How to Reduce Your TMAO Levels

Should we be concerned about high-choline plant foods such as broccoli producing the same toxic TMAO that results from eating high-choline animal foods such as eggs?

Choline- and carnitine-rich foods—meat, eggs, and dairy—can be converted by our gut flora into trimethylamine, which in our livers is then turned into TMAO, a toxic compound that may increase our risk of heart failure, kidney failure, and atherosclerosis, or heart attacks and strokes. The good news, though, is that this “opens up exciting new nutritional and interventional prospects” for prevention, as I discuss this in my video How to Reduce Your TMAO Levels.

Okay, so how do we do it? Well, if our gut bacteria can take meat, dairy, and eggs and turn them into TMAO, all we have to do is…destroy our gut flora! We could give people antibiotics to eliminate the production of TMAO. However, that could also kill our good bacteria and “facilitate the emergence of antibiotic-resistant bacterial strains.”

What about probiotic supplements? Maybe if we add good bacteria, they will crowd out the ones that take the meat, egg, and dairy compounds and turn them into the TMA that our liver turns into TMAO. But, that doesn’t work. Adding good bacteria doesn’t seem to get rid of the bad. What if we added new bacteria that could somehow siphon off the TMA made by the bad bacteria? Well, there’s a bacterium inside the guts of cows and sheep that turns trimethylamine into methane. Could we use that bacterium to get rid of some of the trimethylamine from our gut, like a cow fecal transplant? There’s a problem with that. If it didn’t take, you’d have to keep giving it to people: “Continuous administrations may be necessary if subjects do not become colonized.” So, might the fact that Consumer Reports found fecal contamination in every sample of beef it tested be a good thing? No. Methane-producing bacteria may be able to eat up our TMAO, but, unfortunately, these bacteria may be associated with a variety of diseases, from gum disease down to colorectal cancer, as you can see at 2:15 in my video.

If antibiotics and probiotics aren’t going to work to prevent gut bacteria from taking meat, dairy, and eggs and turning them into the trimethylamine, which our liver makes TMAO out of, I guess we have no choice but to cut down on…our liver function!

That was the billion-dollar answer to cholesterol. The same foods—meat, dairy, and eggs—raise our cholesterol, but dietary change isn’t very profitable. So, the drug industry developed statin drugs that cripple the liver’s enzyme that makes cholesterol. Could “pharmacologic inhibition” of the enzymes in our liver that make TMAO “potentially serve as a therapy for CVD [cardiovascular disease] risk reduction”? Trimethylaminuria is a genetic condition in which this enzyme is naturally impaired, in which there is a build-up of trimethylamine in the bloodstream. The problem is that trimethylamine is so stinky it makes you smell like “dead fish.” So, “given the known adverse effects…from sufferers of fish odor syndrome, the untoward odorous side effects of inhibiting this enzyme make it a less attractive [drug] target.”

Do we have to choose between smelling like dead fish or suffering from heart and kidney disease? If only there were some other way we could stop this process from happening. Well, what do those with trimethylaminuria often do to cut down trimethylamine levels? They stop eating animal products.

About a third of those who complain of bad body odor despite good personal hygiene test positive for the condition, but reducing or eliminating meat, egg, and dairy intake can be a real lifesaver. But, given what we now know about how toxic the end product TMAO can be for normal people, cutting down on animal products may not just save the social lives of people with a rare genetic disorder, but help save everyone else’s actual lives.

The “simplest point of intervention” is to simply limit the consumption of foods rich in choline and L-carnitine, which “can be an effective strategy to limit circulating TMAO.” But, wait! We could always try to genetically engineer a bacterium that eats up trimethylamine, but “the simplest and safest recommendation” may just be to eat more healthfully. You can completely eliminate carnitine from the diet, since our body makes all we need, but choline is an essential nutrient so we do need some. Thankfully, we can get all we need in fruits, vegetables, beans, and nuts. “However excess choline, such as that found in eggs, may be worth avoiding.”

Need we worry about high-choline plant foods, like broccoli? Consumption of cruciferous vegetables is associated with a significantly longer life and less cardiovascular disease mortality, as you can see at 5:34 in my video. To see what was going on, researchers took the vegetable highest in choline, brussels sprouts, and had people eat two cups a day for three weeks. What happened? Their TMAO levels actually went down. It turns out that brussels sprouts appear to naturally downregulate that TMAO liver enzyme—not enough to make you stinky, but just enough to drop TMAO.

And, people who eat completely plant-based may not make any TMAO at all—even if you try. You can give a vegan a steak, which contains both choline and carnitine, and there will not even be a bump in TMAO because vegetarians and vegans have different gut microbial communities. If we don’t eat steak, then we don’t foster the growth of steak-eating bacteria in our gut. So forget the cow—how about getting a fecal transplant from a vegan? From a TMAO standpoint, we may not have to eat like a vegan as long as we poop like one.


Can you sense my frustration as I read paper after paper proposing those ridiculous (but profitable!) answers when the safe, simple, side-effect-free solution was staring them in the face the whole time? It makes me think of so many parallels, not the least of which are:

For more on TMAO, the “smoking gun” of diet-microbiome-disease interactions, 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:

Cancer Risk from Arsenic in Rice and Seaweed

A daily half-cup of cooked rice may carry a hundred times the acceptable cancer risk of arsenic. What about seaweed from the coast of Maine?

“At one point during the reign of King Cotton, farmers in the south central United States controlled boll weevils with arsenic-based pesticides, and residual arsenic still contaminates the soil.” Different plants have different reactions to arsenic exposure. Tomatoes, for example, don’t seem to accumulate much arsenic, but rice plants are really good at sucking it out of the ground—so much so that rice can be used for “arsenic phytoremediation,” meaning you can plant rice on contaminated land as a way to clear arsenic from the soil. Of course, you’re then supposed to throw the rice—and the arsenic—away. But in the South, where 80 percent of U.S. rice is grown, we instead feed it to people.

As you can see at 0:52 in my video Cancer Risk from Arsenic in Rice and Seaweed, national surveys have shown that most arsenic exposure has been measured coming from the meat in our diet, rather than from grains, with most from fish and other seafood. Well, given that seafood is contributing 90 percent of our arsenic exposure from food, why are we even talking about the 4 percent from rice?

The arsenic compounds in seafood are mainly organic—used here as a chemistry term having nothing to do with pesticides. Because of the way our body can deal with organic arsenic compounds, “they have historically been viewed as harmless.” Recently, there have been some questions about that assumption, but there’s no question about the toxicity of inorganic arsenic, which you get more of from rice.

As you can see at 1:43 in my video, rice contains more of the toxic inorganic arsenic than does seafood, with one exception: Hijiki, an edible seaweed, is a hundred times more contaminated than rice, leading some researchers to refer to it as the “so-called edible hijiki seaweed.” Governments have started to agree. In 2001, the Canadian government advised the public not to eat hijiki, followed by the United Kingdom, the European Commission, Australia, and New Zealand. The Hong Kong Centre for Food Safety advised the public not to eat hijiki and banned imports and sales of it. Japan, where there is actually a hijiki industry, just advised moderation.

What about seaweed from the coast of Maine—domestic, commercially harvested seaweed from New England? Thankfully, only one type, a type of kelp, had significant levels of arsenic. But, it would take more than a teaspoon to exceed the provisional daily limit for arsenic, and, at that point, you’d be exceeding the upper daily limit for iodine by about 3,000 percent, which is ten times more than reported in a life-threatening case report attributed to a kelp supplement.

I recommend avoiding hijiki due to its excess arsenic content and avoiding kelp due to its excess iodine content, but all other seaweeds should be fine, as long as you don’t eat them with too much rice.

In the report mentioned earlier where we learned that rice has more of the toxic inorganic arsenic than fish, we can see that there are 88.7 micrograms of inorganic arsenic per kilogram of raw white rice. What does that mean? That’s only 88.7 parts per billion, which is like 88.7 drops of arsenic in an Olympic-size swimming pool of rice. How much cancer risk are we talking about? To put it into context, the “usual level of acceptable risk for carcinogens” is one extra cancer case per million. That’s how we typically regulate cancer-causing substances. If a chemical company wants to release a new chemical, we want them to show that it doesn’t cause more than one in a million excess cancer cases.

The problem with arsenic in rice is that the excess cancer risk associated with eating just about a half cup of cooked rice a day could be closer to one in ten thousand, not one in a million, as you can see at 4:07 in my video. That’s a hundred times the acceptable cancer risk. The FDA has calculated that one serving a day of the most common rice, long grain white, would cause not 1 in a million extra cancer cases, but 136 in a million.

And that’s just the cancer effects of arsenic. What about all the non-cancer effects? The FDA acknowledges that, in addition to cancer, the toxic arsenic found in rice “has been associated with many non-cancer effects, including ischemic heart disease, diabetes, skin lesions, renal [kidney] disease, hypertension, and stroke.” Why, then, did the FDA only calculate the cancer risks of arsenic? “Assessing all the risks associated with inorganic arsenic would take considerable time and resources and would delay taking any needed action to protect public health” from the risks of rice.

“Although physicians can help patients reduce their dietary arsenic exposure, regulatory agencies, food producers, and legislative bodies have the most important roles” in terms of public health-scale changes. “Arsenic content in U.S.-grown rice has been relatively constant throughout the last 30 years,” which is a bad thing.

“Where grain arsenic concentration is elevated due to ongoing contamination, the ideal scenario is to stop the contamination at the source.” Some toxic arsenic in foods is from natural contamination of the land, but soil contamination has also come from the dumping of arsenic-containing pesticides, as well as the use of arsenic-based drugs in poultry production and then the spreading of arsenic-laced chicken manure on the land. Regardless of why south central U.S. rice paddies are so contaminated, we shouldn’t be growing rice in arsenic-contaminated soil.

What does the rice industry have to say for itself? Well, it started a website called ArsenicFacts. Its main argument appears to be that arsenic is everywhere, we’re all exposed to it every day, and it’s in most foods. But shouldn’t we try to cut down on the most concentrated sources? Isn’t that like saying look, diesel exhaust is everywhere, so why not suck on a tailpipe? The industry website quotes a nutrition professor saying, “All foods contain arsenic. So, if you eliminate arsenic from your diet, you will decrease your risk…and you’ll die of starvation.” That’s like Philip Morris saying that the only way to completely avoid secondhand smoke is to never breathe—but then you’ll asphyxiate, so you might as well just start smoking yourself. If you can’t avoid it, you might as well consume the most toxic source you can find?!

That’s the same tack the poultry industry took. Arsenic and chicken? “No need to worry” because there’s a little arsenic everywhere. That’s why it’s okay the industry fed chickens arsenic-based drugs for 70 years. If you can’t beat ’em, join ’em.

How can the rice industry get away with selling a product containing a hundred times the acceptable cancer risk? I cover that and so much more in my other videos on arsenic and rice, which also include concrete recommendations on how to mediate your risk.


Check out:

Pesticides were not the only source of arsenic. Poultry poop, too, if you can believe it! I cover that story in Where Does the Arsenic in Chicken Come From? and Where Does the Arsenic in Rice, Mushrooms, and Wine Come From?.

Chronic low-dose arsenic exposure is associated with more than just cancer. See The Effects of Too Much Arsenic in the 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:

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: