Does Nutritional Yeast Trigger Crohn’s Disease?

Is the exaggerated reaction of many Crohn’s disease patients to baker’s, brewer’s, and nutritional yeast just a consequence of their inflamed leaky gut, or might the yeast be a contributing cause?

“Baker’s Yeast in Crohn’s Disease—Can It Kill You?” is the inflammatory title (no pun intended) of a 1999 journal article. Crohn’s disease is an inflammatory bowel disease. Might baker’s yeast, which is the same yeast as brewer’s yeast, which is the same yeast as nutritional yeast, play a role in Crohn’s disease? I explore this in my video Does Nutritional Yeast Trigger Crohn’s Disease?

It all started with a study published in 1988 that showed that people with Crohn’s disease tend to have more antibodies to yeast than people without Crohn’s, as you can see at 0:32 in my video. Antibodies are like homing devices our immune system makes to attack foreign invaders, and cell-mediated immunity, where our white blood cells attack invaders directly, is another part of our immune system. The same hypersensitive reaction to yeast was found in the white blood cells of Crohn’s disease patients, as well.

If you draw blood from healthy people—even bakers who are around yeast all the time—and then you expose their immune system’s white blood cells to yeast, nothing happens. The white blood cells just ignore the yeast because it’s typically harmless. But, “[i]n striking contrast with healthy controls,” if you do the same with Crohn’s disease patients, they show “a marked increase in their lymphocyte proliferation when exposed to yeast” as their white blood cells go crazy.

Now, when I say yeast is “typically harmless,” if you have cancer or AIDS or are immunocompromised, you could potentially get infected from home-brewed beer or probiotic yeast supplements, but researchers don’t think the yeast is actually infecting Crohn’s patients. People with Crohn’s may just be hypersensitive to exposure to the inactive, dead yeast in typical food products, which may help explain why they get better when they rest their bowels by fasting.

In fact, that’s why we add yeast extracts and proteins to vaccines as an adjuvant, an irritant like aluminum, to make the vaccines work better by heightening the immune response. But might that be raising the risk of autoimmune disease, boosting our immune response a little too much, especially in people who may be genetically susceptible, like those with Crohn’s?

The greater the anti-yeast response, the more severe the disease. This was seen in children and may also be the case for adults, too. Should we try a yeast-free diet for Crohn’s patients to see whether they get better? Hold on. Just because anti-yeast antibodies are associated with Crohn’s disease doesn’t mean the reaction to yeast is causing the Crohn’s disease. Maybe the Crohn’s disease is causing the reaction to yeast.

Think about it: Crohn’s causes an inflamed, leaky gut, so maybe the Crohn’s came first and allowed yeast particles to leak into the bloodstream, which resulted in the anti-yeast reaction. Instead of the yeast reaction triggering the Crohn’s, maybe the Crohn’s triggered the yeast reaction. “Whether these antibodies are triggering IBD [inflammatory bowel disease] or are only a consequence of gut inflammation without a disease-aggravating role remained elusive.” How could we test it? If anti-yeast antibodies are just a consequence of food particles leaking through the gut, Crohn’s patients should have antibodies to all sorts of common foods, but they don’t. As you can see at 3:18 in my video, there were higher anti-yeast antibodies in Crohn’s disease patients compared with controls, but there was no greater reaction in Crohn’s patients to milk, wheat, or egg proteins, all of which would presumably leak through, too.

We can also look at it the other way. Instead of other foods, what about other inflammatory bowel disorders? Ulcerative colitis and acute gastroenteritis could cause guts to get inflamed and leaky, too, yet there is no increased yeast reaction. There does appear to be something unique about the relationship between yeast and Crohn’s, but might inflamed Crohn’s intestines just uniquely and selectively allow yeast through? If you cut out the Crohn’s, can you stop the yeast reaction? Crohn’s gets so bad that most patients have to go under the knife and get sections of their intestines removed. So, when the inflamed segments are removed, does the yeast reaction go away? No, as you can see at 4:18 in my video, there is no post-operative change. So, a change in Crohn’s activity doesn’t lead to a change in the yeast reaction, but we still have to prove that the yeast reaction comes first.

Thankfully, the Israeli military systematically draws blood from its recruits and follows their health for years, so we can go back and check the blood of newly diagnosed Crohn’s victims. And, indeed, those who went on to have Crohn’s were disproportionately reacting to yeast years earlier. So, it’s not as though yeast reactions were low until Crohn’s hit and then shot up. As you can see at 4:54 in my video, yeast reactivity crept up year after year before the diagnosis. It is possible there was some subclinical gut leakiness in the years preceding diagnosis that led to the yeast reaction, but there doesn’t appear to be any association between yeast reactivity and gut leakiness. Given that, do high blood levels of anti-yeast antibodies result from leakiness of the gut barrier in Crohn’s disease? No, that does not appear to be the case. So, if Crohn’s isn’t leading to the yeast reaction, does that mean the yeast reaction is leading to the Crohn’s?

Any time two things appear to be associated—in this case, reacting to yeast (X) and Crohn’s disease (Y)—they can appear tied together because X causes Y or Y causes X. Well, as we’ve discussed, it appears that Y, Crohn’s disease, does not cause X, a yeast reaction, but does that mean that X causes Y? There’s another option. There may be a third factor, Z, that causes both X and Y independently. Maybe the only reason yeast reactivity and Crohn’s disease appear to go together is that there’s a third factor causing them both—for instance, Candida, which I cover in my video Is Candida Syndrome Real?.

This is something I warned people about long ago on social media. It takes some time from when I first research a topic until the video is produced and uploaded to the site, so for breaking or important news, I rely on our Facebook, Twitter, Instagram, and YouTube channels to let everyone know as quickly as I can. Please consider following along and joining in on the conversation.


Warned about? So is yeast really a potential problem? Yes, and not just for Crohn’s. This is the first of a four-part video series. See also:

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:

Treating Advanced Prostate Cancer with Diet

Dr. Dean Ornish showed that a plant-based diet and lifestyle program could apparently reverse the progression of prostate cancer for early stage, localized, watch-and-wait cancer. What about for more advanced stage life-threatening disease?

Dr. Dean Ornish showed that a plant-based diet and lifestyle program could apparently reverse the progression of prostate cancer by making men’s bloodstreams nearly eight times better at suppressing cancer cell growth. But this was for early-stage, localized, watch-and-wait prostate cancer.

What about for more advanced-stage, life-threatening disease? There have been sporadic case reports in the literature suggesting benefit. For example, a man with extensive metastatic disease who had been given about three years to live went on a strict plant-based diet. Four years later, it appeared the cancer had disappeared. After six years, he got a little too comfortable, backslid a bit on the diet and began eating “turkey, tuna fish, and chicken,” then the cancer came raging back and he died. But that could have been a total coincidence. That’s the problem with case reports, which are kind of glorified anecdotes. You have no idea how representative the outcome is unless it’s studied formally. But, throughout the 20th century, all we had were these kinds of case reports for more advanced prostate cancer until 2001.

We had “preliminary evidence” based on all the case reports that “prostate cancer may be sensitive to diet even after metastasis develops. Plant-based diets may be associated with prolonged survival and instances of remission of bone metastasis in men with advanced disease.” So, researchers decided to put it to the test in a four-month intervention. They thought that too much saturated fat, too little fiber, and too much meat may be the biggest players in tumor promotion and progression, so they put people on a whole food plant-based diet of whole grains, beans, seeds, and fruits. Figuring this would be quite the departure from their regular diet, the researchers included a stress reduction component in hopes of improving dietary compliance.

Who were the subjects? The ten men in the study didn’t just have prostate cancer—they had all undergone a radical prostatectomy to remove their primary tumor and then subsequently had increasing PSA levels, indicative of probable metastatic disease. PSA stands for prostate-specific antigen. It’s only made by prostate cells, but the ten men had just had their entire prostates removed so their levels should have been zero. The fact that they not only still had some PSA, but that it was rising suggests that the surgery had failed, and the cancer had spread and was making a comeback.

At 2:43 in my video Treating Advanced Prostate Cancer with Diet: Part 1, you can view a graph showing the PSA levels for each of the men before the study began and see the speed at which their PSAs went up. If their PSA trajectories had stayed the same after four months of eating healthfully, it would mean the diet had had no effect. In that case, presumably, the cancer would have still been powering away and spreading just as fast as before. Instead, in two of the men, it looked as if the cancer had accelerated and grew even faster, but in the other eight men, the intervention appeared to work, apparently slowing down cancer growth. And, in three of the ten men, it didn’t just slow or stop, but appeared to reverse and shrink.

Why the different responses? Well, in the Ornish study, the more people complied with the diet and lifestyle recommendations, the better they did, as you can see at 3:31 in my video. Dietary changes only work if you actually do them. Just because you tell people to start eating a whole food plant-based diet, doesn’t mean patients actually do it. One can use fiber intake as a proxy for dietary compliance because all whole plant foods have fiber, and Ornish’s patients about doubled their fiber intake from 31 grams to 59 grams.

How did the ten men in the 2001 study do? They started out even worse, averaging 14 grams of fiber a day, and only made it up to 19 grams a day. That’s not a whole food plant-based diet—that doesn’t even meet the recommended minimum daily intake. As you can see at 4:18 in my video, only four of the ten men even increased their fiber intake at all, so that may explain the different responses. In fact, the man whose fiber improved the most had the best PSA result, and the man whose fiber intake dropped the most had the worst PSA result. Indeed, it appears the more changes they made to their diet, the better their results.

The researchers concluded that “a plant-based diet delivered in the context of MBSR [Mindfulness-Based Stress Reduction]…may slow the rate of tumor progression,” and, unlike other treatments, may give patients some control over their disease. And, as Ornish pointed out, “the only side effects are beneficial ones.”

Dr. Ornish and colleagues were able to show an apparent reversal in the progression of early-stage, localized prostate cancer with a plant-based diet and lifestyle program, and researchers at the University of Massachusetts and elsewhere showed a similar diet may help slow the progression of even advanced prostate cancer over a period of four months.

How about over six months? As I discuss in my video Treating Advanced Prostate Cancer with Diet: Part 2, researchers at University of California, San Diego put cancer patients through the same protocol as the four-month study. Once again, these were patients who had already been treated for invasive prostate cancer by either radical prostatectomy or radiation therapy, yet still had rising PSA levels, suggesting the treatment didn’t work and the cancer was on the move. “In those who have undergone a [cancer] recurrence, PSA typically tends to rise exponentially after prostatectomy or radiation therapy, reflecting the gradual, inexorable growth of the cancer in the body. After local treatment, the rate of PSA rise is the single best predictor of…development of overt metastatic disease, as well as of overall survival.” The next step would be hormonal therapy, which is chemical or surgical castration, but that has a list of side effects, including loss of libido, sexual function, strength, and vitality. “Therefore, many physicians employ a strategy of active surveillance” and try to hold off for as long as possible. If we’re just waiting, why not give diet a try?

Patients were “taught to increase intake of whole grains, vegetables, fruit, and legumes and to decrease meat, dairy, and refined carbohydrates.” Of all possible lifestyle interventions, why a whole food plant-based diet? If you look around the world, there are huge differences in prostate cancer rates, as you can see at 1:42 in my video, and our We’re #1! USA! USA! rates are up to a hundred times higher than some places in Asia, for example—and it’s not just genetic. Within one generation of migrating to the United States, cancer rates shoot up, and the grandkids of the immigrants end up with the same top-of-the-pile “approximate US rates.” A whole range of lifestyle factors have been looked at, but diet appears to have the greatest influence.

Specifically, “consumption of meat and dairy appears to increase risk, and consumption of plant-based foods appears to decrease risk.” Hence, the plant-based diet. A possible mechanism found in both meat and dairy products is arachidonic acid, an inflammatory compound that we make from omega-6-rich oils, like corn, sunflower, safflower, and cottonseed oils. It also comes “preformed” in animal-based foods and, in the American diet, is found particularly in chicken and eggs. In a petri dish, arachidonic acid appears to stimulate prostate cancer cell growth as much 200 percent, as you can see at 2:43 in my video.

So what happened when those researchers at University of California, San Diego asked men to remove processed and animal foods from their diet for six months? At 2:57 in my video, you can see a graph showing how fast the cancer patients’ PSA levels had been rising before starting the study. “In the absence of treatment, absolute levels of PSA tend to increase exponentially,” but upon eating more healthfully, nine of the ten study subjects showed an apparent slowing of cancer growth and four of the nine showed an apparent reversal in cancer growth. The average doubling time, an estimate of how long it would take for their cancer to double in size, slowed from doubling every year to closer to every ten years.

Other studies have used various diets and nutritional interventions, like vitamin supplements, but none has worked as well as this one—and the subjects’ compliance wasn’t even all that great. As you can see at 3:41 in my video, they did well in boosting their whole grain consumption in the first three months, but then backslid a bit, and they ate more vegetables, including a serving of greens, and an extra serving of fruit, at least early on. And, in the beginning, they at least ate one whole serving of legumes a day. So the researchers “did observe some [dietary] recidivism by 6 months,” with subjects sliding back into old habits. Given that, they checked to see if the study participants were better able to beat off the disease during that earlier period. And, indeed, at the end of the first three months, on average, there was PSA reversal. “Changes in the rate of rise in PSA, an indicator of disease progression, were in the opposite direction as changes in the intake of plant-based food groups, raising the provocative possibility that PSA may have inversely tracked intake of these foods and suggesting that adoption of a plant-based diet may have therapeutic potential in the management of this condition.”

Their findings suggest that, without further surgery, radiation, or chemotherapy, disease progression can be slowed or even reversed, despite “the prevailing scientific consensus…that cancer progression is largely irreversible.” The researchers state their “findings do not refute the benefits of standard therapies or guarantee that a plant-based diet and stress reduction will always induce remission,” but their results “do contribute to a growing [medical] literature that suggests that in at least some circumstances, cancer may be partly reversible and that modification of dietary and lifestyle factors may be able to help prevent disease spread”—all without getting their testicles cut off.

Hold on. We can make men’s bloodstreams nearly eight times better at suppressing cancer cell growth? See How Not to Die from Cancer.

It’s not all or nothing, though. Any movement we make towards healthy eating may help. See Prostate Cancer Survival: The A/V Ratio .


You may also be interested 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:

Coconut Oil and the Boost in HDL “Good” Cholesterol

The effects of coconut oil were compared to butter and tallow. Even if virgin coconut oil and other saturated fats raise LDL “bad” cholesterol, isn’t that countered by the increase in HDL “good” cholesterol?

According to “the experience and wisdom of 200 of the country’s leading experts in cardiovascular diseases,” in a report representing 29 national medical organizations, including the American Heart Association and the American College of Cardiology, we’ve known for nearly half a century that “coconut oil is one of the most potent agents for elevating [blood] serum cholesterol level.” As I discuss in my video Coconut Oil and the Boost in HDL “Good” Cholesterol, studies showing coconut oil elevates cholesterol date back to 1955, when it was first shown experimentally that switching someone from coconut oil to soybean oil could drop cholesterol from around 200 down to 150, as you can see at 0:39 in my video.

Coconut oil can significantly raise cholesterol levels within hours of consumption. In fact, a significant increase in blood cholesterol was found within hours of eating a slice of cake made from either coconut oil (or cod liver oil for that matter), but not from the same cake made from flaxseed oil.

As you can see at 1:10 in my video, coconut oil may even be worse than tallow, or beef fat, but it is not as bad as butter. An interventional trial was published in March 2017: a month-long randomized, controlled, crossover study looking at the impact of two tablespoons per day of virgin coconut oil. The result? Coconut oil elevated cholesterol about 14 percent over the control, which was consistent with seven other interventional trials published to date in a 2016 review.

Hold on. Saturated fats can make HDL, the so-called good cholesterol, go up, so what’s the problem? The problem is that it doesn’t seem to help. Having a high blood HDL level is “no longer regarded as protective.” What? Wait a second. Higher HDL levels are clearly associated with lower risk of heart disease, as you can see at 2:01 in my video. In fact, HDL levels “are among the most consistent and robust predictors of CVD [cardiovascular disease] risk.” Ah, but there are two types of risk factors: causal and non-causal. Association does not mean causation—that is, just because two things are tightly linked, it doesn’t mean one causes the other.

Let me give you an example, which you can see at 2:30 in my video. I bet that the number of ashtrays someone owns is an excellent predictor of lung cancer risk and that study after study would show that link. But, that does not mean that if you intervene and lower the number of ashtrays someone has, their lung cancer risk will drop, because it’s not the ashtrays that are causing the cancer, but the smoking. The ashtrays are just a marker of smoking, an indicator of smoking, as opposed to playing a causal role in the disease. So, just like having a high number of running shoes and gym shorts might predict a lower risk of heart attack, having a high HDL also predicts a lower risk of heart attack. But, raising HDL, just like raising the number of gym shorts, wouldn’t necessarily affect disease risk. How do you differentiate between causal and non-causal risk factors? You put them to the test. The reason we know LDL cholesterol truly is bad is because people who were just born with genetically low LDL cholesterol end up having a low risk of heart disease. And, if you intervene and actively lower people’s LDL through diet or drugs, their heart disease risk drops—but not so with HDL.

People who live their whole lives with high HDL levels don’t appear to have a lower risk of heart attack, and if you give people a drug that increases their HDL, it doesn’t help. That’s why we used to give people high-dose niacin—to raise their HDL. But, it’s “time to face facts.” The “lack of benefit of raising the HDL cholesterol level with the use of niacin…seriously undermine[s] the hypothesis that HDL cholesterol is a causal risk factor.” In simple terms: “High HDL may not protect the heart.” We should concentrate on lowering LDL. So, specifically, as this relates to coconut oil, the increase in HDL “is of uncertain clinical relevance,” but the increase in LDL you get from eating coconut oil “would be expected to have an adverse effect” on atherosclerotic cardiovascular disease risk.

But, what about the MCTs, the medium-chain triglycerides? Proponents of coconut oil, who lament “that ‘coconut oil causes heart disease’ has created this bad image of [their] national exports,” assert that the medium-chain triglycerides, the shorter saturated fats found in coconut oil, aren’t as bad as the longer-chain saturated fats in meat and dairy. And, what about that study that purported to show low rates of heart disease among Pacific Islanders who ate large amounts of coconuts? I cover both of those topics in my video What About Coconuts, Coconut Milk, and Coconut Oil MCTs?.


I love topics that give me an excuse to talk about scientific concepts more generally, like various study designs in my video Prostate Cancer and Organic Milk vs. Almond Milk or my discussion of direct versus indirect risk factors in this one.

How do we know LDL is bad? Check out How Do We Know That Cholesterol Causes Heart Disease?.

But, wait. Isn’t the whole saturated fat thing bunk? No. 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: