This test is most useful if any of these apply to you.
Faecalibacterium is often less abundant in people with inflammatory bowel disease. That is a repeated finding in gut microbiome research, but it hasn't yet become a reliable way to diagnose a flare or choose treatment. Your stool result provides an exploratory view of this group of bacteria.
There are no validated healthy or optimal cutpoints for the genus, and trials haven't established that choosing treatment to raise this result improves health. Diet, illness, medications and measurement differences can all affect the number. A low result alone doesn't establish that your gut is inflamed.
Faecalibacterium is a genus of gut bacteria. A genus contains closely related species. This stool result estimates the abundance of the genus from bacterial DNA. Much of the older research used the name Faecalibacterium prausnitzii for bacteria that newer methods now separate into several species. Findings about a particular species or strain therefore don't translate directly into findings about the total genus.
That distinction matters in practice. A study of Japanese adults found that other Faecalibacterium species were more abundant than F. prausnitzii. Two people with similar genus totals can have different mixtures of species.
These bacteria grow in the low-oxygen environment of the colon. They use fermentable carbohydrates and products supplied by neighboring bacteria, including acetate, to make butyrate. Butyrate is a short-chain fatty acid that colon-lining cells use for fuel. It also helps regulate the gut barrier and immune activity.
Researchers have identified a protein from bacteria historically classified as F. prausnitzii that reduced inflammatory signaling in cultured cells and protected mice against experimentally induced colitis. Those experiments help explain the interest in these bacteria, but a stool DNA result doesn't measure the protein or establish that these effects are occurring in your gut.
Studies following infants found that Faecalibacterium became more common during late infancy. Babies with older siblings acquired it earlier, although that difference was no longer apparent in toddlerhood.
Experimental research suggests that intestinal inflammation changes the colon's oxygen and chemical environment in ways that can disadvantage oxygen-sensitive bacteria. Losing bacteria that produce butyrate may also affect the gut lining and immune responses. These mechanisms support a possible two-way relationship.
Most human studies compare people with and without disease at one point in time. They can show that lower abundance accompanies inflammation, but usually can't establish which came first. Treatment, diet and changes in bowel habits can also contribute to the differences.
The most consistent disease associations concern inflammatory bowel disease, which includes Crohn's disease and ulcerative colitis. Stool studies repeatedly find less F. prausnitzii in affected groups. In one ulcerative colitis study, lower abundance was associated with more active disease. These are species-level findings, although studies of the broader genus also commonly report depletion.
A study distinguishing several Faecalibacterium species found F. prausnitzii more often in people whose Crohn's disease was in remission than in those having a flare. Reduced abundance can also persist during remission, so the result doesn't reliably separate active from inactive disease.
Some research has linked lower F. prausnitzii to recurrence after Crohn's surgery. An early study measured bacteria on surgically removed intestinal tissue. That is a different specimen from stool, and its findings cannot be applied directly to this genus result.
Treatment-response research is promising but inconsistent. An analysis of a Crohn's drug trial associated higher baseline stool Faecalibacterium with remission after ustekinumab. In a separate analysis of 287 people with ulcerative colitis receiving infliximab or etrolizumab, associations differed by bacterial species and treatment. Some Faecalibacterium species were more abundant in people who reached remission, while F. prausnitzii was more abundant in infliximab nonresponders. These studies haven't validated a standalone genus result for selecting a drug or predicting your response.
A Finnish study followed 6,372 adults for a median of nearly 20 years and recorded 240 cases of sepsis. Sepsis is a life-threatening response to infection that damages organs. Higher baseline stool abundance of an F. prausnitzii subgroup was associated with lower subsequent sepsis risk after adjustment for established risk factors.
The estimate was about a fifth lower risk for each step up in abundance on the study's own statistical scale. That comparison doesn't define a target percentage for a stool report. It also concerns a species subgroup rather than the total genus.
A Dutch cohort measured the genus and found an association in the same direction, but the result was statistically inconclusive. Adding microbiome information did not improve sepsis prediction beyond the clinical factors in the Finnish analysis. Neither cohort tested whether increasing these bacteria prevents infection.
Across eight European studies pooling 7,415 adults, higher BMI was associated with less stool Faecalibacterium after accounting for age and sex. A systematic review also found that Faecalibacterium and F. prausnitzii were commonly less abundant in people with type 2 diabetes. These associations don't establish that low abundance causes weight gain or diabetes.
In a study of 371 people, stool F. prausnitzii was less abundant in groups with coronary artery disease than in healthy controls. The same paper investigated possible protective effects in mice; those treatment experiments don't establish a benefit in people.
Among 59 people with an ischemic stroke, higher stool Faecalibacterium was associated with less severe stroke symptoms and better function three months later. The samples were collected after the stroke, so the finding cannot show that the bacteria prevented injury. These studies haven't established a role for this result in choosing cardiovascular or diabetes treatment.
Faecalibacterium appears in research on bacterial signatures of colorectal cancer, but a genus result alone is not a validated cancer screen. Some studies find lower abundance, while others identify associations involving particular species or strains.
A study involving 903 people examined ratios of Fusobacterium nucleatum to F. prausnitzii and Bifidobacterium. The combined ratios showed promising accuracy, including for early-stage cancer, but also flagged some people without cancer. Those results describe a combined research classifier, not this test.
A pooled analysis of 3,741 stool samples from 18 cohorts found particular genetic subgroups of F. prausnitzii associated with late-stage colorectal cancer. A genus total cannot distinguish those subgroups. Neither a high nor a low result can rule cancer in or out.
In a study of 90 young adults, major depression was associated with lower stool Faecalibacterium. A meta-analysis found depletion of this genus across several psychiatric disorders, including depression, bipolar disorder, psychosis and anxiety. Its occurrence across different conditions limits its usefulness for identifying any one of them.
Another population study associated Faecalibacterium with better reported quality of life. Research in ME/CFS found less F. prausnitzii, reduced capacity for butyrate production and an association between lower species abundance and worse fatigue. These findings concern associations, and the ME/CFS result is species-specific. They don't establish this test as a way to explain your symptoms or choose mental health or fatigue treatment.
Some studies have found higher stool Faecalibacterium in illness, including a pediatric COVID-19 cohort and a study of severe gum disease. These observations don't establish that the bacteria caused the illness or that the increase was a protective response.
An analysis of a trial involving 100 stem cell transplant recipients assigned to fecal microbiota transplantation or placebo associated expansion of Faecalibacterium with subsequent graft-versus-host disease. In this condition, donor immune cells attack the recipient's tissues. The association arose in a highly disrupted gut environment and does not establish that higher abundance is harmful in healthy adults.
Together with the species-specific findings in cancer and inflammatory bowel disease, these results argue against interpreting every increase as improvement or every decrease as harm.
Longitudinal studies suggest that Faecalibacterium can be comparatively stable within a person. One year-long study reported high repeatability, while a Swedish study found that meaningful changes in the wider gut community also occurred within individuals over time.
That makes repeated measurements potentially useful for exploring change, but stability alone doesn't establish clinical usefulness. There is no validated size of change that identifies improvement or deterioration, and a personal baseline doesn't turn the result into a disease-monitoring test.
Evidence-backed interventions that affect your Faecalibacterium level
Faecalibacterium is best interpreted alongside these tests.
Faecalibacterium 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.