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:

The Risks and Benefits of Taking Low-Dose Aspirin

Salicylic acid, the active ingredient in aspirin, has been used for thousands of years as an anti-inflammatory painkiller in the form of willow tree bark extract, which Hippocrates used to “treat fever and to alleviate pain during childbirth.” It became trademarked as a drug named Aspirin™ in 1899 and, to this day, “remains the most commonly used drug in the world.” One reason for its on-going popularity, despite the availability of better painkillers now, is that aspirin also acts as a blood thinner. Millions of people take aspirin on a daily basis to treat or prevent heart disease, which I explore in my video, Should We All Take Aspirin to Prevent Heart Disease?.

It all started in 1953 with the publication of the landmark study “Length of life and cause of death in rheumatoid arthritis” in the New England Journal of Medicine. The paper began with the sentence: “It has often been said that the way to live a long life is to acquire rheumatism.” The researchers found fewer deaths than expected from accidents, which could be explained by the fact that people with rheumatoid arthritis likely aren’t skiing or engaging in other potentially risky activity, but they also found significantly fewer deaths from heart attacks. Why would this be? Perhaps all the aspirin the subjects were taking for their joints was thinning their blood and preventing clots from forming in their coronary arteries in their heart. To find out, in the 1960s, there were calls to study whether aspirin would help those at risk for blood clots, and we got our wish in the 1970s: studies suggesting regular aspirin intake protects against heart attacks.

Today, the official recommendation is that low-dose aspirin is recommended for all patients with heart disease, but, in the general population (that is, for those without a known history of heart disease or stroke) daily aspirin is only recommended “when the potential cardiovascular [heart] disease benefit outweigh the risk of gastrointestinal bleeding.”

The bleeding complications associated with aspirin use may be considered an underestimated hazard in clinical medical practice. For those who have already had a heart attack, the risk-benefit analysis is clear. If we took 10,000 patients, daily low-dose aspirin use would be expected to prevent approximately 250 “major vascular events,” such as heart attacks, strokes, or, the most major event of all, death. However, that same aspirin “would be expected to cause approximately 40 major extracranial bleeding events,” meaning bleeding so severe you have to be hospitalized. Thus, the net benefit of aspirin for secondary prevention—for example, preventing your second heart attack—“would substantially exceed the bleeding hazard. For every 6 major vascular events prevented, approximately 1 major bleeding event would occur; therefore, the value of aspirin for secondary prevention is not disputed.”

If we instead took 10,000 patients who hadn’t ever had a heart attack or stroke and tried to use aspirin to prevent clots in the first place, that is, for so-called primary prevention, daily low-dose aspirin would only “be expected to prevent 7 major vascular events and cause 1 hemorrhagic stroke [bleeding within the brain] and 3 major extracranial bleeding events.” So, the benefits are approximately only 2 to 1, which is a little too close for comfort. This is why the new European guidelines do not recommend aspirin for the general population, especially given the additional risk of aspirin causing smaller bleeds within the brain as well.

If only there were a safe, simple solution free of side effects…and there is! Drs. Ornish and Esselstyn proved that even advanced, crippling heart disease could not only be prevented and treated, but also reversed, with a plant-based diet centered around grains, beans, vegetables, and fruits, with nuts and seeds treated as condiments, and without oils, dairy, or meat (including poultry and fish).

Long-time director of the longest-running epidemiological study in the world, the famous Framingham Heart Study, “Dr. William Castelli was asked what he would do to reverse the CAD [coronary artery disease] epidemic if he were omnipotent. His answer: ‘Have the public eat the diet of the rural Chinese as described by Dr. T. Colin Campbell…’” In other words, as he , “‘If Americans adopted a vegetarian diet, the whole thing would disappear,’ Castelli says of the heart disease epidemic.”

Dr. Esselstyn clarified that we’re not just talking about vegetarianism. “This new paradigm” of heart disease reversal means “exclusively plant-based nutrition.”


Did you know preventing heart disease and stroke aren’t the only benefits of an aspirin a day? A daily aspirin may also decrease the risk of certain cancers. In that case, should we take an aspirin a day after all? See Should We All Take Aspirin to Prevent Cancer? and Plants with Aspirin Aspirations.

For more on preventing, arresting, and reversing heart disease, 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:

Is Type 1 Diabetes Triggered by the Bovine Insulin in Milk?

The tight correlation among countries between the incidence of type 1 diabetes in children and cow’s milk consumption didn’t account for Iceland. Indeed, studies correlating dairy intake in children and adolescents with the incidence of type 1 diabetes deliberately excluded the Icelandic data. Why? Is it because of genetics? Perhaps, yes and no. The people of Iceland are similar genetically to other Nordic countries, but their cows are not. As I discuss in my video Does Bovine Insulin in Milk Trigger Type 1 Diabetes?, there are two main types of the cow milk protein casein: A1 and A2. Icelandic cattle, who “have been isolated from interbreeding with other cattle breeds for over 1,100 years,” are unusual in that they produce mostly A2 milk, which may explain the lower incidence of type 1 diabetes in Iceland.

Unlike A2 casein, A1 casein breaks down into casomorphin, which has opioid properties that may alter immune function, perhaps increasing susceptibility to infections that may themselves trigger type 1 diabetes. That’s what’s in the milk from the classic black-and-white patterned Holstein cows, who make up about 95 percent of the U.S. dairy herd and much of the global herd—A1 casein. This issue has even caused dairy boards to begin taking out patents on methods for selecting “nondiabetogenic” milk to avoid triggering of Type 1 diabetes. Indeed, looking only at A1 casein consumption certainly restores that tight linear relationship between milk intake and type 1 diabetes and you can see at 1:47 in the video.

These so-called ecological, or country-by-country, studies, however, primarily serve to suggest possibilities that then need to be put to the test. For example, a study was designed where hundreds of siblings of type 1 diabetics were followed for about ten years and found that those who drank a lot of milk did have about five times the risk of coming down with the disease, too. By the mid-1990s, more than a dozen such studies were done.

Overall, researchers found that early cow’s milk exposure appears to increase the risk of type 1 diabetes by about 50 percent. Those data were enough for the American Academy of Pediatrics to decide that “cow’s milk protein may be an important factor” in the initiation of the process that destroys our insulin-producing cells. The organization went on to say that the avoidance of cow’s milk protein may reduce or delay the onset of type 1 diabetes. As such, the American Academy of Pediatrics emphasizes that breast milk is best and, for those at higher risk of the disease, strongly encourages the avoidance of products containing cow’s milk protein that is intact, as opposed to hydrolyzed formula where the milk proteins are broken up into tiny pieces.

Typically, hydrolyzed formula is given to children with dairy allergies and could potentially make it less risky, but we don’t know until we put it to the test. Based on the population studies and meta-analyses of antibody studies, which suggested that “cow’s milk may serve as a trigger of Type 1 diabetes,” a pilot study was initiated the following year. Researchers wanted to see if babies at high genetic risk for the disease would be less likely to develop antibodies that would then attack their own pancreas if they drank hydrolyzed casein—that is, casein that was chopped up. The hydrolyzed formula did seem to reduce the appearance of at least one autoimmune antibody, but not two or more, which is much more predictive of the development of the disease.

Nevertheless, that was enough for the investigators to embark on the ambitious Trial to Reduce Incidence of Diabetes in Genetically at Risk, also known as the TRIGR study. This multinational, randomized prospective trial involved randomizing thousands of newborns across 15 countries. In 2010, preliminary data suggested the hydrolyzed formula may have helped, but they didn’t quite reach statistical significance, approximately meaning there was greater than a 1 in 20 chance the findings could have just been a fluke. Indeed, when the final autoimmune antibody results were published, the special hydrolyzed formula didn’t seem to help at all.

The researchers only looked at a special group of children, though—ones who were at high genetic risk with diabetes running in the family—whereas the great majority of children who get type 1 diabetes do not have any afflicted close relative. Perhaps most importantly, however, as the researchers themselves emphasized, their study wasn’t designed to test whether cow’s milk is or is not a trigger for the disease. Instead, it aimed to analyze the potential effects of the hydrolyzed casein formula. Maybe it’s not the casein, though. Maybe it’s the bovine insulin.

Insulin autoantibodies—antibodies our body produces to attack our own insulin—often appear as the first sign in prediabetic children. “Because cow’s milk contains bovine insulin,” around the same time researchers were looking into casein, another team “followed the development of insulin-binding antibodies in children fed with cow’s milk formula.” They found significantly more antibodies to bovine insulin in the cow’s milk formula group compared to the exclusively breastfed group, who may have only been exposed to cow proteins through their mom’s breast milk (if their mothers consumed dairy). Furthermore, the bovine antibodies cross-reacted with human insulin, potentially being that caught-in-the-crossfire cause triggering at least some cases of type 1 diabetes.

Of course, we can’t know for sure until we put it to the test. Researchers ran another randomized, double-blind trial, but, this time, tried a cow’s milk formula from which the bovine insulin had been removed. And, indeed, without the bovine insulin exposure, the children built up significantly fewer autoimmune antibodies. What we don’t know yet is whether this will translate into fewer cases of diabetes.


You may also want to check out:

For more on the concerns with cow’s milk exposure in infancy and childhood, see:

I’ve developed a six-part series on the role of gluten-free, casein-free diets in the treatment of autism:

What’s The Best Baby Formula? Breast milk!

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: