Do the Pros of Brown Rice Outweigh the Cons of Arsenic?

Are there unique benefits to brown rice that would justify keeping it in our diet despite the arsenic content?

For years, warnings had been given about the arsenic levels in U.S. rice potentially increasing cancer risk, but it had never been put to the test until a study out of Harvard. The finding? “Long-term consumption of total rice, white rice or brown rice[,] was not associated with risk of developing cancer in US men and women.” This was heralded as good news. Indeed, no increased cancer risk found even among those eating five or more servings of rice per week. But, wait a second: Brown rice is a whole grain, a whole plant food. Shouldn’t brown rice be protective and not just neutral? I discuss this in my video Do the Pros of Brown Rice Outweigh the Cons of Arsenic?.

If you look at whole grains in general, there is “a significant inverse”—or protective—“association between total whole-grain intake and risk of mortality from total cancers,” that is, dying from cancer. My Daily Dozen recommendation of at least three servings of whole grains a day was associated with a 10 percent lower risk of dying from cancer, a 25 percent lower risk of dying from heart attacks or strokes, and a 17 percent lower risk of dying prematurely across the board, whereas rice consumption in general was not associated with mortality and was not found to be protective against heart disease or stroke. So, maybe this lack of protection means that the arsenic in rice is increasing disease risk, so much so that it’s cancelling out some of the benefits of whole-grain brown rice.

Consumer Reports suggested moderating one’s intake of even brown rice, but, given the arsenic problem, is there any reason we should go out of our way to retain any rice in our diet at all? With all of the other whole grain options out there, should we just skip the rice completely? Or, are there some unique benefits we can get from rice that would justify continuing to eat it, even though it has ten times more arsenic than other grains?

One study showed that “a brown rice based vegan diet” beat out the conventional Diabetes Association diet, even after adjusting for the extra belly fat lost by the subjects on the vegan diet, but that may have been due to the plant-based nature of their diet rather than just how brown rice-based it was.

Another study found a profound improvement in insulin levels after just five days eating brown rice compared to white rice, but was that just because the white rice made people worse? No, the brown rice improved things on its own, but the study was done with a South Indian population eating a lot of white rice to begin with, so this may have indeed been at least in part a substitution effect. And yet another study showed that instructing people to eat about a cup of brown rice a day “could significantly reduce weight, waist and hip circumference, BMI, Diastole blood pressure,” and inflammation—and not just because it was compared to white. However, a larger, longer study failed to see much more than a blood pressure benefit, which was almost as impressive in the white-rice group, so, overall, not too much to write home about.

Then, another study rolled around—probably the single most important study on the pro-rice sideshowing a significant improvement in artery function after eight weeks of eating about a daily cup of brown rice, but not white, as you can see at 3:18 in my video, and sometimes even acutely. If you give someone a meal with saturated fat and white rice, you can get a drop in artery function within an hour of consumption if you have some obesity-related metabolic derangements. But, if you give brown rice instead of white, artery function appears protected against the adverse effects of the meal. Okay, so brown rice does show benefits in interventional studies, but the question is whether it shows unique benefits. Instead, what about oatmeal or whole wheat?

Well, first, researchers needed to design an artery-crippling meal, high in saturated fat. They went with a Haagen Daaz, coconut cream, and egg milkshake given with a bowl of oatmeal or “a comparable bowl of whole rolled wheat.” What do you think happened? Do you think these whole grains blocked the artery-damaging effects like the brown rice did? The whole oats worked, but the whole wheat did not. So, one could argue that brown rice may have an edge over whole wheat. Do oats also have that beneficial long-term effect that brown rice did? The benefit was of a similar magnitude but did not reach statistical significance.

So, what’s the bottom line? Until we know more, my current thinking on the matter is that if you really like rice, you can moderate your risk by cutting down, choosing lower arsenic varieties, and cooking it in a way to lower exposure even further. But, if you like other whole grains just as much and don’t really care if you have rice versus quinoa or another grain, I’d choose the lower arsenic option.

Tada! Done with arsenic in the food supply—for now. Should the situation change, I’ll produce another video on the latest news. Make sure you’re subscribed so you don’t miss any updates.


Here are all 13 videos in the series, in case you missed any or want to go back and review:

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

In health,

Michael Greger, M.D.

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

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?

What?!

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:

Açaí vs. Wild Blueberries for Artery Function

“Plant-based diets…have been found to reduce the risk of cardiovascular disease” and some of our other leading causes of death and disability. “Studies have shown that the longest living and least dementia-prone populations subsist on plant-based diets.” So why focus on açaí berries, just one plant, for brain health and performance?

Well, “foods rich in polyphenols…improve brain health,” and açaí berries contain lots of polyphenols and antioxidants, so perhaps that’s why they could be beneficial. If you’re only looking at polyphenols, though, there are more than a dozen foods that contain more per serving, like black elderberry, regular fruits like plums, flaxseeds, dark chocolate, and even just a cup of coffee.

As you can see at 1:02 in my video The Benefits of Açaí vs. Blueberries for Artery Function, in terms of antioxidants, açaí berries may have ten times more antioxidant content than more typical fruits, like peaches and papayas, and five times more antioxidants than strawberries. But blackberries, for instance, appear to have even more antioxidants than açaí berries and are cheaper and more widely available.

Açaí berries don’t just have potential brain benefits, however. Might they also protect the lungs against harm induced by cigarette smoke? You may remember the study where the addition of açaí berries to cigarettes protected against emphysema—in smoking mice, that is. That’s not very helpful. There is a long list of impressive-looking benefits until you dig a little deeper. For example, I was excited to see a “[r]eduction of coronary disease risk due to the vasodilation effect” of açaí berries, but then I pulled the study and found they were talking about a vasodilator effect…in the mesenteric vascular bed of rats. There hadn’t been any studies on açaí berries and artery function in humans until a study published in 2016.

Researchers gave overweight men either a smoothie containing about two-thirds of a cup of frozen açaí pulp and half a banana or an artificially colored placebo smoothie containing the banana but no açaí. As you can see at 2:26 in my video, within two hours of consumption of their smoothie, the açaí group had a significant improvement in artery function that lasted for at least six hours, a one or two point bump that is clinically significant. In fact, those walking around with just one point higher tend to go on to suffer 13 percent fewer cardiovascular events like fatal heart attacks.

As I show at 2:52 in my video, you can get the same effect from wild blueberries, though: about a one-and-a-half-point bump in artery function two hours after blueberry consumption. This effect peaks then plateaus at about one and a half cups of blueberries, with two and a half cups and three and a half cups showing no further benefits.

What about cooked blueberries? As you can see at 3:12 in my video, if you baked the blueberries into a bun, like a blueberry muffin, you get the same dramatic improvement in artery function.

Cocoa can do it, too. As shown at 3:30 in my video, after having one tablespoon of cocoa, you gain about one point, and two tablespoons gives you a whopping four points or so, which is double what you get with açaí berries.

One and a quarter cups’ worth of multicolored grapes also give a nice boost in artery function, but enough to counter an “acute endothelial insult,” a sudden attack on the vulnerable inner layer of our arteries? Researchers gave participants a “McDonald’s sausage egg breakfast sandwich and two hash browns.” They weren’t messing around! As you can see at 3:56 in my video, without the grapes, artery function was cut nearly in half within an hour, and the arteries stayed stiffened and crippled three hours later. But when they ate that McMuffin with all those grapes, the harmful effect was blunted.

Eat a meal with hamburger meat, and artery function drops. But if you eat that same meal with some spices, including a teaspoon and a half of turmeric, artery function actually improves.

What about orange juice? Four cups a day of commercial orange juice from concentrate for four weeks showed no change in artery function. What about freshly squeezed orange juice? Still nothing. That’s one of the reasons berries, not citrus, are the healthiest fruits.

For a beverage that can improve your artery function, try green tea. Two cups of green tea gives you that same effect we saw with cocoa, gaining nearly four points within just 30 minutes. And, as you can see at 5:05 in my video, that same crazy effect is also seen with black tea, with twice as powerful an effect as the açaí berries.

So, why all the focus on just that one plant? Why açaí berries? Well, the real reason may be because the author owns a patent on an açaí-based dietary supplement.


How do the antioxidant effects of açaí berries compare to applesauce? See The Antioxidant Effects of Açaí vs. Apples.

What about the effects of other foods on artery function? Coronary artery disease is, after all, our leading cause of death for men and women. See:

What else can blueberries do? Check out:

In health,

Michael Greger, M.D.

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

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:

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:

The Food Industry’s “model of systemic dishonesty”

In 1993, the Harvard Nurses’ Health Study found that a high intake of trans fat may increase the risk of heart disease by 50 percent. That’s where the trans fat story started in Denmark, ending a decade later with a ban on added trans fats in 2003. It took another ten years before the United States even started considering a ban. All the while, trans fats were killing tens of thousands of Americans every year. With so many people dying, why did it take so long for the United States to even suggest taking action? I explore this in my video Controversy Over the Trans Fat Ban.

One can look at the fight over New York City’s trans fat ban for a microcosm of the national debate. Not surprisingly, opposition came from the food industry, complaining about “government intrusion” and “liken[ing] the city to a ‘nanny state.’” “Are trans fat bans…the road to food fascism?”

A ban on added trans fats might save 50,000 American lives every year, which could save the country tens of billions of dollars in healthcare costs, but not so fast! If people eating trans fat die early, think about how much we could save on Medicare and Social Security. Indeed, “smokers actually cost society less than nonsmokers, because smokers die earlier.” So, “we should be careful about making claims about the potential cost-savings of trans fat bans….more research is needed on the effects of these policies, including effects on the food industry.” Yes, we might save 50,000 lives a year, but we can’t forget to think about the “effects on the food industry”!

How about “education and product labeling” rather than “the extreme measure of banning trans fats”? As leading Danish cardiologist “puts it bluntly, ‘Instead of warning consumers about trans fats and telling them what they are, we’ve [the Danes] simply removed them.’” But we’re Americans! “As they say in North America: ‘You can put poison in food if you label it properly.’”

People who are informed and know the risks should be able to eat whatever they want, but that assumes they’re given all the facts, which doesn’t always happen “due to deception and manipulation by food producers and retailers.” And, not surprisingly, it’s the unhealthiest of foods that are most commonly promoted using deceptive marketing. It’s not that junk food companies are evil or want to make us sick. “The reason is one of simple economics”—processed foods simply “offer higher profit margins and are shelf-stable, unlike fresh foods such as fruit and vegetables.” The food industry’s “model of systemic dishonesty,” some argue, “justifies some minimal level of governmental intervention.”

But is there a slippery slope? “Today, trans fats; tomorrow, hot dogs.” Or, what about the reverse? What if the government makes us eat broccoli? This argument actually came up in the Supreme Court case over Obamacare. As Chief Justice Roberts said, Congress could start ordering everyone to buy vegetables, a concern Justice Ginsburg labeled “the broccoli horrible.” Hypothetically, Congress could compel the American public to go plant-based, however, no one can offer the “hypothetical and unreal possibility…of a vegetarian state” as a credible argument. “Judges and lawyers live on the slippery slope of analogies; they are not supposed to ski it to the bottom,” said one legal scholar.

If anything, what about the slippery slope of inaction? “Government initially defaulted to business interests in the case of tobacco and pursued weak and ineffective attempts at education” to try to counter all the tobacco industry lies. Remember what happened? “The unnecessary deaths could be counted in the millions. The U.S. can ill afford to repeat this mistake with diet.”

Once added trans fats are banned, the only major source in the American diet will be the natural trans fats found in animal fat. For more on this, see Banning Trans Fat in Processed Foods but Not Animal Fat and Trans Fat in Meat and Dairy.

Ideally how much trans fat should we eat a day? Zero, and the same goes for saturated fat and cholesterol. See Trans Fat, Saturated Fat, and Cholesterol: Tolerable Upper Intake of Zero, Good, Great, Bad, and Killer Fats, and Lipotoxicity: How Saturated Fat Raises Blood Sugar.


More on industry hysterics and manipulation in:

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:

Food Combining for Prostate Cancer

What would happen if you secretly gave cancer patients four of the healthiest foods?

In my video Pomegranate vs. Placebo for Prostate Cancer, I discussed how pomegranate pills appeared useless in the treatment for prostate cancer, and the same disappointing results were seen with a pomegranate beverage, but that was just a pomegranate extract as well. So, maybe the pomegranate itself “cannot be blamed for the ineffectiveness seen in the study” but rather the low dose of the pomegranate active principles in the extract. But what is the active principle? Extracts will boast about the level of ellagic acid, definitely “one of the most potent of the phytochemicals found in pomegranate. However, it is not as strong as pomegranate” itself.

What researchers mean is that the components may act synergistically: The whole may be greater than the sum of its parts. As you can see at 1:07 in my video Best Supplements for Prostate Cancer, human prostate cancer cells in a petri dish churned away at 100 percent growth, but after dripping on a pomegranate fraction, the cancer growth rate was cut by 30 percent. However, dripping on a different fraction appeared useless. What do you think would happen if you added them both together? 30% suppression + 0% suppression = 70% suppression! That’s synergy, where 1 + 1 is greater than 2. Under a microscope, prostate cancer cells appeared sparser with the combination of fractions. “Any attempt to characterize the phytoceutical power of a medicinal food by standardizing a single chemical is missing the entire point” of plant-based medicine. So, the standardized extracts represent a “cynical, lucre-driven [money-driven] attempt to replace the power of the pomegranate with the power of ellagic acid. The pomegranate needs no such tricks or enhancements.” It’s powerful as is. So, why don’t researchers just try the fruit on cancer patients?

Because you can’t stuff a pomegranate in a pill, so you can’t compare it to an indistinguishable sugar pill placebo. Drugs are easy to study. People don’t know if they are taking the active drug or a placebo, but they tend to notice if they’re eating a pomegranate or not. So, if you gave a bunch of cancer patients some pomegranates to eat and the cancer slowed down, you wouldn’t know if it was the pomegranates or just the placebo effect. Of course, the patients wouldn’t care. They’d just care that they got better. But, to change medical practice, we want to know if the fruit is actually something special. I suppose you could create some kind of pomegranate smoothie versus a fake smoothie, but that sounds logistically difficult. So, researchers tried powdering it. Three times a day, 199 men with prostate cancer got either a placebo or a tablet containing 100 mg of powdered whole pomegranate—the whole fruit with just the water taken out. How much can fit in a tablet? It comes out to be about six pomegranate seeds’ worth a day, about 1/100th of a pomegranate each day. Since so little could fit into a pill, researchers tried to maximize their chances of beating back the cancer using diversity.

As you can see at 4:01 in my video, two groups of people ate approximately the same amount of fruits and vegetables, but one group ate a relatively low biological diversity diet, where they ate tons of really healthy foods but just less variety than did a second group who ate smaller servings of a high diversity diet. Which group do you think would win in terms of protecting their DNA from free radical damage? The high diversity group. This suggests that “smaller amounts of many phytochemicals may have greater potential to exert beneficial effects than larger amounts of fewer phytochemicals.”

Same result for inflammation. Greater variety in fruit and vegetable intake is associated with lower inflammation even if you eat the same number of servings. Same with improving cognitive function, too. Greater variety in fruit and vegetable intake is also associated with a better mental status, executive function, attention, and memory function in some cases, even after adjustment for total quantity. So, if you have two people eating the same number of servings of healthy foods, the one eating a greater variety may do better.

Going back to the study with the 199 prostate cancer patients getting either a placebo or a tablet with 100 mg of powdered whole pomegranate three times daily, the researchers didn’t just put in pomegranate powder. They also added powdered broccoli, powdered turmeric, and powdered green tea concentrate. So, the tablet contained a fruit, a vegetable, a spice, and a leaf in tiny amounts—about one floret of broccoli a day, less than an eighth of a daily teaspoon of turmeric, and about one sixth of a tea bag worth of green tea. All great plants, but could such tiny amounts actually affect the progression of cancer? Yes. As you can see at 5:55 in my video, in the group of men with early stage prostate cancer trying to avoid surgery, the PSA levels in the placebo group rose nearly 50 percent, indicating that the cancer continued to flourish, whereas the PSAs didn’t rise at all in the pomegranate, broccoli, turmeric, and green tea food supplement group. And, in those with more advanced disease—patients who had already had surgery or radiation and were trying to avoid chemo—there was a 70 percent greater rise in PSA levels in the placebo group. This was enough to significantly delay some of these more toxic treatments. Indeed, the study found significant, short-term, favorable effects. However, they only had enough money to run the study for six months, because it was a “non-commercial” endeavor, funded by charities, not some supplement company. In fact, there was no supplement until the investigators dreamed it up from scratch for the study. Of course, now there’s a supplement, given the study’s extraordinary results, but the only reason the researchers put the foods in pill form was to match it with a placebo. In my mind, what this study should tell cancer patients is to eat curried broccoli with fruit for dessert and to sip some green tea. A completely plant-based diet may even shrink the tumor, not just slow it down, but there’s no reason we can’t do both with a plant-based diet chock full of especially powerful plants.

I love that study! You and I both know why these types of studies aren’t performed more often. Who would profit? (Other than the millions of people suffering and dying from cancer, of course!)

The note I ended on, the landmark Ornish study, is detailed in Cancer Reversal Through Diet. For those unwilling or unable to make such significant dietary changes, there’s still something you can do. See Prostate Cancer Survival: The A/V Ratio. Changing a Man’s Diet After a Prostate Cancer Diagnosis isn’t easy!


For more on the 2 + 2 > 4 concept, see Food Synergy.

What about preventing prostate cancer in the first place? Check out my videos like Prostate Cancer and Organic Milk vs. Almond Milk and Eggs, Choline, and Cancer to get a sense of what you might want to avoid. But, in terms of what to eat, see The Role of Soy Foods in Prostate Cancer Prevention and Fermented or Unfermented Soy Foods for Prostate Cancer Prevention?.

Also, 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:

Pill-Free Ways to improve Your Sex Life

“Sex is important to health,” according to the Harvard Health Letter. “Frequent sexual intercourse is associated with reduced heart attack risk.” But, as I discuss in my video Do Men Who Have More Sex Live Longer?, that seems to be the perfect case of reverse causation. They’re implying that more sex leads to healthier arteries, but isn’t the opposite more likely—that is, healthier arteries lead to more sex? Blood flow in the penis is so reflective of blood flow elsewhere that penile Doppler ultrasound can predict cardiovascular disease. However, low frequency of sexual activity may predict cardiovascular disease in men independently of erectile dysfunction. This suggests that sex may be more than “just fun” and may also be therapeutic, or at least so says an editor of the Journal of Sexual Medicine and colleagues in discussing whether or not “frequent sexual activity can be prescribed” to improve general health. In men, they suggest it’s because more sex means more testosterone.

When men have sex, they get a big spike in testosterone levels in their blood, but, interestingly, in contrast, they don’t get a testosterone boost when they masturbate, as you can see at 1:21 in my video. This may be because “testosterone increases with competitive success,” like if you win a sports game. While sex “is not usually regarded as a competitive event…one’s mental state following coitus could nevertheless be something like that of a winner,” as opposed to the mental state after masturbation.

As you can see at 2:00 in my video, the spike in sex hormones in the blood is so great that men’s beards actually grow faster on days they have sex. And, since low testosterone levels are associated with increased risk of mortality, this could help explain the health benefits of having sex.

So, do men who have more sex actually live longer? I searched Pubmed for sexual activity and longevity and found a study supported by the U.S. Department of Agriculture, titled “Sexual activity and longevity of the southern green stink bug”—clearly an example of our taxpayer dollars hard at work. I was less interested in whether or not screwworms live up to their namesake and more interested in a study on sex and death, in which the objective was “to examine the relation between frequency of orgasm and mortality.” The researchers found that men with “high orgasmic frequency” appeared to cut their risk of premature death in half and, apparently, the more, the better: There was an associated 36 percent drop in mortality odds for every additional 100 orgasms a year. “Conclusion: Sexual activity seems to have a protective effect on men’s health”—but, apparently, not if you cheat. “Unfaithfulness in men seems to be associated with a higher risk of major cardiovascular events,” like heart attacks and strokes. “Extramarital sex may be hazardous and stressful because the lover is often younger…[and] a secret sexual encounter” may be more stressful.

In a large autopsy series, the majority of cases of sudden death during sex occurred in men during extramarital intercourse. The absolute risk is low—“only one out of 580 men might be expected to suffer a sudden death attributable to sexual intercourse”—but for those at high risk, research shows that “[s]ex in familiar surroundings, in a comfortable room temperature, and with the usual partner adds less stress to the heart” and may be safer.

Speaking of safe sex, you thought drinking and driving was bad? “While it is generally assumed that sexual behavior happens in parked cars, there is little discussion…in the research literature of sexual activity in moving vehicles.” About one in five college students report engaging in sex while driving, nearly half while going more than 60 miles an hour. Researchers suggest maybe this is something students should be warned about in health class.

When done right, though, love may protect your lover’s life. Given the benefits of sexual activity, “intervention programmes could also be considered, perhaps based on the exciting ‘At least five a day’ campaign aimed at increasing fruit and vegetable consumption—although the numerical imperative may have to be adjusted.”

What are some pill-free ways to improve your sex life? Exercising, quitting smoking, not drinking too much alcohol, not weighing too much, and eating a healthy diet. But what does it mean to “eat a healthy diet”? As I discuss in my video Best Foods to Improve Sexual Function, heart-healthy lifestyle changes are sex-healthy lifestyle changes, which have been demonstrated in studies from around the world, including in women (for whom there is sadly a dearth of research about in the biomedical literature). “Sexual function in women is significantly affected” by coronary artery disease, atherosclerotic narrowing of blood flow through our arteries, including the arteries that supply our pelvis. So, high cholesterol may mean “lower arousal, orgasm, lubrication, and satisfaction,” and the same holds for high blood pressure.

Given this, putting women on a more plant-based diet may help with sexual functioning.   Researchers found that improvements in female sexual function index scores were related to an increased intake of fruits, vegetables, nuts, and beans, and a shift from animal to plant sources of fat. The same for men: a significant improvement in international Index of Erectile Function scores. In fact, the largest study on diet and erectile dysfunction found that each additional daily serving of fruits or vegetables may reduce the risk of ED by 10 percent. But why? It may be due to the anti-inflammatory effects. Two years on a healthier diet resulted in a significant reduction in systemic inflammation, as indicated by reduced levels of C-reactive protein. Fiber itself may play an anti-inflammatory role. Those who eat the most fiber tend to have significantly lower levels of inflammation in their bodies, as you can see at 2:06 in my video. The opposite was found for saturated fat, “associated with an increased likelihood of elevated CRP”, C-reactive protein levels.

We’re used to seeing changes in inflammatory markers over weeks, months, or years, but people don’t realize that the level of inflammation in our bodies can change after only a single meal. For example, there’s a pro-inflammatory signaling molecule in our bodies called interleukin 18, thought to play a role in destabilizing atherosclerotic plaque. As such, the level of interleukin 18 in the blood “ is a strong predictor” of cardiovascular death.

What would happen if you fed people one of three different types of meals: sausage-egg-butter-oil sandwiches, cheeseless pizza with white flour crust, or the same cheeseless pizza but with whole-wheat crust? Within hours of eating the sausage sandwich, interleukin 18 levels shot up about 20 percent, an effect not seen after eating the plant-based pizza. In contrast, those eating the whole food, plant-based pizza made with the whole-wheat crust had about a 20 percent drop in interleukin 18 levels within hours of consumption, reinforcing dietary recommendations to eat a diet high in fiber and starches, and low in saturated fat to prevent chronic diseases.

But the billions in profits are in pills, not plants, which is why the pharmacology of the female orgasm has been studied ever since 1972 when a researcher at Tulane University implanted tubes deep within the brain of a woman so he could inject drugs directly into her brain and was able to induce repetitive orgasms. A man who had electrodes placed into similar parts of his brain was given a device for a few hours that allowed him to press the button himself to stimulate the electrode. He pressed the button up to 1,500 times.


For more on male reproductive health, see:

Also check out my other men’s health videos, such as:

What effect might that inflammation directly following an unhealthy meal have on our artery function? Check out my three-part endotoxins series starting with The Leaky Gut Theory of Why Animal Products Cause Inflammation.

And why exactly is fiber anti-inflammatory? Watch my video Prebiotics: Tending Our Inner Garden.

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:

Medical Meat Bias

When famed surgeon Michael DeBakey was asked why his studies published back in the 1930s linking smoking and lung cancer were ignored, he had to remind people about what it was like back then. We were a smoking society. Smoking was in the movies, on airplanes. Medical meetings were held in “a heavy haze of smoke.” Smoking was, in a word, normal. Even the congressional debates over cigarettes and lung cancer took place in literal smoke-filled rooms. (This makes me wonder what’s being served at the breakfast buffets of the Dietary Guidelines Committee meetings these days.)

I’ve previously talked about a famous statistician by the name of Ronald Fisher, who railed against what he called “propaganda…to convince the public that cigarette smoking is dangerous.” “Although Fisher made invaluable contributions to the field of statistics, his analysis of the causal association between lung cancer and smoking was flawed by an unwillingness to examine the entire body of data available…” His smokescreen may have been because he was a paid consultant to the tobacco industry, but also because he was himself a smoker. “Part of his resistance to seeing the association may have been rooted in his own fondness for smoking,” which makes me wonder about some of the foods nutrition researchers may be fond of to this day.

As I discuss in my video Don’t Wait Until Your Doctor Kicks the Habit, it always strikes me as ironic when vegetarian researchers are forthright and list their diet as a potential conflict of interest, whereas not once in the 70,000 articles on meat in the medical literature have I ever seen a researcher disclose her or his nonvegetarian habits––because it’s normal. Just like smoking was normal.

How could something that’s so normal be bad for you? And, it’s not as if we fall over dead after smoking one cigarette. Cancer takes decades to develop. “Since at that time most physicians smoked and could not observe any immediate deleterious effects, they were skeptical of the hypothesis and reluctant to accept even the possibility of such a relation”—despite the mountain of evidence.

It may have taken 25 years for the Surgeon General’s report to come out and longer still for mainstream medicine to get on board, but now, at least, there are no longer ads encouraging people to “Inhale to your heart’s content!” Instead, today, there are ads from the Centers for Disease Control and Prevention fighting back.

For food ads, we don’t have to go all the way back to old ads touting “Meat…for Health Defense” or “Nourishing Bacon,” or featuring doctors prescribing meat or soda, or moms relieved that “Trix are habit-forming, thank heavens!” You know things are bad when the sanest dietary advice comes from cigarette ads, as in Lucky Strike’s advertisements proclaiming “More Vegetables––Less Meat” and “Substitute Oatmeal for White Flour.” (You can see these vintage ads from 2:34 in my video).

In modern times, you can see hot dogs and sirloin tips certified by the American Heart Association, right on their packaging. And, of all foods, which was the first to get the Academy of Nutrition and Dietetics’ “Kids Eat Right” logo on its label? Was it an apple? Broccoli, perhaps? Nope, it was a Kraft prepared cheese product.

Now, just as there were those in the 1930s, 40s, and 50s at the vanguard trying to save lives, today, there are those transforming ads about what you can do with pork butt into ads about what the pork can do to your butt: “Hot Dogs Cause Butt Cancer—Processed meats increase colorectal cancer risk” reads an for the Physicians Committee for Responsible Medicine’s “Meat Is the New Tobacco” campaign, which you can see at 3:56 in my video. As Dr. Barnard, PCRM president, tried to convey in an editorial published in the American Medical Association’s Journal of Ethics, “Plant-based diets are the nutritional equivalent of quitting smoking.”

How many more people have to die before the Centers for Disease Control encourages people not to wait for open-heart surgery to start eating healthfully?

Just as we don’t have to wait until our doctor stops smoking to give up cigarettes ourselves, we don’t have to wait until our doctor takes a nutrition class or cleans up his or her diet before choosing to eat healthier. No longer do doctors hold a professional monopoly on health information. There’s been a democratization of knowledge. So, until the system changes, we have to take personal responsibility for our health and for our family’s health. We can’t wait until society catches up with the science again, because it’s a matter of life and death.

Dr. Kim Allan Williams, Sr., became president of the American College of Cardiology a few years back. He was asked why he follows his own advice to eat a plant-based diet. “I don’t mind dying,” Dr. Williams replied. “I just don’t want it to be my fault.”


I find this to be such a powerful concept that I have come at it from different angles. For other takes, check out Taking Personal Responsibility for Your Health and How Smoking in 1959 Is Like Eating in 2019. Are the health effects of smoking really comparable to diet, though? Check out Animal Protein Compared to Cigarette Smoking.

The food industry certainly uses the same kind of misinformation tactics to try to confuse consumers. See, for example:

In health,
Michael Greger, M.D.

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

What Meat and Eggs Do to Our Microbiome

As I’ve explored before, whether young or old, male or female, smoker or non-smoker, with high blood pressure or low blood pressure, high cholesterol or low, having high levels of a toxic compound called TMAO—trimethylamine oxide—in the bloodstream is associated with a significantly higher risk of having a heart attack, stroke, or dying over a three-year period. Where does TMAO come from? As I investigate in my video How to Develop a Healthy Gut Ecosystem, the choline in foods like eggs can be turned by gut bacteria into TMAO, which is then absorbed back into our system. And, the more eggs we eat, the higher the levels climb, as you can see at 0:41 in my video.

Given the similarity in structure between carnitine and choline, Cleveland Clinic researchers wondered if carnitine found in red meat, energy drinks, and supplements might also lead to TMAO production and put it to the test. As you can see at 1:00 in my video, if you feed omnivores, those who regularly eat meat, a steak, their TMAO levels shoot up. Those who eat strictly plant-based may start out with almost no TMAO in their system, presumably because they’re not eating any meat, eggs, or dairy. But, even if vegans eat a sirloin, still almost no TMAO is made. Why? Presumably, they don’t have steak-eating bacteria in their guts. Indeed, it was found that no TMAO is produced if you don’t have TMAO-producing bacteria in your gut. If you don’t regularly eat meat, then you’re not fostering the growth of the meat-eating microbes that produce TMAO.

This suggests that once we develop a plant-based gut ecosystem, our bacteria will not produce TMAO, even if we eat meat every once and awhile. However, we still don’t know how rapidly gut bacteria shift after a shift in our diet—but it does not appear to be all or nothing. If men eating the standard American diet are given two sausage, egg, and cheese biscuits before and after just five days of eating lots of similarly high-fat meals, their TMAO production boosts even higher, as you can see at 2:09 in my video. So, it’s not just whether we have the bad bugs or not. Apparently, we can breed more of them the more we feed them.

Meat-free diets, on the other hand, can also have been “demonstrated to have a profound influence on human metabolism.”Just by analyzing a urine sample, we can tell what kind of diet people eat, based on measurements like how low TMAO levels are in the urine of those eating egg-free vegetarian diets, as you can see at 2:26 in my video. At 2:43 in my video, you’ll see that we can even take the same people rotate them through three different diets, and determine who is on a high-meat diet, low-meat diet, or no-meat diet, based in part on the different compounds churned out by the different gut flora or different flora activity after just about two weeks on the different diets. It’s possible that some of the beneficial effects of whole plant foods may be mediated by the effects they have on our gut bacteria. At the same time, the standard American diet may increase the relative abundance of undesirables that produce toxic compounds including TMAO (as you can see at 3:07 in my video).

Strictly plant-based diets have gained acceptance as a dietary strategy for preventing and managing disease. Perhaps, in part, this is because of their rather unique gut flora, with less of the disease-causing bacteria and more of the protective species. So, all along, we thought the reason those eating plant-based had lower heart disease rates was because they were eating less saturated fat and cholesterol, but maybe their lower TMAO levels may also be contributing to their benefits, thanks to their reduced ingestion of carnitine and choline.

I talked about the egg industry response to the choline revelation in Egg Industry Response to Choline and TMAO. How has the carnitine supplement industry reacted? In response to the research implicating carnitine in TMAO production, the former vice president of AdvoCare—a multilevel marketing company that sells carnitine supplements like AdvoCare Slam while getting slammed with lawsuits finding them guilty of being “engaged in false, misleading or deceptive acts or practices” and forced to pay more than a million dollars—questioned whether there was a secret vegan conspiracy at the Cleveland Clinic. Restricting our intake of meat or carnitine supplements to prevent our gut bacteria from making TMAO, he argued, is like trying to prevent car accidents by restricting the sale of fuel.

Okay…but there are benefits to transportation. We’re talking about TMAO, which may be fueling our epidemic of heart disease, the number-one killer of men and women in this country. As far as I’m concerned, the more we can cut the fuel for that, the better.


For more background on TMAO, see Carnitine, Choline, Cancer, and Cholesterol: The TMAO Connection, then find out How to Reduce Your TMAO Levels.

Our gut flora are what we eat. Check out:

In health,
Michael Greger, M.D.

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

The Role of Meat and Dairy in Triggering Type 1 Diabetes

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

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

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

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

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

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

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

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

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

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

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

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


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

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

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

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

In health,
Michael Greger, M.D.

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