflammation biomarker CRP nearly in half after just ten days eating a lot of broccoli. Broccoli appears to cut inflammation in nonsmokers as well, which may explain in part why eating more than two cups of broccoli, cabbage, cauliflower, kale, or other cruciferous veggies a day is associated with a 20 percent reduced risk of dying, compared to eating a third of a cup a day or less, as you can see at 3:41 in my video.

What about air pollution? We know that the cruciferous compound “is the most potent known inducer” of our detox enzymes, so most of the research has been on its ability to fight cancer. But, for the first time, researchers tried to see if it could combat the pro-inflammatory impact of pollutants, such as diesel exhaust. They put some human lung lining cells in a petri dish, and, as you can see at 4:11 in my video, the number of detox enzymes produced after dripping on some broccoli goodness skyrocketed. Yes, but we don’t inhale broccoli or snort it. We eat it. Can it still get into our lungs and help? Yes. After two days of broccoli sprout consumption, researchers took some cells out of the subjects’ noses and found up to 100 times more detox enzyme expression compared to eating a non-cruciferous vegetable, alfalfa sprouts. If only we could squirt some diesel exhaust up people’s noses. That’s just what some UCLA researchers did, at an amount equal to daily rush hour exposure on a Los Angeles freeway. Within six hours, the number of inflammatory cells in their nose shot up and continued to rise. But, in the group who had been getting a broccoli sprout extract, the inflammation went down and stayed down, as you can see at 4:58 in my video

Since the dose in those studies is equivalent to the consumption of one or two cups of broccoli, their study “demonstrates the potential preventive and therapeutic potential of broccoli or broccoli sprouts,” but if broccoli is so powerful at suppressing this inflammatory immune response, might it interfere with normal immune function? After all, the battle with viruses like influenza can happen in the nose. So what happens when some flu viruses are dripped into the nostrils of broccoli-sprout eaters compared with people consuming non-cruciferous alfalfa sprouts? After eating broccoli sprouts, we get the best of both worlds—less inflammation and an improved immune response. As you can see at 5:55 in my video, after eating alfalfa sprouts, there is a viral spike in their nose. After eating a package of broccoli sprouts every day, however, our body is able to keep the virus in check, potentially offering “a safe, low-cost strategy for reducing influenza risk among smokers and other at risk populations.”

So, better immune function, yet less inflammation, potentially reducing the impact of pollution on allergic disease and asthma, at least for an “enthusiastic broccoli consumer.” But what about cancer and detoxifying air pollutants throughout the rest of our body? We didn’t know, until now. Off to China, where “levels of outdoor air pollution…are among the highest in the world.” By day one, those getting broccoli sprouts were able to get rid of 60 percent more benzene from their bodies. “The key finding…was the observed rapid and highly durable elevation of the detoxification of… a known human carcinogen.” Now, this was using broccoli sprouts, which are highly concentrated, equivalent to about five cups of broccoli a day, so we don’t know how well more modest doses would work. But if they do, eating broccoli could “provide a frugal means to attenuate…the long-term health risks” of air pollution. More on air pollution here.

I’ve been reading about the terrible effects of air pollution for a long time and I am thrilled there’s something we can do other than uprooting our families and moving out to the countryside.

For more on cruciferocity, see my videos Lung Cancer Metastases and Broccoli and Breast Cancer Survival Vegetable.

There’s a secret to maximizing broccoli’s benefits. See Flashback Friday:Second Strategy to Cooking Broccoli.

For more on Cooking Greens: How to Cook Greens and Best Way to Cook Vegetables.

What about broccoli sprout pills? See Broccoli: Sprouts vs. Supplements.

Speaking of respiratory inflammation, what about dietary approaches to asthma? Learn more:

There are sources of indoor pollution, too. See Throw Household Products Off the Scent.

There is one way what we eat can directly impact air pollution, beyond just personal protection. Check out Flashback Friday: Diet and Climate Change: Cooking Up a Storm.

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:

Eating Seaweed Salad May Boost Immune Function

Eating seaweed salad may boost the efficacy of vaccinations and help treat cold sores, herpes, Epstein-Barr virus, and shingles.

Billions of pounds of seaweed are harvested each year, the consumption of which “has been linked to a lower incidence of chronic diseases,” both physical and mental. For example, women who eat more seaweed during pregnancy appear to be less depressed and experience fewer seasonal allergy symptoms. There’s a problem with these cross-sectional, correlational studies, however, in that they can’t prove cause and effect. Maybe seaweed consumption is just an indicator that people generally are following “traditional Japanese dietary customs,” which have lots of different aspects that could protect against disease. To know for certain whether seaweed can modulate immune function, you have to put it to the test.

As I discuss in my video How to Boost Your Immune System with Wakame Seaweed, typically, researchers start out with in vitro studies, meaning in a test tube or a petri dish, which make for quicker, cheaper, and easier experiments. One study, for example, took eight different types of seaweed and essentially made seaweed teas to drip onto human immune system cells in a petri dish. Studies like these showed that the seaweed wakame, which is the kind you find in seaweed salad, can quadruple the replication potential of T cells, which are an important part of our immune defense against viruses like herpes simplex virus.

No one actually gave seaweed to people with herpes until a study published in 2002. Researchers gave people suffering from various herpes infections about two grams a day of pure powdered wakame, which is equivalent to about a quarter cup of seaweed salad. “All fifteen patients with active Herpetic viral infections”—including herpes virus 1, the cause of oral herpes, which causes cold sores; herpes virus 2, which causes genital herpes; herpes virus 3, which causes shingles and chicken pox; and herpes virus 4, also known as Epstein-Barr virus, which causes mono—“experienced significant lessening or disappearance of symptoms,” as you can see at 2:06 in my video. There was no control group in the study, but with no downsides to eating seaweed, why not give it a try?

Researchers also found that wakame boosted antibody production, so could it be useful to boost the efficacy of vaccines? The elderly are particularly vulnerable to suffering and dying from influenza. While the flu vaccine can help, ironically, the elderly are less likely to benefit from it because immune function tends to decline as we get older. So, researchers took 70 volunteers over the age 60. As you can see at 2:50 in my video, their baseline level of antibodies against a flu virus was about 10 GMT. What you’re looking for in a vaccination is to get a two-and-a-half-fold response, so we’d like to see that antibody level get up to at least 25 GMT to consider it an effective response. The vaccine only boosted levels to 15 to 20 GMT, though. What happened after the subjects were given some wakame extract every day for a month before the vaccination? Their levels jumped up to 30 to 35 GMT. The researchers used an extract in a pill rather than the real thing, though, so they could perform this randomized placebo-controlled study. After all, it’s kind of hard to make a convincing placebo seaweed salad.

“It is hoped that the popular seaweeds eaten daily in Japan, though almost unknown around the world outside of Japanese restaurants, will be consumed…for possible immunopotentiation”—that is, immune-boosting potential—“and for attenuating the burden of infectious diseases in the elderly.”

What else can seaweed salad do (other than taste delicious)? See my video Wakame Seaweed Salad May Lower Blood Pressure.

In general, sea vegetables are good sources of iodine, as I discuss in Iodine Supplements Before, During, and After Pregnancy, and may also be one reason Japanese women have historically had such low rates of breast cancer, which I cover in Which Seaweed Is Most Protective Against Breast Cancer?.

What else can we do to boost our immunity? Check out my videos:

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:

Boosting Antiviral Immune Function with Green Tea

Unlike most antiviral drugs, green tea appears to work by boosting the immune system to combat diseases such as genital warts (caused by HPV) and the flu (caused by the influenza virus).

According to one study, “The belief in green tea as a ‘wonder weapon’ against diseases dates back thousands of years.” I’ve talked about it in relation to chronic disease, but what about infectious disease? I explore this in my video Benefits of Green Tea for Boosting Antiviral Immune Function. Interest in the antimicrobial activity of tea dates back to a military medical journal in 1906, which suggested that servicemen fill their canteens with tea to kill off the bugs that caused typhoid fever. “However, this effect of tea was not studied further until the late 1980s” when tea compounds were pitted against viruses and bacteria in test tubes and petri dishes, but what we care about is whether it works in people. I had dismissed this entire field of inquiry as clinically irrelevant until I learned about tea’s effect on genital warts. External genital warts, caused by human wart viruses, “are one of the most common and fastest-spreading venereal diseases worldwide.”

Patients with external genital warts “present with one or several cauliflower-like growths on the genitals and/or anal regions…associated with…considerable impairment of patients’ emotional and sexual well-being.” But rub on some green tea ointment, and you can achieve complete clearance of all warts in more than 50 percent of cases.

If it works so well for wart viruses, what about flu viruses? As you can see at 1:41 in my video, it works great in a petri dish, but what about in people? Well, tea-drinking school children seem to be protected, but you don’t know about the broader population until it’s put to the test. If you give healthcare workers green tea compounds, they come down with the flu about three times less often than those given placebo, as you can see at 2:02 in my video. In fact, just gargling with green tea may help. While a similar effect was not found in high school students, gargling with green tea may drop the risk of influenza infection seven or eight-fold compared to gargling with water in elderly residents of a nursing home, where flu can get really serious.

Unlike antiviral drugs, green tea appears to work by boosting the immune system, enhancing the proliferation and activity of gamma delta T cells, a type of immune cell that acts as “a first line defense against infection.” According to the researchers, “Subjects who drank six cups of tea per day had up to a 15-fold increase in [infection-fighting] interferon gamma production in as little as one week”—but why?

There is in fact a molecular pattern shared by cancer cells, pathogens, and “edible plant products such as tea, apples, mushrooms, and wine.” So, eating healthy foods may help maintain our immune cells on ready alert, effectively priming our gamma delta T cells so they “then can provide natural resistance to microbial infections and perhaps tumors.” I guess I shouldn’t have been so surprised; tea, after all, is a “vegetable infusion.” You’re basically drinking a hot water extraction of a dark green leafy vegetable.

For more on what green tea can (and cannot) do, check out videos such as:

How else can we improve our immune function? 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:


Takeaways from My Webinar on COVID-19

On December 30, 2019, Dr. Li Wenliang, an ophthalmologist at Wuhan Central Hospital in the Hubei province of China, messaged his fellow physicians, alerting them to the appearance of what he thought as SARS. Thirty-nine days later, after becoming infected with the very virus he tried to warn his colleagues about, he was dead at thirty-three. By that time, the disease we now know as COVID-19 had already spread to dozens of countries.

Before the SARS outbreak in 2002, only two coronaviruses were known to cause disease in humans, but neither caused much more than the common cold. The SARS coronavirus, however, went on to kill about one in ten people it infected. A decade later, in 2012, MERS, another deadly coronavirus, emerged. Like SARS, MERS spread to infect thousands of people across dozens of countries, but that time, one in three died. Today, we’re fighting to protect ourselves from—and to defeat—the COVID-19 coronavirus.

Where are these emerging infectious diseases emerging from?

All human viral infections are believed to originate in animals.

To understand COVID-19 and other deadly viral outbreaks, we have to understand their history and evolution if we’ll ever have a chance at preventing future pandemics. We also have to look back and take lessons from the past. How did we successfully beat back SARS? Why is it more difficult with COVID-19? What do we have to do to slow the pandemic today before we even have a hope at a vaccine?

I covered all of that in my recent four-hour webinar—from origin stories of past killer pandemics to what we should be doing today to stay safe—and then dove into the clinical side of COVID-19 and discussed what the disease looks like and the best way to treat it. If you missed the webinar, the following is an overview of what I covered.

Please note: Recommendations for mitigation and slowing the spread vary by location. Be sure to follow your region’s safety guidelines. Further, as data on COVID-19 is continually changing, we recommend the following sources: 


The Emergence of MERS

  • Most human coronaviruses appear to have arisen originally in bats, thought to be the primordial hosts, but jumping the species barrier to infect people appears to require intermediate hosts.
  • In the case of MERS, the intermediate hosts were found to be camels.
  • Although we domesticated camels three thousand years ago and MERS had long been circulating in them for decades without crossing the species barrier into humans, more recent intensification of camel production—from foraging outdoors to, today, primarily being confined indoors at high stocking densities—is thought to be what helped drive the spillover of MERS from camels to people.
  • The first human cases of MERS were reported in 2011, the year after open grazing was banned in Qatar, the Middle Eastern country with the highest camel density.

The Emergence of SARS

  • The first new global disease outbreak of the 21st century was SARS, even before MERS.
  • In the case of SARS, the intermediate hosts were found to be civet cats.
  • SARS-CoV causes the SARS coronavirus, and SARS-CoV-2 causes the COVID-19 coronavirus.
  • Many of the first cases of SARS were found in the same type of place most of the first cases of our current COVID-19 pandemic have been found: live animal “wet” markets in China.
  • At wet markets, crowded cages of animals, including exotic animals, are contaminated with the feces, urine, and blood of different species mixed together, and animals may be slaughtered. These conditions lead to a perfect storm for zoonotic (animal-to-human) disease transmission.
  • The virus uses the spikes on its corona like a key in a lock to access host receptors. Just as a new lock needs a new key, in order to switch from infecting one species to another, the genes coding the spikes must mutate to fit into the new host’s receptors.
  • Both viruses that cause SARS and COVID-19, SARS-CoV and SARS-CoV-2, respectively, attach to an enzyme coating the cells of our lungs. By the time bat coronaviruses made it into civets, the virus’s docking spikes were just two mutations away from locking in the configuration to bind to human receptors—and then the human-to-human SARS epidemic was born.

The Emergence of COVID-19

  • Ground zero for the COVID-19 pandemic was the Hua’nan Market in Wuhan, China, named in Dr. Li’s “7 SARS cases confirmed” message. It wasn’t a SARS-coronavirus, though. It was a virus to be named SARS coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 2019, or COVID-19.
  • The new COVID-19 coronavirus is about 80 percent identical to the original SARS virus, but it’s more than 95 percent identical to a coronavirus found in a bat in 2013.
  • The current theory: COVID-19 originated in bats before jumping to humans after passing through an intermediate host, thought to be the pangolin, the most trafficked mammal in the world.
  • Coronaviruses found in two different groups of diseased pangolins being smuggled into China were found to be about 90 percent identical with the COVID-19 virus. As well, the pangolin coronavirus spike protein’s critical receptor binding region is virtually identical to the human strain.

Coronaviruses Infect Pigs Right Off the Bat

  • COVID-19 is the fourth coronavirus to jump from bats to cause large deadly outbreaks in the 21st  century. First was SARS in 2002, MERS in 2012, and then SADS—Swine Acute Diarrhea Syndrome—in 2016, which devastated commercial pig farms in the same part in China where SARS had broken out. SADS was traced to a coronavirus discovered in a nearby bat cave.
  • Other emerging and re-emerging coronavirus diseases include Porcine Epidemic Diarrhea and Porcine Deltacoronavirus among pigs, and Infectious Bronchitis Virus in chickens. Increasingly, coronaviruses are emerging and circulating among farm animal populations, and the more novel coronaviruses mix in greater numbers of animals, the greater the likelihood that strains with the potential to spark a pandemic may emerge.

COVID-19 May Not Have Been the First Coronavirus Pandemic

  • The second most common cause of the common cold are coronaviruses.
  • To date, four human cold coronaviruses have been discovered, which means seven coronaviruses in all can cause human disease as far as we know. We believe we got SARS from civets, MERS from camels, and COVID-19 perhaps from pangolins.
  • Though we still don’t know where two of the four mild coronaviruses originated, one—human coronavirus 229E—has been traced back to camels and the other—OC43—traced back to cattle or pigs.
  • Molecular clock analyses dating human coronavirus OC43’s emergence suggest that the bovine coronavirus now causing “shipping fever” disease in cattle, jumped to humans around 1890. Indeed, that same year, 1890, there was a pandemic, presumed to be influenza.
  • Because of the timing of the emergence of human coronavirus OC43, some conjecture it actually may have been a COVID-19-like interspecies transmission of a coronavirus. This is supported by the fact that cattle herds the world over were being devastated by a deadly respiratory disease, resulting in massive culling operations between 1870 and 1890.


Slowing an Outbreak

  • There were more COVID-19 cases in the first month of reporting than SARS ever caused. Why? The primary reason revolves more around when it is contagious than how contagious it is.
  • Microbes most likely to cause pandemics have three characteristics: (1) novelty, therefore, without pre-existing immunity; (2) respiratory spread; and (3) transmission before the onset of symptoms.
  • SARS, despite spreading to twenty-nine countries and regions, was not considered a pandemic. And, we were able to stop it within only a few months, after approximately 8,000 cases and 800 deaths. Why? SARS was spread via respiratory droplets but lacked significant spread before symptoms arise.
  • SARS’s average incubation period—from first becoming infected to first coming down with symptoms—was around five days, but viral loads took another six to eleven days to ramp up. So, SARS patients weren’t very infectious in the first five or so days of the illness. In that way, transmission from person to person could be stopped if patients were isolated within the first few days after symptoms arose.
  • One hundred percent of SARS patients developed a fever, as did 98 percent of MERS patients. However, as many as 36 percent—more than one in three—of COVID-19 patients do not present with fever at the onset of symptoms and, more seriously, may be infectious while completely symptom-free during the incubation period.
  • People can potentially spread COVID-19 before even knowing they have it, even while they’re feeling completely fine, which is why isolation may slow the spread of disease without knowing who is infectious.

Social Distancing

Slowing a Pandemic

  • China enacted “wartime control measures” and initiated the most expansive containment effort in history, affecting about three quarters of a billion people, confining them to their homes.
  • The seemingly impossible was achieved: the containment of a widely circulating respiratory infection. Ground zero of COVID-19, Hubei Province, reported its first day of no new local cases within two months.
  • That same day, the world confirmed its 200,000th 
  • Countries able to rapidly control the disease quickly relied on testing and tracing—mass testing to identify all cases and tracing every patient’s every possible contact—to block as many paths of transmission as possible through isolation and quarantine.
  • Rapid response varied wildly. By the middle of March, South Korea had tested more than a quarter million people, more than five thousand out of every million citizens, compared to fewer than a hundred per million in the United States.
  • When the window on containment closes, as it did in the United States, the strategy pivots to suppression and mitigation.
  • Closing nonessential businesses, cancelling gatherings, and encouraging people to stay at home and shelter in place all attempt to break every possible link in the chain of viral transmission—to “flatten the curve,” that is, to flatten the epidemic curve to slow the spread of disease to more evenly distribute the cases over time.
  • Until there is wide availability of an effective vaccine, thought unlikely until 2021 at the earliest, population lockdowns can help slow the spread by removing susceptible hosts from the virus’s reach. Once such stay-at-home measures are relaxed, though, the disease could attack again as it did in the 1918 pandemic when some U.S. cities suffered a second peak in mortality after social-distancing measures were lifted.
  • Triage protocols have been published, establishing a hierarchy of care in anticipation of too few resources, such as hospital beds and ventilators, and too many patients. Wrote a preeminent group of medical ethics experts in the New England Journal of Medicine, “[W]e believe that removing a patient from a ventilator or an ICU bed to provide it to others in need is also justifiable and that patients should be made aware of this possibility at admission,” adding, “the decision to withdraw a scarce resource to save others is not an act of killing and does not require the patient’s consent.”


Symptoms of COVID

The Clinical Course of COVID-19

  • COVID-19 is thought to have an average incubation period of about five days, which means we are infected and possibly infectious for almost a week before we may even know we have the disease.
  • Not all infected people show symptoms, but of those who do, about 98 percent start exhibiting them by day twelve, which explains why quarantine after a potential exposure are for two weeks.
  • After infection, the virus may shed for more than a month (with an average of twenty days), but it is unclear how contagious survivors are during that period.
  • The most common symptoms are fever (90 percent of patients) and cough (70 percent). About four in ten experience fatigue, three in ten cough up phlegm, two in ten have muscle aches, and one in ten may suffer gastrointestinal symptoms, such as nausea or diarrhea, or common cold-type symptoms, like runny nose, sore throat, or headache.
  • Difficulty breathing has been the only symptom found predictive of a more severe course of COVID-19 and has resulted in more than six times the odds of eventually being admitted into the ICU.
  • COVID-19’s severity varies widely based on pre-existing conditions: People with high blood pressure are twice as likely to suffer a severe course and three times as likely with cardiovascular disease, and those with either condition are about four times as likely to end up in the ICU. Those with chronic obstructive pulmonary diseases (COPD) like emphysema appear to be at the highest risk (six times the odds of a severe course) and nearly eighteen times the odds of ICU admission.
  • As with SARS and MERS, those with diabetes appear to be at higher risk.
  • Excess body fat also seems to be a risk factor. Those with a body mass index (BMI) of 28 or more appear to have nearly six times the odds of suffering a severe COVID-19 course. (The average BMI in the United States exceeds 29)
  • Even without taking weight into account, most adult Americans over fifty suffer from a “co-morbidity” that may put them at risk. It’s important to note that the major comorbid conditions for COVID-19 severity and death—obesity, heart disease, hypertension, type 2 diabetes—may all be controlled or even reversed with a healthy enough plant-based diet.
  • Although newborns through seniors in their nineties have been infected, most COVID-19 patients are between thirty and seventy-nine, but the severity of the disease disproportionately affects older patients. Compared with people aged nineteen to sixty-four, in the United States, those sixty-five and older without underlying conditions or other risk factors appear to be hospitalized or end up in the ICU at approximately three times the rate.
  • The best data come from South Korea: Of confirmed cases, about 1 in 1,000 died in their thirties and forties, 1 in 150 of those in their fifties, 1 in 50 in their sixties, 1 in 15 in their seventies, and 1 in 5 in their eighties. U.S. data are less reliable due to the relative lack of testing, these age-related death risks are similar based on the first few thousands of American cases that were reported.
  • On autopsy, the lung’s respiratory surface appears obliterated by scar tissue. Pulmonary fibrosis (lung scarring) is expected to be a long-term complication among survivors of serious COVID-19 infection.
  • Death from COVID-19 is the result of progressive “consolidation” of the lung—your lungs start filling up with something other than air. In COVID-19 pneumonia, postmortems show you drown in lungs “filled with clear liquid jelly.”

How to Treat COVID-19

  • Presently, there is no specific proven therapy for COVID-19.
  • Although there are more than 400 clinical treatment trials underway, we should not expect an effective antiviral drug or vaccine anytime soon.
  • I support commonsense advice to stay healthy during the crisis, as recommended by trusted authorities such as the American College of Lifestyle Medicine and the World Health Organization, including getting sufficient sleep (seven to nine hours), reducing stress, keeping active, staying connected (remotely) to friends and family, and eating healthfully (a diet centered around whole plant foods).

Lifestyle Choices _ Immunity(click to enlarge)

  • Given our near-total ignorance of the immunological aspects of COVID-19, I will not jump on the snake-oily spamwagon to promote foods to boost immunity. We just don’t know if enhancing specific arms of the immune system could make things even worse.
  • There is an assumption that seniors are more susceptible to serious COVID-19 courses due to their waning, aging immune systems, but that may not be correct. Similarly, though young children, with their relatively immature immune systems, typically suffer disproportionally from infections such as the flu, that doesn’t appear to be with the case with COVID-19 (or SARS or MERS). Likewise, immunosuppressed patients may not be at greater risk of severe complications from COVID-19, although they normally are from respiratory viruses.
  • Our own immune response may be the primary driver of damage to the lungs during coronavirus infection—somewhat akin to an autoimmune reaction where the body over-reacts and the lungs get caught in the crossfire as the coronavirus is attacked.

How to Avoid COVID-19

  • Although cancelling gatherings, meetings, and events may slow COVID-19’s spread by as much as 35 percent, according to preliminary evidence from Japan, that has not been enough to contain the outbreak.
  • Our best course of action is to shelter-in-place—stay home to reduce contact with those outside our households as much as possible—and to do so now.
  • By the time a community has its first death from the disease, it’s likely that hundreds or even thousands of cases are present.
  • If you must leave your home to provide essential services such as direct care or food delivery, maintain a safe distance from others and sanitize your hands every time you touch a public surface. It’s critical not to touch your mucous membranes—your eyes and the inside of your nose or mouth—with unsanitized hands.

shopping for essentials

  • The virus can’t pass through your skin. It can only replicate in live cells, and our skin’s outer layer is covered by protective dead skin cells. To get into your lungs, the virus has to find its way to your mucous membranes, the moist lining of your eyes, nostrils, or mouth.
  • To the best of our current understanding, the COVID-19 coronavirus is thought to be transmitted from person to person via respiratory droplets coughed out by the infected into the air and then landing in the eyes, nose, or mouth of another. You can also infect yourself by touching your eyes, nose, or mouth with hands contaminated by a virus-laden object or surface—for instance, by picking your nose or rubbing your eyes after shaking someone’s hand or touching a public surface like a door knob or an elevator button.
  • The levels of virus in the snot of COVID-19 patients can reach almost a million per drop.
  • The COVID-19 coronavirus has been detected in stool samples, suggesting another way toilets may potentially transmit infection, beyond just touching the flush handle. Modern flush toilets aerosolize up to 145,000 droplets of toilet water into the air, which can float around for at least thirty minutes, so be sure to close the lid before you flush and then, of course, thoroughly wash your hands.
  • Coronaviruses are “enveloped” viruses. As they emerge from our infected cells, they cover themselves in the outer layer of our cells. Although that oily coating makes it harder for our immune system to detect them because they look like us, it also makes them susceptible to disinfection and environmental inactivation.
  • The COVID-19 virus appears to survive for less than three hours on printing paper but may last for one day on cloth. On the outer layer of surgical masks, though, it can survive for a week. COVID-19 virus’s half-life is about six hours on steel or plastic, so, although about 99 percent is gone by forty-eight hours, it may be up to 96 hours for all infectivity to be extinguished.

How to Inactivate COVID-19

  • Hands can be disinfected by properly washing your hands with soap and water. The CDC recommends washing them for at least twenty seconds. Researchers found the fingertips, thumbs, and backs of hands are the most frequently missed areas when washing, so be sure to wash thoroughly.
  • There is no need to use hot water when washing your hands.

wash hands1

  • Researchers found that the COVID-19 virus could be inactivated within thirty seconds by 30% alcohol (ethyl or isopropyl). Most vodka, rum, brandy, gin, and whisky exceed 30% alcohol by volume. Note that 30% alcohol isn’t enough to kill many other pathogens, so I still recommend sanitizers with 60% to 80% alcohol. (One rub to rule them all!) But, if you can’t find them, it’s nice to know you can make your own.

DIY Hand Sanitizer

Basic Recipe: The easiest method would probably be to just use 80-proof liquor straight up as a hand-sanitizing rub. Pour it into a squirt or spray bottle and apply enough to completely cover all surfaces of your hands and then rub them together and leave on for 30 seconds. The addition of a gelling agent such as aloe vera is not recommended as it might compromise antiviral efficacy.

Fancy Recipe: Assuming you have all of the ingredients, you can make a gallon of COVID-19 hand sanitizer by combining 12 cups of an 80-proof liquor (40% alcohol-by-volume) with ¼ cup of glycerine (also spelled glycerin or called glycerol) and a teaspoon of regular strength (3%) hydrogen peroxide and then just fill the rest of the gallon container with water. To make just a quart, simply quarter the recipe: 3 cups liquor, 1 tablespoon glycerine, ¼ teaspoon hydrogen peroxide, and water. Again, don’t add anything else.

  • Bleach is recommended for disinfection of inanimate surfaces—1 part household bleach diluted in 49 parts water, so about 1 teaspoon bleach per cup of water.
  • This 1:50 recommendation is for standard bleach (5% sodium hypochlorite). If you have 2.5% hypochlorite bleach, use two teaspoons per cup, and if you have 10% hypochlorite bleach, you only need a half teaspoon per cup.
  • Prepare the bleach solution fresh and leave it on the surface you’re disinfecting for at least ten minutes. Surfaces visibly contaminated with bodily secretions like snot, blood, or poop may require a stronger bleach solution (1 part standard bleach to 9 parts water, left for ten minutes).
  • NEVER mix bleach with any other cleanser as it reacts with ammonia (found in many glass cleaners) to create hazardous gases and reacts with acids (like vinegar, or some toilet bowl, drain, and automatic dishwashing detergents) to create chlorine gas, which is also toxic.

  DIY Hand Sanitizer  DIY Hand Sanitizer English Metric

(click to enlarge: imperial & metric)

What If You Come Down with COVID-19?

  • The best option is to try to recover at home, isolated as much as possible from others in your household. Preferably, you should avoid contact with both people and pets, and be cordoned off in a “sick room” with a separate bathroom if possible.
  • Most people who get infected with the COVID-19 virus recover without medical intervention. If you do come down with it, protect those around you, rest, hydrate, and monitor your symptoms. If you experience difficulty breathing or persistent pain or pressure in the chest, seek medical attention—but, first call your doctor or emergency room before heading in, since they may have special instructions for suspect cases in your area.
  • Practice good hygiene and social-distancing etiquette: Wash your hands often. Cough or sneeze into a tissue, covering your nose and mouth, then throw the used tissue into a lined bin and immediately sanitize your hands. Don’t share eating utensils, towels, bedding, or other personal household items. Routinely disinfect all high-touch objects (e.g., doorknobs and toilet surfaces) in your sick room and bathroom yourself, but have someone else disinfect the rest of the house. Be sure to wear gloves while cleaning and disinfecting, and open windows if possible and wear a surgical mask.
  • If you’re sick but must share a room with someone else, wear a face mask. That’s what they were originally designed for: source control, rather than self-protection.


(click to enlarge)

  • It’s important to understand that respiratory droplets are not just gobs of mucus. When you’re outside on a cold day and your breath fogs, those are respiratory droplets. That vapor plume you’re exhaling is made up of tiny water droplets straight from your lungs. On a warm day, you breathe out that same cloud—you just can’t see it.
  • Should everyone cover their face in public since infected individuals are exhaling virus before they even know they have it? The CDC recommends “wearing cloth face coverings in public settings where other social distancing measures are difficult to maintain” such as grocery stores or pharmacies. The U.S. Surgeon General is featured in a video demonstrating how to improvise masks out of a bandana and rubber bands, and the CDC has easy no-sew instructions at


(click to enlarge)

  • Cloth coverings, which should be washed regularly, are no substitute for masks, but may be better than nothing. Scarves, pillowcases, and 100 percent cotton t-shirts are probably the most suitable household materials for making homemade masks, blocking various bacteria and viruses about 60 percent as well as surgical masks.
  • What about N95 masks? Also known as N95 respirators, these are cup-like masks that fit tighter to the face and, unlike surgical masks, are intended to protect the wearer. The CDC and its European counterpart recommend N95 masks for healthcare workers during routine care of patients, while the World Health Organization suggests surgical masks are sufficient.
  • Until we know more about how the COVID-19 virus is transmitted, it seems prudent for those in close contact with coughing patients use eye protection (at least a face shield) and N95 respirators.
  • According to the CDC, once your symptoms start improving, you’ve been fever-free for three full days off of fever-reducing medicines, and it’s been at least one week since your symptoms first appeared, only then can you start relaxing your home isolation. The World Health Organization is more conservative, though, and recommends self-quarantine for a full fourteen days for anyone with symptoms or living with anyone with symptoms.

 prevent-cleaning kitchen

  • A note on pets: Dogs have been found infected with the COVID-19 coronavirus in rare cases, but it replicates poorly in dogs and doesn’t seem to make them sick, and they don’t appear to pass the virus along to others. In cats, however, the virus has been shown to reproduce And, cats have been able to experimentally transmit the virus to other cats even though they may not themselves become sick. In the United States, the only confirmed case of animal infection that I know of is a sickened tiger at the Bronx Zoo.


  • We shouldn’t count on COVID-19 going away naturally when the weather gets warmer. Every recent flu pandemic emerged in the spring or summer months, but secondary waves tended to hit the following winter.
  • Even if the COVID-19 virus’s contagiousness drops in the Northern Hemisphere this summer, thanks to warmer, wetter weather, that’s not expected to make a big impact on the pandemic curve.
  • Herd immunity would stop the pandemic—when a critical portion of the population is immune to the virus. When there are no longer enough susceptible individuals for a virus to infect, jumping from person to person, the chains of transmission are broken.
  • Mass vaccination is the ideal way to accomplish this. Without a vaccine, the only way to achieve herd immunity is through mass infection.
  • Based on estimates for the COVID-19 virus from large outbreaks in affected countries and simplistic mathematical models, the minimum population immunity required varies from approximately 30 percent (based on South Korea’s data) to more like 80 percent (based on an estimate from Spain).
  • This is why “flattening the curve” is critical. We can’t wait until 80 percent of the population is infected.
  • One trait the COVID-19 virus shares with HIV is its rapid mutation rate. The possibility that the virus could transform in the near future to become even more transmissible or dangerous cannot be ruled out.
  • A “best guess” estimate presented to the American Hospital Association was about a half a million U.S. deaths if the virus stayed the course. That may be reduced to under 100,000 with sufficient social distancing.
  • The CDC developed a Pandemic Severity Index, modelled after the Hurricane Severity Index to define the destructive capacity of a storm. In the 1918 pandemic, about one in three became infected and, of those, about 2 percent died, classifying it as a category 5 pandemic, analogous to a “super typhoon” with sustained winds exceeding 150 miles per hour. COVID-19 infection fatalities are much lower, probably closer to 0.5 percent, meaning 1 in 200 cases dying.
  • For more than a century, we’ve known about the pandemic potential of the flu virus, but that 2 percent fatality of the 1918 influenza appears to be the deadliest it ever got. In 1997, however, a flu virus was found in chickens that appears to have killed more than 50 percent of the people it infected. What if a virus like that triggered an outbreak?

PREVENTING FUTURE PANDEMICS: Having Our Meat and Eating It Too

  • We were spared by the last pandemic: In 2009, swine flu only triggered a category 1 pandemic, killing a half million people. It did, however, reveal that industrial pork production was a new origin point for pandemic viruses.
  • The emergence of H5N1 and other bird flu viruses infecting humans has been blamed on industrial poultry production.
  • The CDC considers H7N9, a bird flu virus, to be our gravest pandemic flu threat, one that could kill millions of Americans. To date, H7N9 has killed about 40 percent of the people it has infected. Two in five.
  • At this time, neither H5N1 nor H7N9 has acquired the capacity for easy human-to-human transmission, but neither has been eradicated. They’re still out there, still mutating.
  • How can we stop the emergence of pandemic viruses in the first place? Whenever possible, treat the cause.
  • The largest and oldest association of public health professionals in the world, the American Public Health Association, has called for a moratorium on factory farming for nearly two decades. Its journal published an editorial entitled “The Chickens Come Home to Roost” that went beyond calling for a deintensification of the pork and poultry industries:

“It is curious, therefore, given the pandemic threat, that changing the way humans treat animals, most basically ceasing to eat them, or at the very least, radically limiting the quantity of them that are eaten—is largely off the radar as a significant preventive measure. Such a change, if sufficiently adopted or imposed, could still reduce the chances of the much-feared influenza epidemic. It would be even more likely to prevent unknown future diseases that, in the absence of this change, may result from farming animals intensively and killing them for food. Yet humanity doesn’t even consider this option.”

  • This may be changing, thanks to food innovations like plant-based milks, egg products, and meats.
  • Our food choices don’t just affect our personal health but our global health. Not just in terms of climate change, but in terms of pandemic risk.
  • Major meat producers have started blending in vegetable proteins to make hybrid meats like Tyson’s “Whole Blends” sausage links and Perdue’s “next generation” chicken nuggets. The world’s largest pork producer, Smithfield, recently launched a whole line of plant-based products. Egg-free mayo has taken the sandwich spread sector by storm, and Quorn, a brand of meat-free meat made from the mushroom kingdom, opened a facility capable of producing the meat equivalent of twenty million chickens per year.
  • While these products may not be the healthiest from a personal standpoint, they tend to be healthier than their animal-product counterparts and, from a pandemic standpoint, they present zero risk.
  • What about cultivated meat? The primary human health benefit of a slaughter-free harvest would be food safety. (If you make meat without intestines, you don’t have to worry about fecal bugs like Salmonella, and if you make meat without lungs, you don’t have to worry about brewing respiratory viruses.) Growing meat directly from muscle cells has been touted for the environmental benefits—reducing water use and greenhouse gas emissions by as much as 96 percent and lower land use by as much as 99 percent—but factoring in pandemic risk, the benefits to human health may rival those to planetary health.


  • In the webinar, I ended by taking a moment to acknowledge all of the first responders and frontline medical workers. Many of them are not only dealing with physical and mental exhaustion, the torment of difficult triage decisions, and the pain of losing patients and colleagues, but are also—quite literally—putting their own lives at risk. Thousands of healthcare workers have been infected, and more than a hundred have died.
  • Crises like these can bring out the worst in people, like all the hate crimes and harassment against Asian-Americans, but they can also bring out the best.
  • You can support those on the front lines from being overwhelmed by staying safe, and, if you can, staying home.


  • During the webinar, I was excited to announce that my entire four-hour lecture will be turned into a month-long series of videos on, so stay tuned.
  • I have also been feverishly working on a new book set to be released on May 26, 2020—How to Survive a Pandemic.
  • Have any questions? I’ll be going live on Thursday, April 16, at 12pm EDT on Facebook and 6pm EDT on YouTube for special COVID-19 live Q&As.
  • I’m working on a second webinar for May. Be sure you’re subscribed to our newsletter to get all of the latest updates first. Click here to subscribe.

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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: