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:

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:

Moderation Kills

What if we don’t want just low risk for a heart attack, but no risk? One great stumbling block has been that government and national health organizations appear to have taken the patronizing view that the public can’t handle the truth and would rather the science be watered down.

However, as Dr. Esselstyn wrote in the Cleveland Clinic Journal of Medicine, in regard to cholesterol lowering, moderation kills. “Even if all Americans kept their total cholesterol below 200 mg/dL, as recommended by the American Heart Association, millions would develop coronary artery disease.” Strong evidence shows we need to keep our total cholesterol under 150 mg/dL in order to stem the American epidemic of coronary artery disease, our number-one killer. What kind of evidence? In many cultures, coronary artery disease is practically unheard of when total serum cholesterol levels are under 150 mg/dL. In the United States, the famous Framingham Heart Study demonstrated that few of those with levels below 150 mg/dL developed heart disease, and none died from it.

In my video Everything in Moderation? Even Heart Disease? you can see the data from a 26-year follow-up of the Framingham Heart Study comparing the cholesterol levels of people who get heart attacks and the cholesterol levels of those who don’t. The study suggests that because we now know that 35% of heart attacks occur in people with total cholesterol levels of 150-200 mg/dL, a target level of only 200 mg/dL guarantees that millions of U.S. citizens will die from coronary artery disease.

Dr. Esselstyn states, “We cannot continue to have public and private organizations on the forefront of health leadership recommend to the public a dietary plan that guarantees that millions will perish from the very disease the guidelines were supposed to prevent. With its lack of fiber and antioxidants, and its emphasis on animal protein, fat, and extreme free-radical production, the US diet is largely responsible for our bitter harvest of [chronic] diseases….” He continues, “If the coronary artery disease epidemic is seen as a raging fire, and cholesterol and fats as the fuels, the AHA [American Heart Association] has merely recommended cutting the flow of fuel. The only tenable solution is to cut off the fuel supply altogether—by reducing cholesterol levels to those proven to prevent coronary artery disease.”

It’s worth closely examining the Framingham data. At first, it seems those who get heart disease and those who don’t have very similar cholesterol levels, but that’s only at “normal” levels. To get an Optimal Cholesterol Level, one has to eat an exceedingly healthy diet. It’s worth it, though, since we’re not just talking life and death with heart disease, but life and the number-one cause of death.


What’s so bad about having high cholesterol? Well, it’s not only involved in the formation of atherosclerotic plaque, as I discuss in my video, Cholesterol Crystals May Tear Through Our Artery Lining. What about fluffy versus dense cholesterol? I cover that in Does Cholesterol Size Matter?. But can’t you just take cholesterol-lowering statin drugs? I encourage you to see The Actual Benefit of Diet vs. Drugs. When should we start monitoring cholesterol? As it turns out, Heart Disease May Start in the Womb.

For more on this concept of being at normal risk and dying from all the normal diseases, watch my video, When Low Risk Means High Risk. I continue questioning the patronizing paternalism of authorities in Optimal Diet: Just Give It To Me Straight, Doc. Finally, check out my latest heart disease overview, How Not to Die from Heart Disease.

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: