Are Lectins in Food Good or Bad for You?

Might lectins help explain why those who eat more beans and whole grains have less cancer?

Lectins are to blame for the great “white kidney bean incident” of 2006 in Japan. One Saturday evening, a TV program introduced a new method to lose weight. The method was simple: toast some dry, raw, white kidney beans in a frying pan for three minutes, grind the beans into a powder, and then dust it onto rice. Within days, a thousand people fell ill, some with such severe diarrhea and vomiting they ended up in the hospital. Why? Lectin poisoning. Three minutes of dry heat is not enough to destroy the toxic lectins in kidney beans. If you don’t presoak them, you need to boil large kidney beans for a full hour to completely destroy all the lectins, though if you first soak them overnight 98 percent of the lectins are gone after boiling for just 15 minutes and all are gone by half an hour, as you can see at 0:44 in my video Are Lectins in Food Good or Bad for You?. And, indeed, when researchers tested the white beans, they found that toasting them for three minutes didn’t do a thing. It’s no wonder people got sick. But, 95 percent of the lectins were inactivated after boiling them for three minutes and completely inactivated after ten minutes of boiling. Evidently, “‘Do not eat raw beans’ is a traditional admonition in Japan to prevent intestinal problems”—and now we know why.

While canning may completely eliminate lectins from most canned beans, some residual lectin activity may remain in canned kidney beans, though apparently not enough to result in toxicity. And, ironically, “How doses of lectins may be beneficial by stimulating gut function, limiting tumor growth, and ameliorating obesity.” What? I thought lectins were toxic.

For as long as people have speculated dietary lectins are harmful, others have conjectured that they may be protective. “If this theory is correct, appropriate lectins by mouth should be of use in the prophylaxis [prevention] (and possibly treatment) of colon cancer.” Or, of course, we could just eat our beans.

Interest in the purported antitumor effect of plant lectins started with the discovery in 1963 that lectins could distinguish between cancer cells and normal cells. Researchers at Massachusetts General Hospital found a substance in wheat germ—the lectin in whole wheat—that appeared to be “tumor cell specific,” clumping together the tumor cells, while the normal cells were left almost completely alone. In fact, it is so specific that you can take a stool sample from someone and, based on lectin binding to the colon lining cells that get sloughed off into the feces, effectively predict the presence of polyps and cancers.

Subsequently, it was discovered that lectins couldn’t only distinguish between the two types of cells, but also extinguish the cancer cells, while largely leaving the normal cells alone. For example, that same white kidney bean lectin, as you can see at 2:53 in my video, was found to almost completely suppress the growth of human head and neck cancer cells, liver cancer cells, breast cancer cells, and cervical cancer cells (at least most of the way), within about three days—but that was in a petri dish. Those petri dish studies are largely the basis of the evidence for the antitumor activity of plant lectins. How do we even know dietary lectins are absorbed into our body?

Colorectal cancer is one thing. The fact that lectins can kill off colon cancer cells in a petri dish may be applicable, since lectins we eat may come in direct contact with cancerous or precancerous cells in our colon, “providing a mechanism” by which bean consumption may help in “the prevention and treatment of colorectal cancer.” Even more exciting is the potential for effectively rehabilitating cancer cells. The “loss of differentiation and invasion are the histological hallmarks of malignant cells,” meaning that when a normal cell transforms into a cancer cell, it tends to lose its specialized function. Breast cancer cells become less breast-like, and colon cancer cells become less colon-like. What these researchers showed—for the first time—is that the lectin in fava beans could take colon cancer cells and turn them back into looking more like normal cells. As you can see at 4:13 in my video, before exposure to the fava bean lectins, the cancer cells were growing in amorphous clumps. But, after exposure to the fava bean lectins for two weeks, those same cancer cells started to go back to growing glandular structures like normal colon issue. Therefore, dietary lectins or putting them in a pill “may slow the progression of colon cancer,” potentially helping to explain why dietary consumption of beans, split peas, chickpeas, and lentils appears to reduce the risk of colorectal cancer based on 14 studies involving nearly two million participants. Okay, but what about cancers outside of the digestive tract?

“Although lectin containing foods,” like beans and whole grains, “are frequently consumed cooked or otherwise processed, these treatments may not always inactivate the lectins…For example, lectins have been detected in roasted peanuts….” Peanuts are legumes, and we don’t tend to eat them boiled but just roasted or even raw. Are we able to absorb the lectins into our system? Yes. As you can see at 5:12 in my video, within an hour of consumption of raw or roasted peanuts, you can detect the peanut lectin in the bloodstream of most people. Same with tomatoes. Some of the non-toxic lectin in tomatoes also makes it down into our gut and into our blood. Wheat germ agglutinin, the wheat lectin known as WGA, doesn’t seem to make it into our bloodstream, though, even after apparently eating the equivalent amount of wheat germ in more than 80 slices of bread. And, if you ate something like pasta, the boiling in the cooking process might wipe out the lectin in the first place anyway.

In terms of phytochemicals in the fight against cancer, lectins are able to “resist digestion resulting in high bioavailability,” potentially allowing “the cellular mechanisms of the host to utilize the full potential of the…dramatic anti-cancer benefits” lectins have to offer. But, these dramatic benefits have yet to be demonstrated in people. We do know, however, that population studies show “that the consumption of a plant-based diet is strongly associated with a reduced risk of developing certain types of cancer.” People eating a plant-based diet could just be eating fewer carcinogens, but plants do have all those active components that do seem to protect against the “initiation, promotion, or progression” of cancer. So, maybe lectins are one of those protective compounds. We know people who eat more beans and whole grains tend to get less cancer overall, but we’re just not sure exactly why. Now, you could say, “Who cares why?” Well, Big Pharma cares. You can’t make as much money on healthy foods as you can on “lectin based drugs.”

Interested in learning more about lectins? Check out my videos Dr. Gundry’s The Plant Paradox Is Wrong and How to Avoid Lectin Poisoning.


Lectins remind me of the story about phytates. Other components of beans and whole grains, phytates were thought at first to be harmful, but, more recently, evidence is coming to light that suggests the opposite may be true. Check out Phytates for Rehabilitating Cancer Cells and Phytates for the Prevention of Osteoporosis.

What else may explain the protective effect of beans? See, for example, Gut Dysbiosis: Starving Our Microbial Self. Soybeans may be particularly protective against certain cancers, as you can see in BRCA Breast Cancer Genes and Soy.

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:

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 to Boost the Fat Burning Hormone FIAF

Although recent increases in the availability of junk food and decreases “in institutionally driven physical activity” have created an obesity-permissive environment, several other factors may contribute. We know, for example, that the use of antibiotics is linked to obesity, so our gut flora may play a role. I discuss this in my video Is Obesity Infectious?.

Recently, specific bacterial species were identified. Eight species seemed protective against weight gain, and they are all producers of a short-chain fatty acid called butyrate.

Early on, we thought there might be some intestinal bacteria that were able to extract additional calories from what we eat, but the relationship between our gut flora and obesity has proven to be more complex, as you can see at 0:49 in my video. Our gut flora may affect how we metabolize fat, for example, such as through the hormone FIAF—fasting-induced adipose factor.

While we’re fasting, our body has to stop storing fat and instead start to burn it off. FIAF is one of the hormones that signals our body to do this, which could be useful for someone who is obese, and may be one way our gut flora manages our weight. Some bacteria repress this hormone, thereby increasing fat storage. In contrast, when we feed fiber to our fiber-eating bacteria, those that secrete short-chain fatty acids like butyrate are able to upregulate this hormone in all human cell lines so far tested.

“Currently, when an individual fails to lose weight…the only other option is surgery,” but “[a]s the mechanisms of the microbiota’s [gut flora’s] role in weight regulation are elucidated, one can envision transplanting intestinal contents from a thin individual into an obese individual.” Such so-called fecal transplants may suffer from “repulsive esthetics,” though. It turns out there may be easier ways to share.

We’ve known that people who live together share a greater similarity in gut bacteria than people living apart. This could be because co-habitants inadvertently swap bacteria back and forth, or possibly because they eat similar diets, living in the same house. We didn’t know…until now. Not only do co-habiting family members share bacteria with one another—they also share with their dogs, who are probably eating a different diet than they are. You may be interested in the charts at 2:22 in my video.

In fact, it’s been “suggest[ed] that homes harbor a distinct microbial fingerprint that can be predicted by their occupants.” Just by swabbing the doorknobs, you can tell which family lives in which house, as shown at 2:35 in my video. And, when a family moves into a new home, “the microbial community in the new house rapidly converged” or shifted toward that of the old house, “suggesting rapid colonization by the family’s microbiota.” Experimental evidence suggests that individuals raised in a household of lean people may be protected against obesity—no fecal transplant necessary. (Indeed, people may be sharing gut bacteria from kitchen stools instead.)

Moreover, as we know, people living together share more bacteria than those living apart, but when a dog is added to the mix, the people’s bacteria get even closer, as you can see at 3:11 in my video. Dogs can act like a bridge to pass bacteria back and forth between people. Curiously, owning cats doesn’t seem to have the same effect. Maybe cats don’t tend to drink out of the toilet bowl as much as dogs do?

Exposure to pet bacteria may actually be beneficial. It’s “intriguing to consider that who we cohabit with, including companion animals, may alter our physiological properties by influencing the consortia of microbial symbionts [or bacteria] that we harbor in and on our various body habitats.” This may be why “[r]ecent studies link early exposure to pets to decreased prevalence of allergies, respiratory conditions, and other immune disorders” as kids grow older. In my video Are Cats or Dogs More Protective for Children’s Health?, I talk about studies in which dog exposure early in life may decrease respiratory infections, especially ear infections. Children with dogs “were significantly healthier,” but we didn’t know why. Indeed, we didn’t know the mechanism until, perhaps, now—with the first study tying together the protection from respiratory disease through pet exposure to differences in gut bacteria. None of the studied infants in homes with pets suffered from wheezy bronchitis within the first two years of life, whereas 15 percent of the pet-deprived infants had. And, when comparing stool samples, this correlated with differences in gut bacteria depending on the presence of pets in the home.

There was a famous study of 12,000 people that found that a “person’s chances of becoming obese increased by 57%…if he or she had a friend who became obese,” suggesting social ties have a big effect. However, given the evidence implicating the role of gut bacteria in obesity, this “raises up the possibility that cravings and associated obesity might not just be socially contagious”—that is, because, for instance, you all go out together and eat the same fattening food—“but rather truly infectious, like a cold.”


Viruses may also play a role in obesity. How? See Infectobesity: Adenovirus 36 and Childhood Obesity. An Obesity-Causing Chicken Virus may help explain the link found between poultry consumption and weight gain, and you may also be interested in Chicken Big: Poultry and Obesity.

The important question: Can Morbid Obesity Be Reversed Through Diet? Find out in my video, and also check out Coconut Oil and Abdominal Fat.

For more on the amazing inner world in our guts, 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: