Trimethyl-amine N-oxide.

A dietary metabolite linked to red meat.

TMAO is a gut microbiota generated metabolite associated with atherosclerosis, stroke, myocardial infarction and cardiovascular death.

High plasma TMAO is associated with cardiovascular disease that is  dose  dependent.

Associated with a more than 60% increased risk of major adverse cardiovascular events and death from causes and people with elevated TMAO levels.

Higher levels are associated with heart failure and chronic renal disease.

TMAO is made from food with choline and L-carnitine, nutrients that are abundant in, poultry, fish, diary and egg is generated by gut microbiota dependent formation of trimethylamine from phosphatidyl choline,the major dietary source of choline.

There is a strong correlation between dietary intake of choline as phosphatidylcholine and cardiovascular disease risk.

Choline consumption is common with over the counter choline containing supplements and multivitamins frequently used to promote brain and heart health or prevent liver damage.

Choline supplementation is often advised during pregnancy to aid fetal neural development.

Foods with high choline content like eggs are regularly consumed in the western diet.

Choline contains a trimethylamine moiety and is a  precursor to TMAO.

Choline  supplementation in animal studies increases circulating TMAO levels and in vivo thrombosis potential, and that interventions blocking microbial production of TMAO attenuated platelet hyperactivity and thrombosis potential in vivo.

There is a strong association between dietary intake of choline has phosphatidylcholine and cardiovascular disease risk.

Enzymes produce TMAO from trimethylamine that is formed when intestinal bacteria breakdown these nutrients.

Red meat is high in L-carnitine and raises TMAO in some individuals substantially more than white meat or non-meat protein consumption.

Plasma levels of TMAO are increased in omnivores compared with vegan/vegetarians and trimethylamine and TMAO generation from oral carnitine is observed to be substantially reduced with the vegetarian diet.

Red meat also shifts the gut microbiome, allowing more bacteria to complete the task breaking down trimethylamine.

Red meat reduces the kidney’s ability to excrete TMAO into the urine.

Individuals with high levels of both L-carnitine and TMAO are more likely to have cardiovascular disease and the future risk of cardiovascular events.

Demonstrates a relationship among food, bacterial metabolism and human metabolism.

It is atherogenic, prothrombotic, and inflammatory.

It creates and alters arterial plaques and increases blood clots, likely reduces cholesterol clearance, increases cholesterol laden foamy cells and pro inflammatory cytokines, and enhances platelet reactivity.

Red meat consumption increases the plasma TMAO level substantially in some individuals more than white meat or non-meat protein consumption.

Red meat decreases the kidneys ability to excrete TMA into the urine.

Circulating levels of TMAO are associated with atherosclerosis development and major adverse cardiovascular events like myocardial infarction, stroke, and death.

TMAO production requires interactions between the environmental exposures, such as dietary intake, the gut microbiome dependent generation of trimethylamine and the conversion of trimethylamine to TMAO by host hepatic flavin monooxygenases.

TMAO generation has been linked to pro atherosclerotic and pro thrombotic effects, and alterations in platelet responsiveness and calcium signaling.

Plant-based meat reduces TMAO levels compared with animal meat.


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