This test is most useful if any of these apply to you.
Bacteroidota is often one of the largest bacterial groups on a stool microbiome report. Your result describes its share of the bacterial DNA detected in that sample. It brings together many different organisms, including members of Bacteroides, Prevotella, Alistipes, and Parabacteroides, whose activities and relationships with health can differ.
This is an exploratory biomarker. There is no validated percentage that defines a healthy gut, diagnoses disease, or serves as a treatment target. The result can describe bacterial composition, but using it to choose treatment or improve long-term health has not been established.
A phylum is a broad branch of the bacterial family tree. Bacteroidota is a phylum; Bacteroides is one genus within it. A finding about Bacteroides, an individual species, or a ratio between bacterial groups does not automatically apply to the whole phylum.
Relative abundance describes a share of a total. That share can rise because Bacteroidota increased, because other bacteria decreased, or both. It cannot establish how many living Bacteroidota cells are present. Stool also samples the organisms leaving your intestine, so the result is not a complete inventory of bacteria throughout your digestive tract.
Many gut members of this group can break down complex plant carbohydrates and sugars in intestinal mucus. Studies of proteins produced by healthy adults' stool microbes have documented machinery involved in these processes. Protein measurements describe microbial activity differently from the DNA-based relative abundance reported here.
Their fermentation commonly produces acetate and propionate. These are short-chain fatty acids made when microbes break down carbohydrates. Butyrate is a major fuel for the cells lining your colon and is produced largely by other bacterial groups. Microbes can also use one another's fermentation products, so the amount of one phylum cannot establish how much useful fermentation is occurring.
Their outer membranes contain lipopolysaccharide, but its immune effects depend on its structure. Experiments with bacterial extracts and human immune cells found that forms produced by common gut Bacteroidales often caused little inflammatory stimulation or inhibited particular inflammatory signals. These laboratory findings do not make a stool percentage a measure of inflammation or of bacterial products entering your bloodstream.
Some members also modify bile acids made by your liver. Bile acids help digest fats. Experiments in bacterial cultures and mice show that particular strains can change bile acid composition and influence metabolism. Those findings concern specific organisms and activities; they do not establish a beneficial or harmful effect from a higher phylum percentage in people.
Large human studies find substantial differences in Bacteroidota abundance among people without a diagnosed intestinal disease. Diet, geography, stool transit, medication use, and analytical methods all contribute. An association between a particular percentage and microbial diversity in one cohort does not establish an optimum.
A comparison group can provide descriptive context, especially when its participants resemble you. Being different from that group's average still does not establish a deficiency, an overgrowth disorder, or a need for treatment.
The speed at which stool moves through your colon is associated with microbial composition. In a study of healthy women, looser stools were associated with a higher Bacteroidetes-to-Firmicutes ratio, and Bacteroides abundance increased with looser stool within one community pattern. These were group-level associations, not a rule that explains every high result.
Transit can change the conditions in which bacteria grow. A difference between a constipated week and a week with loose stools may therefore reflect a real change in the community, without showing that your health improved or worsened.
A separate study collected daily samples from healthy volunteers over several weeks. Absolute counts of some bacterial genera varied by as much as 100-fold during that period. That finding concerned counts of individual genera, not 100-fold daily changes in the relative abundance of this whole phylum.
Repeated samples can describe how your stool community varies. Interpretation still requires separating ordinary variation from sustained change and measurement differences. Even a reproducible change has no established direction of benefit for this phylum.
An evaluation of seven commercial microbiome services tested replicate samples from a standardized stool material. It found discrepancies both within and between providers; differences between providers could be comparable to biological differences between stool donors. Keeping the method consistent reduces one source of variation, but does not make every apparent trend meaningful.
Some of the more promising research concerns whole-community patterns. The Bacteroides 2, or Bact2, enterotype combines a high relative abundance of Bacteroides with features such as low bacterial density and depletion of certain butyrate-producing organisms. A Bacteroidota percentage alone does not identify this pattern.
In an observational study of active Crohn's disease and ulcerative colitis, participants with Bact2 reached remission roughly twice as often with anti-TNF treatment as with vedolizumab. A model combining microbial and stool features with clinical information predicted treatment outcomes better than clinical information alone. Treatment was not randomized according to the microbial profile, so the study did not prove that choosing a drug using that profile improves outcomes.
Other work examined individual species within Bacteroidales using targeted sequencing. In ulcerative colitis, the combined abundance of several species was inversely associated with the extent and severity of inflammation seen during endoscopy. That was a species-level association, not validation of the full phylum as a disease-activity test.
Research panels combining several bacterial species have also distinguished inflammatory bowel disease from comparison groups. Their performance belongs to those specific panels and study populations. It cannot be transferred to this single percentage.
One case-control study found lower stool Bacteroidota relative abundance in people with colorectal cancer. A separate study of 333 people undergoing colorectal cancer surgery associated greater Prevotella abundance with less subsequent cancer progression. The latter finding concerned a genus within the phylum and prognosis after diagnosis.
Researchers have also built models combining multiple bacteria to distinguish people with colorectal lesions in stool-blood-testing cohorts. These are different measurements from Bacteroidota abundance. The phylum percentage has no established role as a substitute for colorectal cancer screening.
An early study of biopsy-confirmed fatty liver disease reported less Bacteroidetes in people with steatohepatitis. Its laboratory measurement targeted Bacteroides and Prevotella and expressed their abundance relative to total bacteria. Although the paper called this Bacteroidetes, it was a narrower measurement than a full-phylum profile.
A prospective study followed participants for about 4.6 years and developed models for new fatty liver disease using microbial functions and chemicals measured in stool and blood. Adding clinical information improved prediction. The model's performance cannot be attributed to Bacteroidota abundance alone.
Lower Bacteroidetes abundance has also been reported during acute hepatic encephalopathy in people with cirrhosis. Such findings describe a community change in serious illness; they do not establish that a low result in someone without liver disease predicts that illness.
Early animal experiments and small human studies helped popularize the idea that a high Firmicutes-to-Bacteroidetes ratio explains obesity. Larger comparisons have been inconsistent. A systematic review and meta-analysis of human studies found no statistically significant pooled difference in Bacteroidetes abundance between adults with and without obesity, with substantial variation between studies.
The ratio has not become a reliable individual measure of obesity or gut health. This does not rule out contributions from particular microbes or microbial activities to metabolism. It means that dividing two broad bacterial groups does not provide a dependable explanation for your body weight.
Studies have reported depletion of this group during Clostridioides difficile infection and enrichment in some cohorts with irritable bowel syndrome, osteoarthritis, or Graves' disease. These findings come from different populations, methods, and disease settings. They do not establish a shared direction of risk.
The species underneath the phylum can also move in different directions. A high total might include organisms associated with useful carbohydrate fermentation, organisms associated with illness in a particular setting, or both. The percentage does not measure their activity or establish why symptoms occur.
Prospective studies have linked some microbial patterns with later cardiovascular events and death, but those patterns are not interchangeable with this test. In HELIUS, associations between several individual bacterial features and cardiovascular events weakened after adjustment for other risk factors. In FINRISK, the clearest mortality associations involved Enterobacteriaceae, a different bacterial family, and adding microbiome information did not improve risk discrimination beyond the clinical model.
A Mayo Clinic study followed a small group of people with cardiovascular risk factors for several years. A community cluster with more Bacteroidetes, including Bacteroides, Alistipes, and Parabacteroides, was associated with a lower risk of a combined outcome including cardiac events, heart failure, and death. This association remained after adjustment for several clinical risk factors. It concerned a community cluster, so it does not establish that increasing the phylum itself protects your heart.
In the CORDIOPREV cohort, a score built from ten bacterial groups was associated with recurrent cardiovascular events in people with coronary heart disease. A separate transplant cohort linked a balance of 19 species with all-cause mortality, while other measures of community disruption were associated with cause-specific deaths. These studies support further investigation of defined microbial signatures; they do not validate a general stool phylum percentage or a commercial dysbiosis score.
A genetic study examined possible causal relationships between gut microbes, microbial chemicals, and chronic disease. Its strongest candidate relationships weakened after accounting for body mass index or alcohol intake. That analysis neither established a causal benefit from higher Bacteroidota nor excluded every possible microbial contribution to disease.
In a large colonoscopy study, stool moisture and other clinical features explained substantial microbial variation. A Bact2 pattern was common both in people with lesions and in those whose colonoscopy found no lesions. A pattern described as dysbiotic therefore does not establish that disease is present, or that it will develop later.
Evidence-backed interventions that affect your Bacteroidota level
Bacteroidota is best interpreted alongside these tests.
Bacteroidota is included in these pre-built panels.
See what your gut microbes are actually doing, not just whether your digestion feels off, and track the balance over time.