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Blocked Arteries

In 4,007 people followed for three years, those with the most of one gut bacterial compound in their blood went on to have the most heart attacks and strokes.

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Microbiome basics

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What is the microbiome?

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The tiny world inside you

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What your gut microbes eat

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How Gut Bacteria Help Build Arterial Plaque


There is strong and repeatedly confirmed evidence that gut bacteria take part in this process. Arteries narrow because fatty deposits called plaque build up inside their walls. That much has been understood for decades. What has emerged more recently is that certain foods only raise risk after gut bacteria have worked on them first. The same meal, eaten by two people, produces different amounts of a harmful compound depending on which bacteria are doing the digesting. Most advice about blocked arteries focuses on cholesterol and saturated fat. This is a separate pathway, running alongside those.


A compound your bacteria build out of your food


Some nutrients contain a chemical structure called trimethylamine. Choline, found in eggs and meat, contains one. So does L-carnitine, which is abundant in red meat.


The body cannot break these structures down on its own. Gut bacteria can. When they do, they release trimethylamine, which travels to the liver and is converted there into trimethylamine N-oxide, usually shortened to TMAO. TMAO is a compound that promotes fatty deposits in artery walls.


Researchers fed L-carnitine to people and measured what happened. Those eating a normal omnivorous diet produced substantially more TMAO than vegans and vegetarians given the same dose. The difference came from the bacteria, not the dose. Long-term diet had shaped which bacteria were present, and those bacteria determined how much of the compound got made.


In mice, feeding L-carnitine accelerated the build-up of plaque, and it only did so when gut bacteria were intact.



Source: Intestinal microbiota metabolism of l-carnitine, a nutrient in red meat, promotes atherosclerosis

What that compound predicts in large numbers


A mechanism in mice is one thing. The question is whether the compound predicts anything in people.


Researchers measured TMAO in 4,007 adults undergoing heart investigations and followed them for three years. Higher levels predicted more heart attacks, strokes and deaths. The link held after adjusting for age, blood pressure, diabetes, cholesterol, smoking, kidney function and how extensive their existing artery disease already was.


That result has since been tested repeatedly. A review pooled 30 prospective studies covering 48,968 people and found raised TMAO associated with both major cardiovascular events and death overall.


One honest caveat belongs here. TMAO may partly be a marker of a diet and a bacterial community that carry risk, rather than the sole cause of the damage. The mouse work argues for a direct role. The human work cannot separate the two completely.



Source: Intestinal microbial metabolism of phosphatidylcholine and cardiovascular risk
Source: Gut microbiota metabolites and risk of major adverse cardiovascular events and death: A systematic review and meta-analysis

Why the vegetarian result is the useful part


Of everything above, one finding points most directly at what a person can do.


The vegans and vegetarians in that carnitine experiment were not protected because they avoided the nutrient on the day of the test. They were given it deliberately. They were protected because years of eating differently had left them with a bacterial community less capable of making the compound in the first place.


That reframes the problem. It is not only about which foods reach the gut on any given day. It is about which bacteria are waiting there, and that population is built slowly through what a person eats over months and years.


Plant-rich eating patterns shift that population, which is one plausible reason they are consistently associated with lower cardiovascular risk.


What this means for you


The chain here is unusually complete. Certain nutrients are converted by gut bacteria into a compound that drives fatty deposits in artery walls. That compound predicts heart attacks and strokes across tens of thousands of people. How much of it a person makes depends on a bacterial community shaped by long-term diet. Chest pain, breathlessness on exertion or pain in the legs when walking need urgent medical assessment rather than dietary experiments. Alongside that, the reason to build meals around plants here is specific rather than general, since the people who made least of this compound were those whose long-term eating had reshaped which bacteria were present. Pulses, whole grains, vegetables, nuts and fruit each feed different parts of that community. That is the idea behind GutLab, where everyday gut health starts with regularly feeding the microbiome, the community of microbes living in the gut, a broad range of plant-rich ingredients.

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Educational information only

The information on this website is for educational purposes only and is not medical advice. Always consult a qualified health professional for personalised guidance.

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