At Coprata, we usually talk about stool. 💩
For Menopause Awareness Month, we are looking slightly beyond the gut, at urinary tract infections, or UTIs. The connection is more direct than it may first appear. The intestine is an important reservoir for bacteria that cause UTIs, and a growing body of research suggests that the composition and metabolic activity of the gut microbiome may influence susceptibility to recurrent infection.
For women going through menopause, this question is particularly relevant. Declining estrogen changes the urinary and vaginal environment at the same time that age, prior antibiotic exposure, and changes in the gut microbiome may alter another important line of defense.
Why UTIs Become Especially Relevant Around Menopause
UTIs are among the most common bacterial infections and disproportionately affect women. Female anatomy plays a central role: bacteria originating in the intestinal and perineal area can more easily reach the urethra and ascend into the bladder.
Menopause adds further complexity. Cells in the urinary and genital tracts carry receptors for sex hormones, particularly estradiol, which helps maintain epithelial integrity and supports local antimicrobial defenses. As estrogen declines during perimenopause and menopause, vaginal and urinary tissues can thin and the local microbial environment shifts. These changes reduce resistance to colonization by potential pathogens, contributing to the increased urinary symptoms and recurrent UTIs commonly seen after menopause.
Many of the bacteria responsible for these infections, however, originate somewhere else entirely: the intestine.
The Gut Is a Reservoir for UTI-Causing Bacteria
Approximately 80 to 90% of community-acquired UTIs are caused by Escherichia coli.
Many of these organisms are classified as uropathogenic E. coli, or UPEC. They can reside within the intestinal microbial community without causing urinary infection. A UTI may begin when these bacteria migrate from the intestinal reservoir to the periurethral area, colonize the urethra, and travel upward into the bladder.
Other organisms can cause UTIs, but E. coli offers a particularly clear illustration of how gut and urinary health may be linked.
Genetic studies support this transmission route. Multiple investigations have recovered near-identical or indistinguishable bacterial isolates from the stool and urine of individual patients with UTIs, pointing to a microbial transmission axis between the gut and bladder.
This raises an important question: why does an organism that can quietly colonize the intestine sometimes become a recurrent urinary pathogen?
It May Not Simply Be About Having E. coli
One tempting hypothesis is that people who develop UTIs simply have more E. coli in their The evidence is more complicated. Some studies report higher E. coli abundance in the gut of people with UTIs, while others find no meaningful difference compared to those without.
This shifts attention away from any single species toward the ecology of the gut microbial community as a whole.
A 2024 narrative review in Nutrients drew on several studies that found evidence of gut dysbiosis) an imbalance in the microbial community (among individuals with UTIs. In one of those studies, women with recurrent UTIs had significantly lower gut microbial richness than controls, along with reductions in bacterial taxa associated with short-chain fatty acid production.
The findings are not entirely consistent across studies, but one pattern emerges repeatedly: microbiomes associated with UTIs tend to have fewer bacteria involved in short-chain fatty acid production.
Short-Chain Fatty Acids May Be an Important Part of the Story
This finding is particularly interesting to us at Coprata because of our MAT test. We have covered short-chain fatty acids, or SCFAs, which are produced when gut bacteria ferment dietary fiber, in prior blogs.
SCFAs shape the intestinal environment in several ways: supporting epithelial barrier integrity, influencing mucus production, regulating immune and inflammatory responses, and reducing conditions favorable to certain pathogens. One key mechanism is acidification of the intestinal environment, which can inhibit pathogen growth and alter bacterial virulence factor expression.
This remains an association, not proof that low SCFA production causes UTIs. Even so, it points to a plausible biological pathway connecting microbial metabolism in the gut with infection elsewhere in the body.
Recurrent UTIs Create an Additional Problem: Antibiotics and the Microbiome
For many women, particularly after menopause, the clinically important problem is not a single UTI but recurrence. Antibiotics are essential for treating bacterial UTIs, but they can also substantially alter the intestinal microbiome and that creates a difficult biological question.
The gut can harbor the organisms that later cause UTIs. But antibiotic exposure reduces microbial diversity and suppresses beneficial commensal organisms, potentially disrupting the ecological environment that ordinarily helps constrain uropathogens.
Notably, antibiotics do not necessarily eliminate the urinary pathogen from its intestinal reservoir. In one study, the bacterial strain causing a woman's UTI frequently matched the organism found on rectal sampling, and treatment did not permanently clear those strains from the gut.
This has led researchers to consider a potential cycle:
intestinal reservoir → UTI → antibiotic treatment → disruption of the gut microbiome → persistence of the intestinal reservoir → recurrent UTI.
It remains a hypothesis, not an established finding. Antibiotic exposure is also a major confounding factor in microbiome research: it is often unclear whether dysbiosis preceded the UTI or resulted from repeated infections and their treatment.
Could Changing the Gut Microbiome Reduce Recurrent UTIs?
If the intestinal microbial community contributes to UTI susceptibility, modifying that community becomes a compelling therapeutic possibility. One unexpected source of evidence comes from fecal microbiota transplantation (FMT). FMT is not an established treatment for UTIs it is primarily used for recurrent Clostridioides difficile infection. But several observations suggest that altering the intestinal microbial ecosystem can influence urinary infections.
Patients receiving FMT for recurrent C. difficile have been reported to experience fewer subsequent UTIs. A case report described reduced UTI frequency following FMT in a patient with intestinal dysbiosis, and a small cohort of five patients with multidrug-resistant UTIs showed reduced UTI incidence after FMT.
These studies are small and cannot establish efficacy, but they raise an important biological question: changing the gut's microbial composition appears capable, at least in some cases, of influencing urinary tract infections.
Probiotics are another active area of investigation. A randomized controlled trial of 174 premenopausal women with recurrent UTIs found fewer infections with vaginal probiotics, used alone or combined with oral probiotics. Oral probiotics alone showed no significant benefit over placebo. The broader evidence is similarly mixed; a systematic review found that only two of nine studies concluded that probiotics reduced UTI risk, with considerable variation in the probiotics and regimens studied.
Microbiome-directed prevention is an appealing concept, but no specific probiotic or microbiome intervention can yet be confidently recommended as a universal strategy for preventing recurrent UTIs.
An Emerging Gut-Bladder Axis
The gut-bladder axis remains an emerging area of research.
The strongest evidence points to a relatively direct connection: the gut serves as a key reservoir for organisms that cause UTIs. The more unsettled question is whether the surrounding microbial environment determines how effectively those organisms are kept in check. The available literature identifies several characteristics that recur in people with UTIs:
- lower microbial richness in some cohorts
- depletion of particular commensal organisms
- reduced abundance of SCFA-producing bacteria
- persistence of uropathogenic strains in the intestine despite antibiotic treatment
- in some populations, greater intestinal abundance of organisms that subsequently cause urinary infection
Back to the Gut
Menopause, UTIs, and the gut microbiome can seem like unrelated topics. The evidence suggests otherwise.
Declining estrogen weakens local defenses in the urinary and vaginal tract. The intestine serves as a reservoir for many of the bacteria that cause UTIs. The ecological conditions within that reservoir (particularly microbial diversity and SCFA-producing bacterial activity) may influence whether potential pathogens stay contained or contribute to recurrent infection.
There is not yet evidence that optimizing the gut microbiome will prevent UTIs, and recurrent urinary symptoms should always be evaluated and treated by a clinician. What the emerging science does offer is another reason to support the microbial functions already associated with a healthy gut: adequate dietary fiber, a diverse microbial ecosystem, and consistent production of short-chain fatty acids.
At Coprata, we focus on that last piece. SCFA production alters the chemistry of the intestinal environment, including fecal pH and fecal pH is one accessible indicator of microbial function. It is what the MAT kit tracks at home, for information and education rather than diagnosis. We cannot yet say that maintaining high SCFA production will prevent UTIs. But as research on the gut-bladder axis develops, supporting a metabolically active, SCFA-producing gut microbiome looks like a reasonable place to start.
References
- Iqbal ZS, Halkjær SI, Ghathian KSA, Heintz JE, Petersen AM. The Role of the Gut Microbiome in Urinary Tract Infections: A Narrative Review. Nutrients. 2024;16(21):3615.
- New FJ, Theivendrampillai S, Juliebø-Jones P, Somani B. Role of Probiotics for Recurrent UTIs in the Twenty-First Century: a Systematic Review of Literature. Current Urology Reports. 2022;23(2):19-28.
- Jeney SES, Lane F, Oliver A, Whiteson K, Dutta S. Fecal Microbiota Transplantation for the Treatment of Refractory Recurrent Urinary Tract Infection. Obstetrics & Gynecology. 2020;136(4):771-773.
- Gupta V, Mastromarino P, Garg R. Effectiveness of Prophylactic Oral and/or Vaginal Probiotic Supplementation in the Prevention of Recurrent Urinary Tract Infections: A Randomized, Double-Blind, Placebo-Controlled Trial. Clinical Infectious Diseases. 2024;78(5):1154-1161.
- Jung C, Brubaker L. The etiology and management of recurrent urinary tract infections in postmenopausal women. Climacteric. 2019;22(3):242-249.
