Distinct gut microbiome profiles characterize obese and non-obese patients with atherosclerosis

If you have been told you have atherosclerosis (the buildup of fatty plaque inside artery walls) and you also carry extra weight, a new study suggests your gut bacteria may be telling a different story than a lean patient's with the same diagnosis. Researchers in Kazakhstan sequenced the gut microbiomes of 188 people and found that obesity, not cholesterol or blood sugar, was the single strongest predictor of how those bacterial communities were organized. One bacterium in particular, Prevotella, stood out as behaving almost like its own island within the gut ecosystem of obese atherosclerosis patients.

Key takeaways:

• In a 188-person study, obesity (BMI of 30 or higher) was the strongest predictor of gut microbiome differences among atherosclerosis patients, outperforming cholesterol, blood sugar, and inflammation markers.
• Obese atherosclerosis patients showed a distinct expansion of Prevotella bacteria that consistently moved opposite to the rest of their gut community, alongside lower microbial diversity.
• The findings are associative: this cross-sectional design cannot say whether the bacterial shifts cause worse outcomes or are a downstream effect of obesity and disease.
• If confirmed in larger, longitudinal studies, Prevotella dominance could eventually serve as a marker doctors use to flag higher-risk patients within the obese-atherosclerosis population.

Obesity, Not Cholesterol, Drives Gut Microbiome Differences

The core finding is that among people with atherosclerosis, obesity status (whether a patient's body mass index, or BMI, a measure of weight relative to height, was 30 or above) explained more of the variation in gut bacterial community structure than any other clinical factor measured. Researchers at Nazarbayev University's Heart Center in Astana, led by Issilbayeva and colleagues, used shotgun metagenomic sequencing (a method that reads nearly all the DNA in a stool sample, not just a handful of marker genes) to compare 27 healthy non-obese controls, 93 non-obese atherosclerosis patients, and 68 obese atherosclerosis patients. The study was published in the Journal of Translational Medicine. When the team statistically tested every clinical and demographic variable against the microbiome data, BMI came out on top (a statistical effect size of F = 3.1, a formal way of ranking how strongly a factor separates groups), ahead of sex, cholesterol, and even the presence of atherosclerosis itself as a stand-alone comparison.

Why This Matters for Heart Disease and Obesity Research

Atherosclerosis and obesity frequently occur together, and doctors already know obesity raises cardiovascular risk through blood pressure, cholesterol, and blood sugar. What this study adds is evidence that obesity does not just pile more of the same gut bacteria changes on top of atherosclerosis, it appears to redirect the microbiome down a different path entirely. The gut microbiome has been linked to cardiovascular disease through inflammation and metabolic byproducts for years, but most prior studies lumped obese and lean cardiovascular patients together. This is one of the more direct comparisons showing that body weight itself reorganizes which bacteria dominate, independent of the artery disease. For readers managing both a weight issue and a cardiovascular diagnosis, or researching whether the two are connected through their gut, this offers a more specific piece of the puzzle than "eat better for your heart" advice.

How the Study Was Designed

This was a cross-sectional study (a single snapshot in time, not a study that follows people over months or years) of 188 adults enrolled between March and December 2024. Participants were grouped by both atherosclerosis diagnosis, confirmed through coronary angiography, imaging, and standard cardiology guidelines, and by BMI. The obese and non-obese atherosclerosis groups were closely matched on age and sex, and researchers ran three separate comparisons between the groups specifically to separate the effects of obesity from the effects of atherosclerosis itself, rather than mixing the two together. Fecal DNA was sequenced on an Illumina NovaSeq 6000 with a minimum of 6 gigabases of data per sample, then analyzed with the same statistical bar (95% confidence intervals excluding zero) applied consistently across every comparison. Community composition differed significantly across the three groups overall (PERMANOVA F = 3.23, p = 0.001, a test for whether entire bacterial communities differ, not just individual species).

What the Prevotella Signal Could Mean for You

The standout finding was Prevotella, a gut bacterium already known for fermenting fiber into short-chain fatty acids (a class of molecules gut bacteria produce from fiber that generally support gut and metabolic health). In obese atherosclerosis patients, Prevotella made up roughly 18% of the identifiable microbial genus-level signal, compared to about 13% in non-obese atherosclerosis patients, a statistically significant difference. But abundance alone was not the interesting part. Prevotella was the only bacterium whose behavior moved in the opposite direction from nearly every other major group of gut bacteria the researchers tracked, both in raw composition and in the metabolic pathways those bacteria carry out. The authors describe this pattern as a Prevotella expansion that consistently opposes the rest of the bacterial community, effectively forming its own isolated cluster rather than fitting into the broader ecosystem. Obese atherosclerosis patients also had measurably lower species richness and evenness (two standard measures of microbiome diversity), a pattern generally associated with less resilient gut ecosystems in other conditions. None of this means a stool test showing high Prevotella is a diagnosis of anything on its own. Prevotella is common in people with fiber-rich diets and is not inherently harmful; its relationship to obesity and inflammation appears to depend heavily on context, including diet and which Prevotella strains are present. Anyone curious about their own gut composition should treat a microbiome test result as a data point to discuss with a doctor, not a verdict.

What This Study Cannot Tell Us

The design of this study cannot establish cause and effect. The researchers themselves are explicit that the cross-sectional design does not allow them to say whether Prevotella expansion contributes to worsening atherosclerosis, is a downstream consequence of obesity and disease, or both. The control group was also relatively small at 27 people, which limits how confidently the findings generalize to the broader population. And the obese and non-obese atherosclerosis groups differed in other ways beyond weight, including blood sugar markers (HbA1c), HDL cholesterol, inflammation (CRP), and rates of fatty liver, any of which could be intertwined with the microbiome differences rather than obesity acting alone. The study's functional pathway analysis, which links bacteria to metabolic activity, was also inferred computationally rather than measured directly, so those mechanistic links remain hypotheses rather than confirmed biology.

What Comes Next

The authors call for longitudinal studies, ones that track the same patients over time, to determine whether Prevotella expansion precedes worsening atherosclerosis or follows it, and whether intervening on diet or the microbiome directly can shift that trajectory. They also flag that Prevotella's relationship to fiber intake is complicated: in some prior research, high-fiber diets increased Prevotella activity in ways linked to inflammation, while low-carbohydrate diets have been shown to sharply reduce Prevotella abundance within weeks. That double-edged relationship is a reminder that no specific diet change is established as a fix based on this study alone. Larger studies replicating this obesity-stratified approach, and eventually testing whether a Prevotella-based marker adds anything to existing cardiovascular risk scores, are the logical next step. Broader context on how gut bacteria contribute to atherosclerotic disease and how the gut-heart relationship functions more generally, as reviewed in Nature Communications, can help place this study's findings in the wider research landscape.

Common Questions

Does having more Prevotella in my gut mean I am at risk for heart disease? No. This study found an association between Prevotella expansion and obesity in people who already had atherosclerosis; it did not test whether Prevotella levels predict future heart disease risk in the general population, and Prevotella is common in healthy, fiber-eating people too.

Is this study saying obesity causes different gut bacteria, or the other way around? Neither can be confirmed here. The cross-sectional design captures a single snapshot, so the researchers cannot determine whether obesity changes gut bacteria, altered gut bacteria contribute to weight gain, or both happen together.

Should I change my diet based on this finding? No specific diet is proven by this study. The researchers note that both high-fiber and low-carbohydrate diets can shift Prevotella levels in different directions, and any dietary changes for cardiovascular or weight-related goals should be discussed with a doctor rather than driven by a single study.

References

Argul Issilbayeva, Elizaveta Vinogradova, Laura Chulenbayeva, et al. (2026). Distinct gut microbiome profiles characterize obese and non-obese patients with atherosclerosis: a metagenomic analysis. Journal of Translational Medicine. https://doi.org/10.1186/s12967-026-08739-1