How the Egg Industry Tried to Bury the TMAO Risk

“Metabolomics is a term used to describe the measurement of multiple small-molecule metabolites in biological specimens, including bodily fluids,” with the goal of “[i]dentifying the molecular signatures.” For example, if we compared the metabolic profile of those with severe heart disease to those with clean arteries, we might be able to come up with a cheap, simple, and noninvasive way to screen people. If heart patients happened to have something in their blood that healthy people didn’t, we could test for that. What’s more, perhaps it would even help us understand the mechanisms of disease. “To refer to metabolomics as a new field is injustice to ancient doctors who used ants to diagnose the patients of diabetes” (because the ants could detect the sugar in the diabetics’ urine).

The first modern foray discovered hundreds of substances in a single breath, thanks to the development of computer technology that made it possible to handle large amounts of information—and that was in 1971, when a computer took up nearly an entire room. “[N]ew metabolomics technologies [have] allowed researchers to measure hundreds or even thousands of metabolites at a time,” which is good since more than 25,000 compounds may be entering our body through our diet alone.

Researchers can use computers to turn metabolic data into maps that allow them to try to piece together connections. You can see sample data and a map at 1:28 in my video Egg Industry Response to Choline and TMAO. Metabolomics is where the story of TMAO started. “Everyone knows that a ‘bad diet’ can lead to heart disease. But which dietary components are the most harmful?” Researchers at the Cleveland Clinic “screened blood from patients who had experienced a heart attack or stroke and compared the results with those from blood of people who had not.”

Using an array of different technology, the researchers identified a compound called TMAO, which stands for trimethylamine N-oxide. The more TMAO people had in their blood, the greater the odds they had heart disease and the worse their heart disease was.

Where does TMAO come from? At 2:19 in my video, you can see a graphic showing that our liver turns TMA into TMAO—but where does TMA come from? Certain bacteria in our gut turn the choline in our diet into TMA. Where is the highest concentration of choline found? Eggs, milk, and meats, including poultry and fish. So, when we eat these foods, our gut bacteria may make TMA, which is absorbed into our system and oxidized by our liver into TMAO, which may then increase our risk of heart attack, stroke, and death.

However, simply because people with heart disease tend to have higher TMAO levels at a snapshot in time doesn’t mean having high TMAO levels necessarily leads to bad outcomes. We’d really want to follow people over time, which is what researchers did next. Four thousand people were followed for three years, and, as you can see in the graph at 3:10 in my video, those with the highest TMAO levels went on to have significantly more heart attacks, strokes, or death.

Let’s back up for a moment. If high TMAO levels come from eating lots of meat, dairy, and eggs, then maybe the only reason people with high TMAO levels have lots of heart attacks is that they’re eating lots of meat, dairy, and eggs. Perhaps having high TMAO levels is just a marker of a diet high in “red meat, eggs, milk, and chicken”—a diet that’s killing people by raising cholesterol levels, for example, and has nothing to do with TMAO at all. Conversely, the reason a low TMAO level seems so protective may just be that it’s indicative of a more plant-based diet.

One reason we think TMAO is directly responsible is that TMAO levels predict the risk of heart attacks, strokes, or death “independently of traditional cardiovascular risk factors.” Put another way, regardless of whether or not you had high cholesterol or low cholesterol, or high blood pressure or low blood pressure, having high TMAO levels appeared to be bad news. This has since been replicated in other studies. Participants were found to have up to nine times the odds of heart disease at high TMAO blood levels even after “controll[ing] for meat, fish, and cholesterol (surrogate for egg) intake.”

What about the rest of the sequence, though? How can we be certain that our gut bacteria can take the choline we eat and turn it into trimethylamine in the first place? It’s easy. Just administer a simple dietary choline challenge by giving participants some eggs.

Within about an hour of eating two hard-boiled eggs, there is a bump of TMAO in the blood, as you can see at 4:51 in my video. What if the subjects are then given antibiotics to wipe out their gut flora? After the antibiotics, nothing happens after they eat more eggs. In fact, their TMAO levels are down at zero. This shows that our gut bacteria play a critical role. But, if we wait a month and give their guts some time to recover from the antibiotics, TMAO levels creep back up.

These findings did not thrill the egg industry. Imagine working for the American Egg Board and being tasked with designing a study to show there is no effect of eating nearly an egg a day. How could a study be rigged to show no difference? If we look at the effect of an egg meal (see 5:32 in my video), we see it gives a bump in TMAO levels. However, our kidneys are so good at getting rid of TMAO, by hours four, six, and eight, we’re back to baseline. So, the way to rig the study is just make sure the subjects hadn’t eaten those eggs in the last 12 hours. Then, you can show “no effect,” get your study published in the Journal of the Academy of Nutrition and Dietetics, and collect your paycheck.


Unfortunately, this appears to be part for the course for the egg industry. For more on their suspect activities, see:

For more on the TMAO story, see:

In health,
Michael Greger, M.D.

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

How to Increase Gut Bacterial Richness

We live in an “obesogenic environment,” with cheap junk food everywhere, thanks in part to subsidies going to the “‘food industrial complex,’ which manufactures obesogenic foods that foster addiction…The root causes…[may] make obesity difficult to escape,” but a lot of people do. If it were simply the external environment, why isn’t everyone obese?

“Some individuals seem to be more susceptible to the obesogenic environment…than others,” which suggests a genetic component, supported by studies of twins and adopted kids, but the genes that have been identified so far account for only 6 to 11 percent of the genetic variation in body mass index between individuals. Perhaps variation in our “other genome”—that is, all the different microbes that inhabit our body, known as the microbiome—may be playing a role. We have a hundred times more bacterial genes inside us than human genes.

As I discuss in my video Gut Microbiome: Strike It Rich with Whole Grains, a study found that people tend to fall into one of two groups: those who have lots of different types of bacteria in their gut (high “gut bacterial richness”) and those with relatively few types. Those with low bacterial richness had more overall body fat, insulin resistance, which is the cause of type 2 diabetes, high triglycerides, and higher levels of inflammatory markers, like C-reactive protein, compared to those with high bacterial richness. Not only did people with lower bacterial richness start out heavier, but the obese individuals with lower bacterial richness also gained more weight over time.

The question then becomes: Can a dietary intervention have any impact “A number of studies have associated increased microbial richness…with diets higher in fruits, vegetables, and fiber.”

Just giving fiber-type supplements doesn’t seem to boost richness, however, but the “compositional complexity” of a whole food, like whole grains, “could potentially support a wider scope of bacterial taxa,” types of bacteria, “thereby leading to an increase in diversity.” Human studies to investigate the effects of whole grains had been neglected, though…until now.

Subjects were given whole-grain barley, brown rice, or a mixture of both for a month, and all three caused an increase in bacterial community diversity. Therefore, it may take a broad range of substrates to increase bacterial diversity, and this can be achieved by eating whole plant foods.

Moreover, the alterations of gut bacteria in the study coincided with a drop in systemic inflammation in the body. We used to think that the way fiber in whole grains helped us was by gelling in our small intestine right off of our stomach, slowing the rate at which sugars were absorbed and blunting the spike in blood sugars one might get from refined carbs. We now know, however, that fiber is broken down in our colon by our friendly flora, which release all sorts of beneficial substances into our bloodstream that can have anti-inflammatory effects, as well. So, perhaps what’s happening in our large intestine helps explain the protective effects of whole grain foods against type 2 diabetes.

Interestingly, the combination of both barley and brown rice worked better than either grain alone, suggesting a synergistic effect. This may help explain “the discrepancy of the health effects of whole grains obtained in epidemiological [population-based] and interventional studies.”

Observational studies “strongly suggest” that those who consume three or more servings of whole grains a day tend to have a lower body mass index, less belly fat, and less tendency to gain weight, but recent clinical trials, where researchers randomized subjects to eat white bread rolls versus whole-wheat rolls, failed to provide evidence of a beneficial effect on body weight. Of course, whole grains are so superior nutritionally that they should continue to be encouraged. However, the “[i]nterventional trials might have failed to show [weight] benefits because they focused on a limited selection of whole grains, while in epidemiological trials [or the population studies], subjects are likely to consume a diverse set of whole grains which might have synergistic activities.”


Until recently, we knew very little about how powerfully our gut bacteria can affect our health. Catch up on the latest science with these related videos:

When it comes to rice, even white rice can be better than many choices, but brown rice is better and pigmented rice is probably the best. See my videos Kempner Rice Diet: Whipping Us Into Shape and Is It Worth Switching from White Rice to Brown? for more.

But what about the arsenic in rice? Learn more:

In health,
Michael Greger, M.D.

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

The Best Source of Resistant Starch

Resistant starch wasn’t discovered until 1982. Before that, we thought all starch could be digested by the digestive enzymes in our small intestine. Subsequent studies confirmed that there are indeed starches that resist digestion and end up in our large intestine, where they can feed our good bacteria, just like fiber does. Resistant starch is found naturally in many common foods, including grains, vegetables, beans, seeds, and some nuts, but in small quantities, just a few percent of the total. As I discuss in my video Getting Starch to Take the Path of Most Resistance, there are a few ways, though, to get some of the rest of the starch to join the resistance.

When regular starches are cooked and then cooled, some of the starch recrystallizes into resistant starch. For this reason, pasta salad can be healthier than hot pasta and potato salad can be healthier than a baked potato, but the effect isn’t huge. The resistant starch goes from about 3 percent up to 4 percent. The best source of resistant starch is not from eating cold starches, but from eating beans, which start at 4 or 5 percent and go up from there.

If you mix cooked black beans with a “fresh fecal” sample, there’s so much fiber and resistant starch in the beans that the pH drops as good bacteria churn out beneficial short-chain fatty acids, which are associated both directly and indirectly with lower colon cancer risk. (See Stool pH and Colon Cancer.) The more of this poopy black bean mixture you smear on human colon cancer, the fewer cancer cells survive.

Better yet, we can eat berries with our meals that act as starch blockers. Raspberries, for example, completely inhibit the enzyme that we use to digest starch, leaving more for our friendly flora. So, putting raspberry jam on your toast, strawberries on your corn flakes, or making blueberry pancakes may allow your good bacteria to share in some of the breakfast bounty.

Another way to feed our good bacteria is to eat intact grains, beans, nuts, and seeds. In one study, researchers split people into two groups and had them eat the same food, but in one group, the seeds, grains, beans, and chickpeas were eaten more or less in a whole form, while they were ground up for the other group. For example, for breakfast, the whole-grain group got muesli, and the ground-grain group had the same muesli, but it was blended into a porridge. Similarly, beans were added to salads for the whole-grain group, whereas they were blended into hummus for the ground-grain group. Note that both groups were eating whole grains—not refined—that is, they were eating whole foods. In the ground-grain group, though, those whole grains, beans, and seeds were made into flour or blended up.

What happened? Those on the intact whole-grain diet “resulted in a doubling of the amount excreted compared to the usual diet and produced an additional and statistically significant increase in stool mass” compared with those on the ground whole-grain diet, even though they were eating the same food and the same amount of food. Why? On the whole-grain diet, there was so much more for our good bacteria to eat that they grew so well and appeared to bulk up the stool. Even though people chewed their food, “[l]arge amounts of apparently whole seeds were recovered from stools,” but on closer inspection, they weren’t whole at all. Our bacteria were having a smorgasbord. The little bits and pieces left after chewing transport all this wonderful starch straight down to our good bacteria. As a result, stool pH dropped as our bacteria were able to churn out so many of those short-chain fatty acids. Whole grains are great, but intact whole grains may be even better, allowing us to feed our good gut bacteria with the leftovers.

Once in our colon, resistant starches have been found to have the same benefits as fiber: softening and bulking stools, reducing colon cancer risk by decreasing pH, increasing short-chain fatty acid production, reducing products of protein fermentation (also known as products of putrefaction), and decreasing secondary bile products.

Well, if resistant starch is so great, why not just take resistant starch pills? It should come as no surprise that commercial preparations of resistant starch are now available and “food scientists have developed a number of RS-enriched products.” After all, some find it “difficult to recommend a high-fiber diet to the general public.” Wouldn’t be easier to just enrich some junk food? And, indeed, you now can buy pop tarts bragging they contain “resistant corn starch.”

Just taking resistant starch supplements does not work, however. There have been two trials so far trying to prevent cancer in people with genetic disorders that put them at extremely high risk, with virtually a 100-percent chance of getting cancer, and resistant starch supplements didn’t help. A similar result was found in another study. So, we’re either barking up the wrong tree, the development of hereditary colon cancer is somehow different than regular colon cancer, or you simply can’t emulate the effects of naturally occurring dietary fiber in plant-rich diets just by giving people some resistant starch supplements.

For resistant starch to work, it has to get all the way to the end of the colon, which is where most tumors form. But, if the bacteria higher up eat it all, then resistant starch may not be protective. So, we also may have to eat fiber to push it along. Thus, we either eat huge amounts of resistant starch—up near the level consumed in Africa, which is twice as much as were tried in the two cancer trials—or we consume foods rich in both resistant starch and fiber. In other words, “[f]rom a public health perspective, eating more of a variety of food rich in dietary fibre including wholegrains, vegetables, fruits, and pulses [such as chickpeas and lentils] is a preferable strategy for reducing cancer risk.”


What’s so great about resistant starch? See my video Resistant Starch and Colon Cancer.

I first broached the subject of intact grains in Are Green Smoothies Bad for You?.

Why should we care about what our gut flora eats? See Gut Dysbiosis: Starving Our Microbial Self.

Did I say putrefaction? See Putrefying Protein and “Toxifying” Enzymes.

Berries don’t just help block starch digestion, but sugar digestion as well. See If Fructose Is Bad, What About Fruit?.

The whole attitude that we can just stuff the effects into a pill is a perfect example of reductionism at work. See Reductionism and the Deficiency Mentality and Why is Nutrition So Commercialized? for more on this.

In health,
Michael Greger, M.D.

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