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TMAO (Trimethylamine N-oxide) is one of the few blood tests that connects what you eat to what your gut bacteria do to how your heart fares over time. When you eat foods rich in certain nutrients, bacteria in your intestine produce a chemical that eventually reaches your bloodstream. Your TMAO level reflects how much of that chemical is circulating, and higher levels are consistently linked to a greater risk of heart attack, stroke, and death from cardiovascular disease.
What makes this test distinctive is that it does not measure something your own cells produce. It measures the output of your gut microbiome, the trillions of bacteria living in your digestive tract. That makes it a window into a biological conversation between your diet, your microbes, and your cardiovascular system.
A large umbrella review and meta-analysis found highly suggestive evidence linking TMAO to all-cause mortality, cardiovascular mortality, major adverse cardiovascular events, hypertension, diabetes, and declining kidney filtration. These are not marginal associations. They span multiple populations and clinical settings, from apparently healthy adults to people already living with heart failure, diabetes, or peripheral artery disease.
The process starts with what you eat. Certain nutrients found mainly in animal products, including choline, a B-vitamin relative found in eggs and meat, L-carnitine, abundant in red meat, and a fat molecule called phosphatidylcholine, serve as raw material for your gut bacteria.
Bacteria in your intestine convert these nutrients into a pungent gas called trimethylamine, or TMA. TMA is absorbed into your bloodstream, travels to the liver, and is rapidly converted into TMAO by a liver enzyme. TMAO then circulates in your blood until your kidneys filter it out.
This is why both your diet and your kidney function matter so much for interpreting your result. If you eat a lot of red meat, your gut bacteria produce more TMA. If your kidneys are not clearing TMAO efficiently, it accumulates regardless of what you eat.
TMAO promotes cardiovascular disease through several mechanisms. It encourages immune cells called macrophages to take up cholesterol and form fatty deposits in artery walls, a key step in atherosclerosis. It interferes with your body's ability to move cholesterol back out of arteries, a cleanup process called reverse cholesterol transport. It also makes blood platelets stickier and more prone to forming clots, which is how heart attacks and strokes actually happen.
In one of the largest studies to date, involving a diverse group of American adults in the Multi-Ethnic Study of Atherosclerosis, TMAO showed a dose-dependent relationship with cardiovascular events. Compared to those with the lowest levels, people in the highest fifth of TMAO had about a 33% greater risk of developing cardiovascular disease (HR 1.33). The risk climbed steadily across each tier.
A level above roughly 6 micromoles per liter, which corresponds to the third or fourth quartile in most study populations, is associated with the highest risk of adverse cardiac events. If your level is above this threshold, it suggests your body is producing more TMAO than average, either because of your diet, your gut bacteria, reduced kidney clearance, or some combination.
Long-term tracking adds another layer. In two large cohort studies following health professionals over 10 years, both increases and decreases in TMAO over time were associated with corresponding changes in coronary heart disease risk. This is encouraging because it suggests that lowering your level may translate into lower risk.
Before interpreting your number, you need to know one critical confounder: kidney function. Your kidneys are the primary route for clearing TMAO, and impaired kidney function can elevate your level independently of diet or gut bacteria. In a study of community-dwelling older adults, the link between TMAO and cardiovascular events appeared to be mediated or confounded by kidney filtration rate. High TMAO predicted cardiovascular events primarily in those with impaired kidney function. If your kidney function is reduced, a high TMAO level may partly reflect poor clearance rather than excess production.
Fish presents another interpretive puzzle. Fish and shellfish are significant dietary sources of TMAO, and fish consumption is generally considered heart-protective. In Asian populations, where seafood intake is high, TMAO levels tend to be elevated, yet cardiovascular risk may not be increased in the same way. This means a high TMAO level driven primarily by fish intake should not be interpreted the same way as one driven by red meat consumption.
In people with end-stage kidney disease on dialysis, where TMAO levels are often extremely elevated (above 25 to 50 micromoles per liter), the added predictive value of the test appears diminished. When levels are uniformly very high, the test has less ability to distinguish risk.
Because TMAO sits at the intersection of diet and gut microbiology, your choices at the table are the most direct lever you have. No clinical trial has yet shown that reducing TMAO levels improves cardiovascular outcomes, but the observational data linking TMAO changes to coronary heart disease risk over time provide a rationale for trying.
Dietary changes: Reducing or eliminating red meat is the single most effective dietary strategy. In a controlled feeding study of healthy adults, chronic red meat consumption increased plasma TMAO more than two-fold compared to white meat or non-meat diets, and the effect reversed within 4 weeks of stopping red meat. An 8-week vegan diet in adults with blood sugar abnormalities or obesity reduced TMAO from 10.7 micromoles per liter to approximately 6 micromoles per liter, though levels rebounded after returning to an unrestricted diet. Vegans and vegetarians consistently show lower circulating TMAO and reduced capacity to generate the precursor molecule TMA in their stool. Preliminary data also support TMAO-lowering effects from calorie restriction, exercise, and intermittent fasting.
If you are currently eating red meat regularly and your TMAO is elevated, a trial of reduced red meat intake for 4 to 8 weeks, followed by retesting, is a reasonable and low-risk strategy.
Prebiotics and plant compounds: A 2025 meta-analysis of 41 studies found that prebiotic and phytochemical interventions significantly reduced serum TMAO levels in clinical trials, with a moderate effect size (SMD = -0.82). These interventions included dietary fibers, phenolic compounds found in fruits and vegetables, and glucosinolates found in cruciferous vegetables like broccoli and cabbage. They appear to work by shifting gut bacteria toward species that produce less TMA, including increases in beneficial bacteria like Akkermansia and Bifidobacterium.
Probiotics: The evidence here is mixed and depends heavily on the specific bacterial strain used. A systematic review identified Lactobacillus rhamnosus GG as the most effective strain for reducing TMAO in both humans and animals. However, a randomized controlled trial of a multi-strain probiotic in healthy young men did not significantly reduce TMAO after a choline-rich challenge, though a higher proportion of the probiotic group did show TMAO decreases (78.9% vs 45.0%). Another probiotic formulation, VSL#3, failed to reduce TMAO after a high-fat diet. Probiotics are not yet a reliable tool for TMAO reduction.
Pharmacological approaches: The most promising drug candidates are compounds that block the bacterial enzyme responsible for producing TMA in the first place. The prototype compound, called DMB, reduces TMAO and slows atherosclerotic plaque development in animal models without killing the bacteria or altering cholesterol levels. Interestingly, DMB has been identified in cold-pressed extra-virgin olive oil. Next-generation versions of these enzyme inhibitors are highly potent and selectively accumulate in the gut, providing sustained inhibition with minimal absorption into the rest of the body. In preclinical studies, they have reduced platelet clumping, improved blood pressure, enhanced blood sugar control, and decreased plaque burden. These agents are not yet available for clinical use. Some existing cardiovascular medications, including aspirin, may partially blunt TMAO elevation after consuming choline or carnitine, but whether this contributes to their clinical benefits is unknown.