How Much Arsenic in Rice Is Too Much?

What are some strategies to reduce arsenic exposure from rice?

Those who are exposed to the most arsenic in rice are those who are exposed to the most rice, like people who are eating plant-based, gluten-free, or dairy-free. So, at-risk populations are not just infants and pregnant women, but also those who may tend to eat more rice. What “a terrible irony for the health conscious” who are trying to avoid dairy and eat lots of whole foods and brown rice—so much so they may not only suffer some theoretical increased lifetime cancer risk, but they may actually suffer arsenic poisoning. For example, a 39-year-old woman had celiac disease, so she had to avoid wheat, barley, and rye, but she turned to so much rice that she ended up with sky-high arsenic levels and some typical symptoms, including “diarrhea, headache, insomnia, loss of appetite, abnormal taste, and impaired short-term memory and concentration.” As I discuss in my video How Much Arsenic in Rice Is Too Much, we, as doctors, should keep an eye out for signs of arsenic exposure in those who eat lots of rice day in and day out.

As you can see at 1:08 in my video, in its 2012 arsenic-in-rice exposé, Consumer Reports recommended adults eat no more than an average of two servings of rice a week or three servings a week of rice cereal or rice pasta. In its later analysis, however, it looked like “rice cereal and rice pasta can have much more inorganic arsenic—a carcinogen—than [its] 2012 data showed,” so Consumer Reports dropped its recommendation down to from three weekly servings to a maximum of only two, and that’s only if you’re not getting arsenic from other rice sources. As you can see from 1:29 in my video, Consumer Reports came up with a point system so people could add up all their rice products for the week to make sure they’re staying under seven points a week on average. So, if your only source of rice is just rice, for example, then it recommends no more than one or two servings for the whole week. I recommend 21 servings of whole grains a week in my Daily Dozen, though, so what to do? Get to know sorghum, quinoa, buckwheat, millet, oatmeal, barley, or any of the other dozen or so common non-rice whole grains out there. They tend to have negligible levels of toxic arsenic.

Rice accumulates ten times more arsenic than other grains, which helps explain why the arsenic levels in urine samples of those who eat rice tend to consistently be higher than those who do not eat rice, as you can see at 2:18 in my video. The FDA recently tested a few dozen quinoa samples, and most had arsenic levels below the level of detection, or just trace amounts, including the red quinoas that are my family’s favorite, which I was happy about. There were, however, still a few that were up around half that of rice. But, overall, quinoa averaged ten times less toxic arsenic than rice. So, instead of two servings a week, following the Consumer Reports recommendation, you could have 20. You can see the chart detailing the quinoa samples and their arsenic levels at 2:20 in my video.

So, diversifying the diet is the number-one strategy to reduce exposure of arsenic in rice. We can also consider alternatives to rice, especially for infants, and minimize our exposure by cooking rice like pasta with plenty of extra water. We found that a 10:1 water-to-rice ratio seemed best, though the data suggest the rinsing doesn’t seem to do much. We can also avoid processed foods sweetened with brown rice syrup. Is there anything else we can do at the dining room table while waiting for federal agencies to establish some regulatory limits?

What if you eat a lot of fiber-containing foods with your rice? Might that help bind some of the arsenic? Apparently not. In one study, the presence of fat did seem to have an effect, but in the wrong direction: Fat increased estimates of arsenic absorption, likely due to the extra bile we release when we eat fatty foods.

We know that the tannic acid in coffee and especially in tea can reduce iron absorption, which is why I recommend not drinking tea with meals, but might it also decrease arsenic absorption? Yes, by perhaps 40 percent or more, so the researchers suggested tannic acid might help, but they used mega doses—17 cups of tea worth or that found in 34 cups of coffee—so it isn’t really practical.

What do the experts suggest? Well, arsenic levels are lower in rice from certain regions, like California and parts of India, so why not blend that with some of the higher arsenic rice to even things out for everybody?


Another wonky, thinking-outside-the-rice-box idea involves an algae discovered in the hot springs of Yellowstone National Park with an enzyme that can volatize arsenic into a gas. Aha! Researchers genetically engineered that gene into a rice plant and were able to get a little arsenic gas off of it, but the rice industry is hesitant. “Posed with a choice between [genetically engineered] rice and rice with arsenic in it, consumers may decide they just aren’t going to eat any rice” at all.

This is the corresponding article to the 11th in a 13-video series on arsenic in the food supply. If you missed any of the first ten videos, watch them here:

You may also be interested in Benefits of Turmeric for Arsenic Exposure.

Only two major questions remain: Should we moderate our intake of white rice or should we minimize it? And, are there unique benefits to brown rice that would justify keeping it in our diet despite the arsenic content? I cover these issues in the final two videos: Is White Rice a Yellow-Light or Red-Light Food? and Do the Pros of Brown Rice Outweigh the Cons of Arsenic?.

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:

Why Was Chicken the Primary Source of Arsenic Exposure in Children?

What was the National Chicken Council’s response to public health authorities calling for the industry to stop feeding arsenic-based drugs to poultry?

“Dietary practices influence our exposure to pesticides, toxic heavy metals, persistent organic pollutants, and industrial pollutants….A diet high in fish and other animal products, for example, results in greater exposure to persistent organic compounds and metals than does a plant-based diet because these compounds bioaccumulate up the food chain.” Researchers at UC Davis analyzed the diets of children and adults in California to see just how bad things have gotten.

Cancer benchmark levels were exceeded by all children—100 percent of children—for arsenic, the banned pesticides dieldrin and DDT, metabolite DDE, as well as dioxins, and not just by a little. As you can see at 0:51 in my video Where Does the Arsenic in Chicken Come From?, researchers found more than a hundred times the acceptable daily exposure for arsenic in preschoolers, school-aged children, parents, and older adults, about ten times the acceptable levels for various pesticides, and up to a thousand times the daily dose for dioxins. Where are all these toxins coming from?

The number-one source of dioxins in the diets of Californian preschoolers, kids, parents, and grandparents appears to be dairy for all age groups, followed by meat, and then white potatoes, refined grains, mushrooms, poultry, and fish.

These days, our DDT legacy is also mostly from dairy. Dieldrin was created as a safer alternative to DDT, but it was banned just two years later, in 1974, though it’s still found in our bodies, mostly thanks to dairy, meat, and, evidently, cucumbers.

Chlordane made it into the 1980s before being banned, though we’re still exposed through dairy (and cukes). Lead is — foodwise — also mostly from dairy, and mercury is not surprisingly mostly from tuna and other seafood. But the primary source of arsenic in children? Surprisingly, mostly from chicken. Why?

Let me tell you a tale of arsenic in chicken. Arsenic is “well known as a poison by anyone who reads mysteries or the history of the Borgias, and with its long and colourful history, arsenic is not something that people want in their food.” So, when a biostatistics student went to the USDA in 2000 in search of a project for his master’s degree, he decided to look into it. He found a startling difference: Arsenic levels in chicken were three times higher than in other meats. His veterinary colleagues weren’t at all surprised and explained that four different types of arsenic-containing antibiotic drugs are fed to poultry—and have been fed to them since 1944.

“While arsenic-based drugs had been fed to poultry since the 1940s, recognition of this source of exposure [for humans] only occurred after appropriate statistical analysis of the data”—that is, after this student churned through the data. It was published in 2004 and expanded upon in 2006. The National Chicken Council (NCC) was none too pleased, saying lots of foods are contaminated with arsenic. “By focusing specifically on chicken, IATP [the Institute for Agriculture and Trade Policy] makes it clear that it is producing a publicity-oriented document focused on the objective of forcing [chicken] producers to stop using these safe and effective products”—by which the NCC means these arsenic-containing drugs. In fact, the NCC admits to using them but says we don’t need to worry because chicken producers use organic arsenic, “not the inorganic form made infamous in ‘Arsenic and Old Lace.’” Okay, so we don’t need to worry—until, apparently, we cook it. When chicken is cooked, it appears that some of the arsenic drug in the meat turns into the ”Arsenic and Old Lace” variety. So, the Poison-Free Poultry Act of 2009 was introduced into Congress, flopped, and was followed by the subsequent introduction of the Poison-Free Poultry Act of 2011. Did the second attempt fare any better? No, legislators once again said pish posh to poison-poor poultry. So, in 2013, a coalition of nine organizations got together and sued the FDA, and by December 31, 2015, all arsenic-containing poultry drugs were withdrawn. As of 2016, arsenic is no longer to be fed to chickens. The bad news is that without giving birds the arsenic-containing drug roxarsone, chicken may lose some of its “appealing pink color.”

In the end, the poultry industry got away with exposing the American public to arsenic for 72 years. “It should be noted that the European Union has never approved drugs containing arsenic for animal consumption” in the first place, saying, Hmm, feed our animals arsenic? No thanks, nein danke, no grazie, non, merci.

Europe has also long since banned the “urgent threat to human health” posed by feeding farm animals millions of pounds of human antibiotics. As you can see at 5:30 in my video, feeding chickens en masse literally tons of drugs like tetracyclines and penicillins to fatten them faster is a problem that gets worse every year instead of better and dates back to 1951 when drug companies whipped out the ALL CAPS in advertisements,  promising “PROFITS…several times higher!”, a dangerous practice the poultry industry has gotten away with for 68 years…and counting.

If you don’t eat poultry and are feeling a little cocky, you may want to check out my 12-video series on arsenic in rice before you gloat too much:

Think feeding arsenic to chickens is weird? Check out Illegal Drugs in Chicken Feathers.

And for more on the critical public health threat posed by antibiotic overuse in animal agriculture, 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:

Kidney Toxins Created by Meat Consumption

As I discuss in my video How to Treat Heart Failure and Kidney Failure with Diet, one way a diet rich in animal-sourced foods like meat, eggs, and cheese may contribute to heart disease, stroke, and death is through the production of an atherosclerosis-inducing substance called TMAO. With the help of certain gut bacteria, the choline and carnitine found concentrated in animal products can get converted into TMAO. But, wait a second. I thought atherosclerosis, or hardening of the arteries, was about the buildup of cholesterol. Is that not the case?

“Cholesterol is still king,” but TMAO appears to accelerate the process. It seems that TMAO appears to increase the ability of inflammatory cells within the atherosclerotic plaque in the artery walls to bind to bad LDL cholesterol, “which makes the cells more prone to gobble up cholesterol.” So TMAO is just “another piece to the puzzle of how cholesterol causes heart disease.”

What’s more, TMAO doesn’t just appear to worsen atherosclerosis, contributing to strokes and heart attacks. It also contributes to heart and kidney failure. If you look at diabetics after a heart attack, a really high-risk group, nearly all who started out with the most TMAO in their bloodstream went on to develop heart failure within 2,000 days, or about five years. In comparison, only about 20 percent of those starting out with medium TMAO levels in the blood went into heart failure and none at all in the low TMAO group, as you can see at 1:21 in my video.

So, those with heart failure have higher levels of TMAO than controls, and those with worse heart failure have higher levels than those with lesser stage heart disease. If you follow people with heart failure over time, within six years, half of those who started out with the highest TMAO levels were dead. This finding has since been replicated in two other independent populations of heart failure patients.

The question is, why? It’s probably unlikely to just be additional atherosclerosis, since that takes years. For most who die of heart failure, their heart muscle just conks out or there’s a fatal heart rhythm. Maybe TMAO has toxic effects beyond just the accelerated buildup of cholesterol.

What about kidney failure? People with chronic kidney disease are at a particularly “increased risk for the development of cardiovascular disease,” thought to be because of a diverse array of uremic toxins. These are toxins that would normally be filtered out by the kidneys into the urine but may build up in the bloodstream as kidney function declines. When we think of uremic toxins, we usually think of the toxic byproducts of protein putrefying in our gut, which is why specially formulated plant-based diets have been used for decades to treat chronic kidney failure. Indeed, those who eat vegetarian diets form less than half of these uremic toxins.

Those aren’t the only uremic toxins, though. TMAO, which, as we’ve discussed, comes from the breakdown of choline and carnitine found mostly in meat and eggs, may be increasing heart disease risk in kidney patients as well. How? “The cardiovascular implication of TMAO seems to be due to the downregulation of reverse cholesterol transport,” meaning it subverts our own body’s attempts at pulling cholesterol out of our arteries.

And, indeed, the worse our kidney function gets, the higher our TMAO levels rise, and those elevated levels correlate with the amount of plaque clogging up their arteries in their heart. But once the kidney is working again with a transplant, your TMAO levels can drop right back down. So, TMAO was thought to be a kind of biomarker for declining kidney function—until a paper was published from the Framingham Heart Study, which found that “elevated choline and TMAO levels among individuals with normal renal [kidney] function predicted increased risk for incident development of CKD,” chronic kidney disease. This suggests that TMAO is both a biomarker and itself a kidney toxin.

Indeed, when you follow kidney patients over time and assess their freedom from death, those with higher TMAO, even controlling for kidney function, lived significantly shorter lives, as you can see at 4:44 in my video. This indicates this is a diet-induced mechanism for progressive kidney scarring and dysfunction, “strongly implying the need to focus preventive efforts on dietary modulation,” but what might that look like? Well, maybe we should reduce “dietary sources of TMAO generation, such as some species of deep-sea fish, eggs, and meat.”

It also depends on what kind of gut bacteria you have. You can feed a vegan a steak, and they still don’t really make any TMAO because they haven’t been fostering the carnitine-eating bacteria. Researchers are hoping, though, that one day, they’ll find a way to replicate “the effects of the vegetarian diet…by selective prebiotic, probiotic, or pharmacologic therapies.”

For more on this revolutionary TMAO story, see:

For more on kidney failure, see Preventing Kidney Failure Through Diet and Treating Kidney Failure Through Diet.

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:

Can Soy Prevent and Treat Prostate Cancer?

As I discuss in my video The Role of Soy Foods in Prostate Cancer Prevention and Treatment, a compilation of 13 observational studies on soy food consumption and the risk of prostate cancer found that soy foods appear to be “protective.” What are observational studies? As opposed to interventional studies, in observational studies, researchers observe what people are eating but don’t intervene and try to change their diets. In these studies, they observed that men who ate more soy foods had lower rates of prostate cancer, but the problem with observational studies is that there could be confounding factors. For example, “people who choose to eat soy also make other lifestyle decisions that lower the risk of cancer (e.g., lower fat intake, higher vegetable and fruit intake, more frequent exercise),” maybe that is why they have less cancer. Most of the studies tried to control for these other lifestyle factors, but you can’t control for everything. What’s more, most of the studies were done in Asia, so maybe tofu consumption is just a sign of eating a more traditional diet. Is it possible that the reason non-tofu consumers got more cancer is that they had abandoned their traditional diet? If only we could look at a Western population that ate a lot of soy. We can: the Seventh-Day Adventists.

In the 1970s, more than 12,000 Adventist men were asked about their use of soy milk and then were followed for up to 16 years to see who got cancer and who did not. So, what did they find? Frequent consumption of soy milk was associated with a whopping 70 percent reduction of the risk of prostate cancer, as you can see at 1:33 in my video. Similarly, in a multiethnic study that involved a number of groups, soy intake appeared protective in Latinos, too.

Prostate cells carry beta type estrogen receptors, which appear to act as a tumor suppressor, a kind of “gatekeeper…inhibiting invasion, proliferation and…preventing” the prostate cells from turning cancerous. And, those are the receptors targeted by the phytoestrogens in soy, like genistein, which inhibits prostate cancer cell invasion and spread in a petri dish at the kind of levels one might get consuming soy foods. The prevention of metastases is critical, as death from prostate cancer isn’t caused by the original tumor, but its spread throughout the body, which explains why it “is recommended that men with prostate cancer consume soy foods, such as soybeans, tofu, miso and tempeh.”

Wait a moment. Dean Ornish and his colleagues got amazing results, apparently reversing the progression of prostate cancer with a plant-based diet and lifestyle program. Was it because of the soy? Their study didn’t just include a vegan diet, but a vegan diet supplemented with a daily serving of tofu and a soy protein isolate powder. There have been studies showing that men given soy protein powders develop less prostate cancer than the control group, but what was the control group getting? Milk protein powder. Those randomized to the milk group got six times more prostate cancer than the soy group, but was that due to the beneficial effects of soy or the deleterious effects of the dairy? Dairy products are not just associated with getting prostate cancer, but also with dying from prostate cancer. Men diagnosed with prostate cancer who then ate more dairy tended to die sooner, and “both low-fat and high-fat dairy consumption were positively associated with an increased risk of fatal outcome.”

The best study we have on soy protein powder supplementation for prostate cancer patients found no significant benefit, and neither did a series of soy phytoestrogen dietary supplements. But, perhaps that’s because they used isolated soy components rather than a whole soy food. “Taking the whole-food approach may be more efficacious,” but it can be hard to do controlled studies with whole foods: You can make fake pills, but how do you give people placebo tofu?

A group of Australian researchers creatively came up with a specially manufactured bread containing soy grits to compare to a placebo regular bread and gave slices to men diagnosed with prostate cancer awaiting surgery. As you can see at 4:31 in my video, they saw a remarkable difference in just about three weeks time. It was the first study to show that a diet incorporating a whole soy food could favorably affect prostate cancer markers, but you can’t just go out and buy soy grit bread. Another study was a little more practical. Twenty men with prostate cancer who had been treated with radiation or surgery but seemed to be relapsing were asked to drink three cups of regular soy milk a day. The PSA levels in each of the 20 patients were all rising before they started the soy milk, suggesting they had relapsing or metastatic cancer growing inside of them. However, during a year drinking soy milk, 6 out of the 20 subjects got better, 2 got worse, and the remaining 12 remained unchanged, as you can see from 5:02 in my video. So, they concluded that soy food may help in a subset of patients.

Based on all these studies, the results Ornish and his colleagues got were probably due to more than just the soy. Similarly, the low prostate cancer rates in Asia are probably because of more than just the soy, since the lowest rates are also found in parts of Africa, where I don’t think they’re eating a lot of tofu. Indeed, in the multiethnic study, other types of beans besides soy also appeared protective for Latinos and all the groups put together, when looking at the most aggressive forms of prostate cancer. So, the protection associated with plant-based diets may be due to eating a variety of healthy foods. 

That soy milk stat from the Adventist study is astounding. What about fermented soy foods, though? That was the subject of Fermented or Unfermented Soy Foods for Prostate Cancer Prevention?.

Reversing the progression of cancer? See How Not to Die from Cancer.

Given the power of diet, it’s amazing to me how difficult Changing a Man’s Diet After a Prostate Cancer Diagnosis can be. It’s not all or nothing, though. Check out Prostate Cancer Survival: The A/V Ratio.

For soy and breast cancer survival, see Is Soy Healthy for Breast Cancer Survivors?.

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:

Fermented or Unfermented Soy?

As you can see at the start of my video Fermented or Unfermented Soy Foods for Prostate Cancer Prevention?, there is an enormous variation in the rates of prostate cancer around the globe, with among the highest rates in the United States and lowest rates in Asia—though that may be changing. The largest increase in prostate cancer rates in the world in recent decades has been in South Korea, for example: a 13-fold increase in prostate cancer deaths nationwide. Researchers suggested the increase in animal foods may have played a role, since that was the biggest change in their diet over that period, with nearly an 850 percent increase.

This is consistent with what we know in general about foods and the prevention and management of prostate cancer. Tomatoes, cruciferous vegetables like broccoli, and soy foods appear to decrease risk, there’s no clear benefit from fish, but there is an increased risk associated with meat and dairy, as you can see at 0:52 in my video. This may be because a diet based around whole plant foods “may effectively reduce inflammation in the body.”

There is also a genetic factor. If you have a first-degree relative with prostate cancer, you may be at three-fold higher risk, but non-genetic factors may increase your risk 300-fold. How do we know the low rates in Asia aren’t genetic? Because when Asians move to the United States, their rates shoot up, “and by the second generation, the incidence rate [is] already approaching that of average Americans.” This may be because of more Burger Kings and Dairy Queens, but could also be because of eating fewer protective foods, such as soy.

A systematic review of all soy and prostate cancer population studies to date confirmed that soy foods are associated with lower the risk, but that’s a relatively broad category. There are all sorts of soy foods. There are fermented soy foods, like miso and tempeh, and unfermented ones, like tofu and soy milk. Which are more protective? Researchers sifted through the studies, and it turns out that only the unfermented soy seemed to help. Tofu and soy milk consumption was associated with about a 30 percent reduction in risk, whereas there didn’t appear to be any protection linked to fermented soy foods.

What about other healthy plant foods, like broccoli and turmeric? See what they can do in Best Supplements for Prostate Cancer.

Dean Ornish and his colleagues got amazing results, apparently reversing the progression of prostate cancer with a plant-based diet and lifestyle program. Do you think it could be because of the soy? It wasn’t just a vegan diet, but a vegan diet supplemented with a daily serving of tofu and a soy protein isolate powder. Find out in The Role of Soy Foods in Prostate Cancer Prevention and Treatment.

More on the number-one cancer among men:

What about soy and breast cancer? I’m glad you asked!

Who Shouldn’t Eat Soy? Watch the video to find 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:

What About the Trans Fat in Animal Fat?

The years of healthy life lost due to our consumption of trans fats are comparable to the impact of conditions like meningitis, cervical cancer, and multiple sclerosis. But, if “food zealots” get their wish in banning added trans fats, what’s next? I explore this in my video Banning Trans Fat in Processed Foods but Not Animal Fat.

Vested corporate interests rally around these kinds of slippery slope arguments to distract from the fact that people are dying. New York Mayor Bloomberg was decried as a “meddling nanny” for his trans fat ban and attempt to cap soft drink sizes. How dare he try to manipulate consumer choice! But isn’t that what the food industry has done? “Soft drink portion sizes have grown dramatically, along with Americans’ waistlines.” In 1950, a 12-ounce soda was the king-sized option. Now, it’s the kiddie size. Similarly, with trans fats, it was the industry that limited our choice by putting trans fats into everything without even telling us. Who’s the nanny now?

New York City finally won its trans fat fight, preserving its status as a public health leader. “For example, it took decades to achieve a national prohibition of lead paint, despite unequivocal evidence of harm,” but New York City’s Board of Health led the way, banning it “18 years before federal action.”

There’s irony in the slippery slope argument: First, they’ll come for your fries; next, they’ll come for your burger. After the trans fat oil ban, one of the only remaining sources of trans fat is in the meat itself. “Trans fats naturally exist in small amounts in the fat in meat and milk,” as I’ve discussed before in my video Trans Fat in Meat and Dairy. Before the trans fat ban, animal products only provided about one fifth of America’s trans fat intake, but since the U.S. trans fat ban exempts animal products, they will soon take over as the leading source. As you can see at 2:09 in Banning Trans Fat in Processed Foods but Not Animal Fat, now that added trans fats are banned in Denmark, for example, the only real trans fat exposure left is from animal products found in the U.S. dairy, beef, chicken fat, turkey meat, lunch meat, and hot dogs, with trace amounts in vegetable oils due to the refining process.

The question is: Are animal trans fats as bad as processed food trans fats? As you can see at 2:38 in my video, a compilation of randomized interventional trials found that they both make bad cholesterol go up and they both make good cholesterol go down. So, both animal trans fats and processed food trans fats make the ratio of bad to good cholesterol go up—which is bad. Therefore, all trans fats cause negative effects “irrespective of their origin.” The researchers suspect that also removing natural trans fats from the diet could prevent tens of thousands of heart attacks, but unlike processed foods, you can’t remove trans fats from milk and meat because trans fats are there naturally.

The livestock industry suggests that a little bit of their trans fats might not be too bad, but you saw the same everything-in-moderation argument coming from the Institute of Shortening and Edible Oils after industrial trans fats were first exposed as a threat. The bottom line is “that intake of all sources of trans fat should be minimized.” The trans fat in processed foods can be banned, and just adhering to the current dietary guidelines to restrict saturated fat intake, which is primarily found in meat and dairy, would automatically cut trans fat intake from animal fats.

The reason no progress may have been made on animal trans fat reduction in Denmark is because The Danish Nutrition Council that pushed for the trans fat ban was a joint initiative of The Danish Medical Association and The Danish Dairy Board. They recognized that “the economic support from The Danish Dairy Council could be perceived as problematic” from a scientific integrity point of view, but, not to worry—“The Danish Medical Association expanded the Executive Board and the funding members to also include the Danish pork industry, the Danish meat industry, The Poultry and Egg Council and The Danish Margarine Industry Association.”

If people want to eat trans fat, isn’t that their right? Yes, but only if they’re informed about the risks—yet The Food Industry Wants the Public Confused About Nutrition.

For more on the industry pushback, see my video Controversy Over the Trans Fat Ban.

There does not appear to be a safe level of exposure to trans fat—or to saturated fat or dietary cholesterol, for that matter. See Trans Fat, Saturated Fat, and Cholesterol: Tolerable Upper Intake of Zero.

If you find these videos about industry influence on public policy compelling, check out my many others, including:

Note that the concept of raising or lowering HDL (the so-called good cholesterol) playing a causal role in heart disease has come into question. See Coconut Oil and the Boost in HDL “Good” Cholesterol.

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 Treat Polycystic Ovary Syndrome (PCOS) with Diet

Given the role that oxidant free radicals are thought to play in aging and disease, one reason fruits and vegetables may be so good for us is that they contain antioxidant compounds. As you can see at 0:20 in my video Benefits of Marjoram for Polycystic Ovary Syndrome (PCOS), different vegetables and herbs have different antioxidant content. When making a salad, for example, spinach, arugula, or red leaf lettuce may provide twice the antioxidants as butterhead lettuce, and choosing purple cabbage over green, or red onions over white can also boost the salad’s antioxidant power.

Fresh herbs are so powerful that even a small amount may double or even quadruple the antioxidant power of the entire meal. For instance, as you can see at 0:50 in my video, the total antioxidants in a simple salad of lettuce and tomato jump up by adding just a tablespoon of lemon balm leaves or half a tablespoon of oregano or mint. Adding marjoram, thyme, or sage not only adds great flavor to the salad, but effectively quadruples the antioxidant content at the same time, and adding a little fresh garlic or ginger to the dressing ups the antioxidant power even more.

Herbs are so antioxidant-rich that researchers decided to see if they might be able to reduce the DNA-damaging effects of radiation. Radioactive iodine is sometimes given to people with overactive thyroid glands or thyroid cancer to destroy part of the gland or take care of any remaining tumor cells after surgery. For days after the isotope injection, patients become so radioactive they are advised not to kiss or sleep close to anyone, including their pets, and if they breathe on a phone, they’re advised to wipe it “carefully” or cover it “with an easily removed plastic bag.” Other recommendations include “avoid[ing] splatter of radioactive urine,” not going near your kids, and basically just staying away from others as much as possible.

The treatment can be very effective, but all that radiation exposure appears to increase the risk of developing new cancers later on. In order to prevent the DNA damage associated with this treatment, researchers tested the ability of oregano to protect chromosomes of human blood cells in vitro from exposure to radioactive iodine. As you can see at 2:25 in my video, at baseline, about 1 in 100 of our blood cells show evidence of chromosomal damage. If radioactive iodine is added, though, it’s more like 1 in 8. What happens if, in addition to the radiation, increasing amounts of oregano extract are added? Chromosome damage is reduced by as much 70 percent. Researchers concluded that oregano extract “significantly protects” against DNA damage induced by the radioactive iodine in white blood cells. This was all done outside the body, though, which the researchers justified by saying it wouldn’t be particularly ethical to irradiate people for experimental research. True, but millions of people have been irradiated for treatment, and researchers could have studied them or, at the very least, they could have just had people eat the oregano and then irradiate their blood in vitro to model the amount of oregano compounds that actually make it into the bloodstream.

Other in vitro studies on oregano are similarly unsatisfying. In a comparison of the effects of various spice extracts, including bay leaves, fennel, lavender, oregano, paprika, parsley, rosemary, and thyme, oregano beat out all but bay leaves in its ability to suppress cervical cancer cell growth in vitro while leaving normal cells alone. But people tend to use oregano orally—that is, they typically eat it—so the relevance of these results are not clear.

Similarly, marjoram, an herb closely related to oregano, can suppress the growth of individual breast cancer cells in a petri dish, as you can see at 3:53 in my video, and even effectively whole human breast tumors grown in chicken eggs, which is something I’ve never seen before. Are there any clinical trials on oregano-family herbs on actual people? The only such clinical, randomized, control study I could find was a study on how marjoram tea affects the hormonal profile of women with polycystic ovary syndrome (PCOS). The most common cause of female fertility problems, PCOS affects up to one in eight young women and is characterized by excessive male hormones, resulting in excess body or facial hair, menstrual irregularities, and cysts in one’s ovaries that show up on ultrasounds.

Evidently, traditional medicine practitioners reported marjoram tea was beneficial for PCOS, but it had never been put to the test…until now. Drinking two daily cups of marjoram tea versus a placebo tea for one month did seem to beneficially affect the subjects’ hormonal profiles, which seems to offer credence to the claims of the traditional medicine practitioners. However, the study didn’t last long enough to confirm that actual symptoms improved as well, which is really what we care about.

Is there anything that’s been shown to help? Well, reducing one’s intake of dietary glycotoxins may help prevent and treat the disease. Over the past 2 decades there has been increasing evidence supporting an important contribution from food-derived advanced glycation end products (AGEs)…[to] increased oxidative stress and inflammation, processes that play a major role in the causation of chronic diseases,” potentially including polycystic ovary syndrome (PCOS). Women with PCOS tend to have nearly twice the circulating AGE levels in their bloodstream, as you can see at 0:33 in my video Best Foods for Polycystic Ovary Syndrome (PCOS). 

PCOS may be the most common hormonal abnormality among young women in the United States and is a common cause of infertility, menstrual dysfunction, and excess facial and body hair. The prevalence of obesity is also higher in women with PCOS. Since the highest AGE levels are found in broiled, grilled, fried, and roasted foods of “mostly animal origin,” is it possible that this causal chain starts with a bad diet? For instance, maybe eating lots of fried chicken leads to obesity, which in turn leads to PCOS. In that case, perhaps what we eat is only indirectly related to PCOS through weight gain. No, because the same link between high AGE levels and PCOS was found in lean women as well.

“As chronic inflammation and increased oxidative stress have been incriminated in the pathophysiology [or disease process] of PCOS, the role of AGEs as inflammatory and oxidant mediators, may be linked with the metabolic and reproductive abnormalities of the syndrome.” Further, the buildup of AGE inside polycystic ovaries themselves suggests a potential role of AGEs contributing to the actual disease process, beyond just some of its consequences.

RAGE is highly expressed in ovarian tissues. The receptor in the body for these advanced glycation end products, the “R” in RAGE, is concentrated in the ovaries, which may be particularly sensitive to its effect. So, AGEs might indeed be contributing to the cause of PCOS and infertility.

Does this mean we should just cut down on AGE-rich foods, such as meat, cheese, and eggs? Or hey, why not come up with drugs that block AGE absorption? We know AGEs have been implicated in the development of many chronic diseases. Specifically, food-derived AGEs play an important role because diet is a major source of these pro-inflammatory AGEs. Indeed, cutting down on these dietary glycotoxins reduces the inflammatory response, but the “argument is often made that stewed chicken would be less tasty than fried chicken…” Why not have your KFC and eat it, too? Just take an AGE-absorption blocking drug every time you eat it to reduce the absorption of the toxins. What’s more, it actually lowers AGE blood levels. This oral absorbent drug, AST-120, is just a preparation of activated charcoal, like what’s used for drug overdoses and when people are poisoned. I’m sure if you took some ipecac with your KFC, your levels would go down, too.

There’s another way to reduce absorption of AGEs, and that’s by reducing your intake in the first place. It’s simple, safe, and feasible. The first step is to stop smoking. The glycotoxins in cigarette smoke may contribute to increased heart disease and cancer in smokers. Then, decrease your intake of high-AGE foods, increase your intake of foods that may help pull AGEs out of your system, like mushrooms, and eat foods high in antioxidants, like berries, herbs, and spices. “Dietary AGE intake can be easily decreased by simply changing the method of cooking from a high dry heat application to a low heat and high humidity…” In other words, move away from broiling, searing, and frying to more stewing, steaming, and boiling.

What we eat, however, may be more important than how we cook it. At 4:00 in my video, I include a table showing the amounts of AGEs in various foods. For instance, boiled chicken contains less than half the glycotoxins of roasted chicken, but even deep-fried potatoes have less than boiled meat. We can also eat foods raw, which doesn’t work as well as for blood pudding, but raw nuts and nut butters may contain about 30 times less glycotoxins than roasted, and we can avoid high-AGE processed foods, like puffed, shredded, and flaked breakfast cereals.

Why does it matter? Because study after study has shown that switching to a low-AGE diet can lower the inflammation within our bodies. Even just a single meal high in AGEs can profoundly impair our arterial function within just two hours of consumption. At 4:54 in my video, you can see the difference between a meal of fried or broiled chicken breast and veggies compared with steamed or boiled chicken breast and veggies. Same ingredients, just different cooking methods. Even a steamed or boiled chicken meal can still impair arterial function, but significantly less than fried or broiled.

“Interestingly, the amount of AGEs administered [to subjects] during the HAGE [high-AGE] intervention was similar to the average estimated daily intake by the general population,” who typically follow the standard American diet. This is why we can decrease inflammation in people by putting them on a low-AGE diet, yet an increase in inflammation is less apparent when subjects switch from their regular diet to one high in AGEs. Indeed, they were already eating a high-AGE diet with so many of these glycotoxins.

Do we have evidence that reducing AGE intake actually helps with PCOS? Yes. Within just two months, researchers found differences from subjects’ baseline diets switched to a high-AGE diet and then to a low-AGE diet, with parallel changes in insulin sensitivity, oxidative stress, and hormonal status, as seen at 5:54 in my video. The take-home learning? Those with PCOS may want to try a low-AGE diet, which, in the study, meant restricting meat to once a week and eating it only boiled, poached, stewed, or steamed, as well as cutting out fast-food-type fare and soda.

What if instead of eating steamed chicken, we ate no meat at all? Rather than measuring blood levels, which vary with each meal, we can measure the level of glycotoxins stuck in our body tissues over time with a high-tech device that measures the amount of light our skin gives off because AGEs are fluorescent. And, not surprisingly, this turns out to be a strong predictor of overall mortality. So, the lower our levels, the better. The “one factor that was consistently associated with reduced [skin fluorescence]: a vegetarian diet.” This “suggests that a vegetarian diet may reduce exposure to preformed dietary AGE…potentially reduc[ing] tissue AGE,” as well as chronic disease risk

What’s so great about antioxidants? See my videos:

Just how many antioxidants do we need? Check out:

For a few simple tips on how to quickly boost the antioxidant content of your food with herbs and spices, see my video Antioxidants in a Pinch.

I touched on the benefits of spearmint tea for PCOS in Enhancing Athletic Performance with Peppermint. Another sorely under-recognized gynecological issue is endometriosis, which I discuss in How to Treat Endometriosis with Seaweed.

Because of AGEs, I no longer toast nuts or buy roasted nut butters, which is disappointing because I really enjoy those flavors so much more than untoasted and unroasted nuts. But, as Dr. McDougall likes to say, nothing tastes as good as healthy feels. For more on why it’s important to minimize our exposure to these toxic compounds, 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:

The Role of Meat and Dairy Viruses in Cancer

“Nearly 20% of cancer cases arising worldwide can be linked to infectious agents, including viruses.” Seven viruses are now conclusively tied to human cancers, and, as new viruses enter into human populations, the incidence and causes of cancer will likely change accordingly.

The foundation of modern tumor virology was laid more than a century ago with the discovery of a cancer-causing chicken virus, for which a Nobel Prize was awarded. Another Nobel Prize went to the “medical doctor-turned-virologist” who discovered that the HPV virus was causing cervical cancer. In his acceptance speech, he mused that there may be a bovine polyoma virus—a multiple tumor virus in cattle—that could be playing a role in human colon cancer, lung cancer, and breast cancer, but no polyoma virus had ever been discovered in meat…until now.

As I discuss in my video The Role of Burger Viruses in Cancer, polyomaviruses are a particular concern—not only because they are known to be carcinogenic, but also because they can survive cooking temperatures. Since a single burger these days can contain meat from “many dozens of animals,” researchers felt “this could present an ideal situation for virus-hunting…” Researchers from the National Cancer Institute purchased meat samples from three separate supermarkets and found three different polyomaviruses in ground beef, as you can see at 1:52 in my video. Now, just because three types of “polyomavirus species are commonly detectable in food-grade ground beef” doesn’t necessarily mean they are causing human disease. What made this Nobel laureate suspect them? Well, for one thing, some people got cancer right where they had been vaccinated for smallpox—a whole bunch of different cancers, in fact. The vaccine had been harvested from the skin of calves, so “it is possible” there could have been some cancer-causing cow virus.

“Many people are exposed to potentially virus-contaminated meat and dairy products” through their diets, but those in the industry, “such as farm workers, butchers, veterinarians, and employees in dairies,” would be even more exposed. Do these groups have higher cancer incidence? Indeed, it now appears to be clear “that workers in the meat industry are at increased risk of developing and dying from cancer.”

Another reason to suspect the involvement of some kind of bovine infectious factor in colorectal cancer is the fact that there appear to be relatively low rates of colorectal cancer in countries where not a lot of beef is eaten. And, when meat consumption suddenly increases, rates shoot up, as you can see at 3:15 in my video. “The only exception is Mongolia where they have low rates of colon cancer and eat a lot of red meat, but there they eat yak.” Maybe yaks don’t harbor the same viruses.

Can’t you just avoid steak tartare? Even steak cooked “medium” may not reach internal temperatures above 70° Celsius, and it takes temperatures higher than that to inactivate some of these viruses, so we would expect viruses to survive both cooking and pasteurization. In fact, researchers followed up with a paper suggesting the consumption of dairy products may “represent one of the main risk factors for the development of breast cancer” in humans. The recent discovery of a larger number of presumably new viruses in the blood, meat, and milk of dairy cows should be investigated, since one might speculate that infectious “agents present in dairy products possess a higher affinity to mammary [breast] cells,” since they came from breast cells. The fact that people with lactose intolerance, who tend to avoid milk and dairy throughout their lives, have lower rates of breast and other cancers could be seen as supporting this concept. Though, there are certainly other reasons dairy may increase cancer risk, such as increasing levels of the cancer-promoting growth hormone IGF-1 or adversely affecting our gut microbiome. Or, for that matter, maybe the plant-based milks they’re drinking instead could be protective. That’s the problem with population studies: You can’t tease out cause and effect. It doesn’t matter how many viruses are found in retail beef, pork, and chicken, as you can see at 5:16 in my video, if we can’t connect the dots.  

Can’t we just look for the presence of these viruses within human tumors? Researchers have tried and did find some, but even if you don’t find any, that doesn’t necessarily mean viruses didn’t play a role. There’s a “viral hit-and-run” theory of cancer development that suggests that certain viruses can slip in and out of our DNA to initiate the cancer, but be long gone by the time the tumor matures.

There’s still a lot of work to be done. But, if the link between bovine polyomaviruses and human disease pans out, the National Cancer Institute researchers envision the development of a high potency vaccine. So, just like the HPV vaccine may prevent cervical cancer from unsafe sex, perhaps one day, vaccines may prevent breast and colon cancer from unsafe sirloin.

This reminds me of the story of bovine leukemia virus and breast cancer. For more on that, see:

What about chicken? Check out The Role of Poultry Viruses in Human Cancers and Poultry and Penis Cancer.

One of the problems with eating other animals is that we put ourselves at risk of their diseases. Not once have I diagnosed anyone with Dutch Elm Disease or a really bad case of aphids. See Eating Outside Our Kingdom for more on this concept.

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 to Block Lead Absorption

Intake of certain nutrients has been associated with lower lead levels in the body. For example, women with higher intake of thiamine, also called vitamin B1, tended to have lower blood lead levels, and the same was found for lead-exposed steel workers—and not just with thiamine, as “content of dietary fiber, iron, or thiamine intake each correlated inversely with blood lead concentrations in workers…” The thinking is that the fiber might glom onto the lead and flush it out of the body, the iron would inhibit the lead absorption, and the thiamine may accelerate lead removal through the bile. So, researchers suggest that eating lots of iron, fiber and especially thiamine-rich foods “may induce rapid removal and excretion of the lead from the tissues.” But thiamine’s never been put to the test by giving it to people to see if their lead levels drop. The closest I could find is a thiamine intervention for lead-intoxicated goats.

And much of the fiber data are just from test tube studies. In one, for example, researchers used simulated intestinal conditions, complete with “flasks” of feces, and both soluble and insoluble dietary fiber were able to bind up large amounts of mercury, cadmium, and lead to such an extent that they may have been able to block absorption in the small intestine. But, when our good gut flora then eat the fiber, some of the heavy metals may be re-released down in the colon, so it’s not completely fail safe. And, as with thiamine, there haven’t been controlled human studies.

But where is thiamine found? At 1:47 in my video How to Lower Lead Levels with Diet: Thiamine, Fiber, Iron, Fat, Fasting?, I feature a list of some of the healthiest sources of thiamine-rich foods that also contain fiber, which include highly concentrated, super healthy foods like beans and greens—foods we should all be eating anyway. So, even if thiamine- and fiber-rich foods don’t actually lower lead levels, we’ll still end up healthier.

What happened when iron was put to the test? It failed to improve the cognitive performance of lead-exposed children and failed to improve behavior or ADH symptoms, which is no surprise, because it also failed to bring down lead levels, as did zinc supplementation. It turns out that while iron may limit the absorption of lead, “it may also inhibit excretion of previously absorbed lead” that’s already in your body. What’s more, iron may not even inhibit lead absorption in the first place. That was based on rodent studies, and it turns out we’re not rodents.

We get the same story with zinc. It may have helped to protect rat testicles, but didn’t seem to help human children. “Nevertheless, iron is routinely prescribed in children with lead poisoning.” But, “given the lack of scientific evidence supporting the use of iron [supplementation] in…children with lead poisoning, its routine use should be re-examined.” Though, obviously, supplementation may help if you have an iron deficiency.

High fat intake has been identified as a nutritional condition that makes things worse for lead-exposed children. In fact, dietary fat has been associated with higher lead levels in cross-sectional, snapshot-in-time type studies, and there is a plausible biological mechanism: Dietary fat may boost lead absorption by stimulating extra bile, which in turn may contribute to lead absorption, but you really don’t know until you put it to the test.

In addition to testing iron, researchers also tested fat. They gave a group of intrepid volunteers a cocktail of radioactive lead and then, with a Geiger counter, measured how much radiation the subjects retained in their bodies. Drinking the lead with iron or zinc didn’t change anything, but adding about two teaspoons of vegetable oil boosted lead absorption into the body from about 60 percent up to around 75 percent, as you can see at 4:17 in my video.

The only thing that seemed to help, dropping lead absorption down to about 40 percent, was eating a light meal with the lead drink. What was the meal? Coffee and a donut. I think this is the first donut intervention I’ve ever seen with a positive outcome! Could it have been the coffee? Unlikely, because if anything, coffee drinking has been associated with a tiny increase in blood lead levels. If fat makes things worse, and the one sugar they tried didn’t help, the researchers figured that what made the difference was just eating food—any food—and not taking in lead on an empty stomach. And, indeed, if you repeat the study with a whole meal, lead absorption doesn’t just drop from 60 percent to 40 percent—it drops all the way down to just 4 percent! That’s extraordinary. That means it’s 15 times worse to ingest lead on an empty stomach.

Lead given 12 hours before a meal was absorbed at about 60 percent, so most of it was absorbed. When the same amount of lead was given three hours after a meal and also seven hours after a meal, most of it was absorbed at those times, too. But, if you get some food in your stomach within a few hours of lead exposure, you can suppress the absorption of some or nearly all of the lead you ingested, which you can see at 0:11 in my video How to Lower Lead Levels with Diet: Breakfast, Whole Grains, Milk, Tofu?.

This is why it’s critical to get the lead out of our tap water. Although it’s estimated that most of our lead exposure comes from food, rather than water, it’s not what we eat that matters, but what we absorb. If 90 percent of the lead in food is blocked from absorption by the very fact that it’s in food, 10 to 20 times more lead could be absorbed into your bloodstream simply by consuming the same amount of lead in water drank on an empty stomach.

And, since children empty their stomachs faster than adults because kids “have more rapid gastric emptying times,” the timing of meals may be even more important. With little tummies emptying in as few as two hours after a meal, offering midmorning and midafternoon snacks in addition to breakfast and regular meals may cut down on lead absorption in a contaminated environment. And, of course, we should ensure that children wash their hands prior to eating.

So, do preschoolers who eat breakfast have lower levels of lead in their blood? In the first study of its kind, researchers found that, indeed, children who ate breakfast regularly did appear to have lower lead levels, supporting recommendations to provide regular meals and snacks to young children at risk for lead exposure.

Is there anything in food that’s particularly protective? Researchers tested all sorts of foods to find out, and it turns out the “effect of a meal was probably largely due to its content of calcium and phosphate salts but lead uptake was probably further reduced by phytate which is plentiful in whole cereals,” but if calcium and phosphates are protective, you’d think dairy would work wonders. And, indeed, they started giving milk “to workers to prevent lead exposure” ever since calcium was shown to inhibit lead absorption in rats. But, in humans, there’s something in milk that appeared to increase lead uptake, and it wasn’t the fat because they found the same problem with skim milk.

“For over a century milk was recommended unreservedly to counteract lead poisoning in industry,” but this practice was abandoned in the middle of the last century once we learned that milk’s “overall effect is to promote the absorption of lead from the intestinal tract.” What’s the agent in milk that promotes the absorption of lead from the gut? It may be the milk sugar, lactose, though the “mechanism by which lactose enhances lead absorption is not clear.”

The bottom line? “In the past…milk was used as a prophylactic agent to protect workers in the lead industry. Recent studies, however, suggest that this practice is unjustified and may even be harmful.” So, giving people whole grains may offer greater protection against lead uptake.

However, the most potently calcium and phytate-rich food would be tofu. Isolated soy phytonutrients may have a neuroprotective effect, at least this was the case in petri dish-type studies. As you can see at 3:45 in my video, if you add a little lead to nerve cells, you can kill off about 40 percent of them, but if you then give more and more soy phytonutrients, you can ameliorate some of the damage. This is thought to be an antioxidant effect. If you add lead to nerve cells, you can get a big burst of free radicals, but less and less as you drip on more soy compounds.

Nevertheless, even if this worked outside of a lab, cutting down on the toxic effects of lead is nice, but cutting down on the levels of lead in your body is even better. “Because tofu has high content of both calcium and phytic acid phytate…it is biologically plausible that tofu may inhibit lead absorption and retention, thus reducing blood lead levels.” But you don’t know, until you put it to the test.

Tofu consumption and blood lead levels were determined for about a thousand men and women in China. For every nine or so ounces of tofu consumed a week, there appeared to be about four percent less lead in their bloodstream. Those who ate up to two and a half ounces a day had only half the odds of having elevated lead levels, compared to those eating less than about nine ounces a week. Those consuming nearly four ounces a day appeared to cut their odds by more than 80 percent. This was just a cross-sectional study, or snapshot in time, so it can’t prove cause and effect. What you need is an interventional study where you randomize people into two groups, giving half of them some food to see if it drives down lead levels. I cover this in my video Best Food for Lead Poisoning: Chlorella, Cilantro, Tomatoes, Moringa?.

Where does all this lead exposure come from anyway? Check out the first five videos on this series:

For more about blocking lead absorption, as well as what to eat to help rid yourself of the lead you’ve already built up, see:

Or, even better, don’t get exposed in the first place. Find out more in these videos:

Some of my other videos on lead include:

And what about lead levels in women? 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 Explains the Egg-Cancer Connection

The reason egg consumption is associated with elevated cancer risk may be the TMAO, considered the “smoking gun” of microbiome-disease interactions.

“We are walking communities comprised not only of a Homo sapiens host, but also of trillions of symbiotic commensal microorganisms within the gut and on every other surface of our bodies.” There are more bacterial cells in our gut than there are human cells in our entire body. In fact, only about 10 percent of the DNA in our body is human. The rest is in our microbiome, the microbes with whom we share with the “walking community” we call our body. What do they do?

Our gut bacteria microbiota “serve as a filter for our largest environmental exposure—what we eat”—and, “technically speaking, food is a foreign object that we take into our bodies” by the pound every day. The “microbial community within each of us significantly influences how we experience a meal…Hence, our metabolism and absorption of food occurs through” this filter of bacteria.

However, as you can see at 1:22 in my video How Our Gut Bacteria Can Use Eggs to Accelerate Cancer, if we eat a lot of meat, including poultry and fish, milk, cheese, and eggs, we can foster the growth of bacteria that convert the choline and carnitine in those foods into trimethylamine (TMA), which can be oxidized into TMAO and wreak havoc on our arteries, increasing our risk of heart attack, stroke, and death.

We’ve known about this “troublesome” transformation from choline into trimethylamine for more than 40 years, but that was way before we learned about the heart disease connection. Why were researchers concerned back then? Because these methylamines might form nitrosamines, which have “marked carcinogenic activity”—cancer-causing activity. So where is choline found in our diet? Mostly from meat, eggs, dairy, and refined grains. The link between meat and cancer probably wouldn’t surprise anyone. In fact, just due to the industrial pollutants, like PCBs, children probably shouldn’t eat more than about five servings a month of meats like beef, pork, or chicken combined. But, what about cancer and eggs?

Studies going back to the 1970s hinted at a correlation between eggs and colon cancer, as you can see at 2:45 in my video. That was based just on so-called ecological data, though, showing that countries eating more eggs tended to have higher cancer rates, but that could be due to a million factors. It needed to be put to the test.

This testing started in the 80s, and, by the 1990s, 15 studies had been published, of which 10 suggested “a direct association” between egg consumption and colorectal cancer, “whereas five found no association.” By 2014, dozens more studies had been published, confirming that eggs may indeed be playing a role in the development of colon cancer, though no relationship was discovered between egg consumption and the development of precancerous polyps, which “suggested that egg consumption might be involved in the promotional” stage of cancer growth—accelerating cancer growth—rather than initiating the cancer in the first place.

This brings us to 2015. Perhaps it’s the TMAO made from the choline in meat and eggs that’s promoting cancer growth. Indeed, in the Women’s Health Initiative study, women with the highest TMAO levels in their blood had approximately three times greater risk of rectal cancer, suggesting that TMAO levels “may serve as a potential predictor of increased colorectal cancer risk.”

As you can see at 4:17 in my video, though there may be more evidence for elevated breast cancer risk with egg consumption than prostate cancer risk, the only other study to date on TMAO and cancer looked at prostate cancer and did indeed find a higher risk.

“Diet has long been considered a primary factor in health; however, with the microbiome revolution of the past decade, we have begun to understand how diet can” affect the back and forth between us and the rest of us inside, and the whole TMAO story is “a smoking gun” in gut bacteria-disease interactions.

Since choline and carnitine are the primary sources of TMAO production, the logical intervention strategy might be to reduce meat, dairy, and egg consumption. And, if we eat plant-based for long enough, we can actually change our gut microbial communities such that we may not be able to make TMAO even if we try.

“The theory of ‘you are what you eat’ finally is supported by scientific evidence.” We may not have to eat healthy for long, though. Soon, Big Pharma hopes, “we may yet ‘drug the microbiome’…as a way of promoting cardiovascular health.”

What did the egg industry do in response to this information? Distort the scientific record. See my video Egg Industry Response to Choline and TMAO.

This is not the first time the egg industry has been caught in the act. See, for example:

For background on TMAO see my original coverage in Carnitine, Choline, Cancer, and Cholesterol: The TMAO Connection and then find out How to Reduce Your TMAO Levels. Also, see: Flashback Friday: How to Reduce Your TMAO Levels.

This is all part of the microbiome revolution in medicine, the underappreciated role our gut flora play in our health. For more, 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 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:

Decreasing Inflammation and Oxidation After Meals

Within hours of eating an unhealthy meal, we can get a spike in inflammation, crippling our artery function, thickening our blood, and causing a fight-or-flight nerve response. Thankfully, there are foods we can eat at every meal to counter this reaction.

Standard American meals rich in processed junk and meat and dairy lead to exaggerated spikes in sugar and fat in the blood, as you can see at 0:13 in my video How to Prevent Blood Sugar and Triglyceride Spikes after Meals. This generates free radicals, and the oxidative stress triggers a biochemical cascade throughout our circulation, damaging proteins in our body, inducing inflammation, crippling our artery function, thickening our blood, and causing a fight-or-flight nerve response. This all happens within just one to four hours after eating a meal. Worried about inflammation within your body? One lousy breakfast could double your C-reactive protein levels before it’s even lunchtime.

Repeat that three times a day, and you can set yourself up for heart disease. You may not even be aware of how bad off you are because your doctor is measuring your blood sugar and fat levels while you’re in a fasting state, typically drawing your blood before you’ve eaten. What happens after a meal may be a stronger predictor of heart attacks and strokes, which makes sense, since this is where most of us live our lives—that is, in a fed state. And it’s not just in diabetics. As you can see at 1:30 in my video, if you follow non diabetic women with heart disease but normal fasting blood sugar, how high their blood sugar spikes after chugging some sugar water appears to determine how fast their arteries continue to clog up, perhaps because the higher the blood sugars spike, the more free radicals are produced.

So, what are some dietary strategies to improve the situation? Thankfully, “improvements in diet exert profound and immediate favorable changes…,” but what kind of improvements? “Specifically, a diet high in minimally processed, high-fiber, plant-based foods such as vegetables and fruits, whole grains, legumes, and nuts,”—antioxidant, anti-inflammatory whole plant foods—“will markedly blunt the post-meal increase” in sugar, fat, and inflammation.

But what if you really wanted to eat some Wonder Bread? As you can see at 2:23 in my video, you’d get a big spike in blood sugar less than an hour after eating it. Would it make a difference if you spread the bread with almond butter? Adding about a third of a cup of almonds to the same amount of Wonder Bread significantly blunts the blood sugar spike.

In that case, would any low-carb food help? Why add almond butter when you can make a bologna sandwich? Well, first of all, plant-based foods have the antioxidants to wipe out any excess free radicals. So, nuts can not only blunt blood sugar spikes, but oxidative damage as well. What’s more, they can even blunt insulin spikes. Indeed, adding nuts to a meal calms both blood sugar levels and insulin levels, as you can see at 3:02 in my video. Now, you’re probably thinking, Well, duh, less sugar means less insulin, but that’s not what happens with low-carb animal foods.

As you can see at 3:23 in my video, if you add steamed skinless chicken breast to your white rice, you get a greater insulin spike than if you had just eaten the white rice alone. So, adding the low-carb plant food made things better, but adding the low-carb animal food made things worse. It’s the same with adding chicken breast to mashed potatoes—a higher insulin spike with the added animal protein. It is also the same with animal fat: Add some butter to a meal, and get a dramatically higher insulin spike from some sugar, as you can see at 3:45 in my video.

If you add butter and cheese to white bread, white potatoes, white spaghetti, or white rice, you can sometimes even double the insulin reaction. If you add half an avocado to a meal, however, instead of worsening, the insulin response improves, as it does with the main whole plant food source of fat: nuts.

I’ve covered the effect adding berries to a meal has on blood sugar responses in If Fructose Is Bad, What About Fruit?, and that raises the question: How Much Fruit Is Too Much?

In addition to the all-fruit jam question, I cover The Effects of Avocados and Red Wine on Postprandial Inflammation.

Vinegar may also help. See Can Vinegar Help with Blood Sugar Control?.

Perhaps this explains part of the longevity benefit to nut consumption, which I discuss in Nuts May Help Prevent Death.

I also talk about that immediate inflammatory reaction to unhealthy food choices in Best Foods to Improve Sexual Function.

Surprised by the chicken and butter reaction? The same thing happens with tuna fish and other meat, as I cover in my video Paleo Diets May Negate Benefits of Exercise.

Also check:

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 About the Sodium in Miso?

According to the second World Cancer Research Fund/American Institute for Cancer Research expert report, “[s]alt is a probable cause of stomach cancer,” one of the world’s leading cancer killers. If the report’s estimate of an 8 percent increase in risk for every extra gram of salt a day is correct, then in a country like the United Kingdom, nearly 1,700 cases of stomach cancer happen every year just because of excess salt intake, as you can see at 0:27 in my video Is Miso Healthy?, and, in a country like the United States, it would be thousands more annually.

The risk of stomach cancer associated with salt intake appears on par with smoking or heavy alcohol use, but may only be half as bad as opium use or increased total meat consumption, as you can see at 0:43 in my video. These findings were based on a study of more than a half million people, which may explain why those eating meatless diets appear to have nearly two-thirds lower risk.

We know dietary salt intake is directly associated with the risk of stomach cancer, and the higher the intake, the higher the risk. A meta-analysis went one step further and looked at specific salt-rich foods: pickled foods, salted fish, processed meat, and miso soup. Habitual consumption of pickled foods, salted fish, and processed meat were each associated with about a 25 percent greater risk of stomach cancer. The pickled foods may explain why Korea, where the pickled cabbage dish kimchi is a staple, appears to have the highest stomach cancer rates in the world, as you can see at 1:39 in my video. But researchers found there was no significant association with the consumption of miso soup. This may be because the carcinogenic effects of the salt in miso soup are counteracted by the anti-carcinogenic effects of the soy, effectively canceling out the risk. And, if we made garlicky soup with some scallions thrown in, our cancer risk may drop even lower, as you can see at 2:06 in my video.

Cancer isn’t the primary reason people are told to avoid salt, though. What about miso soup and high blood pressure? Similar to the relationship between miso and cancer, the salt in miso pushes up our blood pressures, but miso’s soy protein may be relaxing them down. If we compare the effects of soy milk to cow’s milk, for example, and, to make it even more fair, compare soy milk to skim cow’s milk to avoid the saturated butter fat, soy milk can much more dramatically improve blood pressure among women with hypertension, as you can see at 2:43 in my video. But would the effect be dramatic enough to counter all the salt in miso? Japanese researchers decided to put it to the test.

For four years, they followed men and women in their 60s, who, at the start of the study, had normal blood pressure, to see who was more likely to be diagnosed with hypertension in that time: those who had two or more bowls of miso soup a day or those who had one or less. Two bowls a day may add a half teaspoon of salt to one’s daily diet, yet those who had two or more bowls of miso soup every day appeared to have five times lower risk of becoming hypertensive. So, maybe the anti-hypertensive effects of the soy in the miso exceed the hypertensive effects of the salt.

Indeed, miso paste, a whole soy food, can be used as a “green light” source of saltiness when cooking. That’s why I used it in my pesto recipe in How Not to Die and in my How Not to Die Cookbook. It can help you in Shaking the Salt Habit.

Not convinced that salt is bad for you? Check out these videos:

Not convinced that soy is good for you? 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:

How to Prevent the Infection that May Trigger Type 1 Diabetes

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

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

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

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

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

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

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

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

In health,
Michael Greger, M.D.

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

The Role of Meat and Dairy in Triggering Type 1 Diabetes

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

In health,
Michael Greger, M.D.

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