Eating more vegetables appears to improve microbiome-mediated health indicators

There are many diets that have been rigorously shown to decrease metabolic syndrome (obesity, diabetes, etc.) and are generally associated with a healthy lifestyle, such as vegetarian, vegan, and Mediterranean diets.  The one thing they share in common is a high consumption of plant material, and a low consumption of meat.  There are mechanistic reasons for why high veggie - low fat diets should improve health, and many researchers now believe this is partly due to the gut microbiome that these diets create.  In order to help demonstrate the microbiome-mediated health benefits of a high vegetable – low meat diet, a team of researchers from Italy recently measured the microbiome and specific metabolites produced by the microbiome in 153 individuals.  They then compared these results with the diet that the individual had consumed prior to the measurements, and confirmed that these ‘healthy’ diets were creating ‘healthy’ microbiomes.  They published their results in the journal Gut.

The scientists asked 51 vegans, 51 vegetarians, and 51 ominivores individuals to self-declare their eating habits over the past seven days, and then sampled their stool and urine for bacteria and metabolites.  They learned that amongst the different types of diet the individuals’ overall microbiome diversities were relatively similar.  However, they did show that Bacteroidetes were more prevalent in vegetarians and vegans than in ominvores, and that a higher Firmicutes to Bacteroidetes ratio existed in the guts of ominvores than in vegans and vegetarians.  In addition, the abundance of Prevotella, which is normally associated with health, was positively correlated with overall vegetable intake, and on the contrary Ruminococcus was negatively associated with a high vegetable diet.

The scientists also measured specific metabolites in the individuals.  They discovered that short chained fatty acids (SCFAs), which are normally implicated with health, were associated with the consumption of fruits, vegetables, and legumes.  In addition, there were positive associations between SCFAs and specific populations of bacteria, such as Prevotella.  On the other hand, the metabolite trimethylamine oxide (TMAO), which is a microbiome metabolite whose concentration is directly related to atherosclerosis and other diseases, was significantly lower in vegetarian and vegan diets compared to omnivore diets. It was also directly associated with the abundance of the aforementioned Ruminococcus

These relationships between SCFAs and veggies are unsurprising, because SCFAs are the byproducts of bacteria breaking down the complex glycans found in fiber.  In addition, the TMAO is produced by gut bacteria from carnitine and choline, two molecules that exist in red meat and eggs, among other things.  Regardless though, this study should remind us that our diet can shape our microbiome and have lasting health effects.  This study only reinforces that a diet high in veggies that feeds the microbiome is probably a healthy choice.

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The views expressed in the blog are solely those of the author of the blog and not necessarily the American Microbiome Institute or any of our scientists, sponsors, donors, or affiliates.

Red meat, atherosclerosis, and the microbiome

Atherosclerosis is a disease in which plaque accumulates in your blood vessels.  This can lead to heart attack, stroke, and sometimes death.  One of the major risk factors for atherosclerosis is high levels of a molecule called trimethylamine-N-oxide (TMAO).  TMAO is known to interfere with how the body handles cholesterol, and has long been associated with heart disease.  Researchers from the Cleveland Clinic recently published their discovery of the main pathway by which TMAO is formed in the body.  In the article they describe how TMAO is formed after the microbiome breaks down a molecule found in red meat, which is then converted by the liver to TMAO

Red meat is rich in a molecule called L-carnitine.  The researchers fed this molecule to germ free mice, mice on antibiotics, and control mice and discovered that those with a healthy microbiome produced high levels of TMAO.  They proved a new pathway for this conversion, via an intermediate molecule called γ-Butyrobetaine, by detecting genes for its production.  They then proved that γ-Butyrobetaine alone could be converted to trymethyl-amine (TMA) by the microbiome. (TMA is the precursor to TMAO before being acted on by the liver.)  Next, they discovered that a diet consisting of L-carnitine or γ-Butyrobetaine shifted the microbiome to be enriched in bacteria that could efficiently break them down to convert them to TMAO.  Finally, they gave two groups of mice a diet high in γ-Butyrobetaine to demonstrate the microbiome’s importance in atherosclerosis. One group of mice was given antibiotics to disrupt their microbiomes and the other was not.  The group given the antibiotics had less levels of TMAO and less symptoms of atherosclerosis, including plaque build-up, than those mice that had the normal gut microbiome capable of converting γ-Butyrobetaine to TMA.

This paper provides a definitive link between the actions of the microbiome and atherosclerosis.  Interestingly, some people that eat diets high L-carnitine do not produce high levels of TMAO, and are thus at less risk for atherosclerosis.  The paper hypothesizes that these people do not have the bacteria capable of converting L-carnitine to TMA.  The paper also discusses how γ-Butyrobetaine, which is now shown to be a major precursor source of TMAO, can be purchased at nutrition stores as a dietary supplement to help in building muscle.  These supplements are not regulated by the FDA, and no long term studies have been performed on γ-Butyrobetaine as a supplement to humans.  Anyone taking it should be warned that they may be at a much higher risk for heart disease.  There are clearly dangers in taking unregulated supplements, and we encourage all of our readers to be prudent with what they put in their bodies.

Please email blog@MicrobiomeInstitute.org for any comments, news, or ideas for new blog posts.

The views expressed in the blog are solely those of the author of the blog and not necessarily the American Microbiome Institute or any of our scientists, sponsors, donors, or affiliates.