The gut microbiome is the community of trillions of bacteria and other microorganisms that live in the digestive system. While the influence of the microbiome on gut health is clear, its central role in many other aspects of health and wellbeing is becoming increasingly apparent. The microorganisms in the gut can impact immune responses, inflammation, and hormone metabolism, all of which play a role in the development of endometriosis. As a result, there is growing interest in the endometriosis gut microbiome and the gut–reproductive axis. This article explores what is currently known about the relationship between endometriosis and the gut microbiome, and whether diet and probiotics could have a future supportive role.
Endometriosis is a chronic condition in which tissue that resembles the lining of the uterus grows outside the uterus itself 1. It affects around 10% of women and girls of reproductive age worldwide, meaning it impacts around 190 million people 2. The precise causes of endometriosis are not fully understood, but the best-supported model is that menstrual or endometrial-like cells are able to reach locations outside the uterus. This movement of cells is common, but in susceptible people, the cells are not properly cleared and can attach, survive, and establish a blood supply 3.
These abnormal cells, known as endometriotic lesions, cause local inflammation and can lead to severe pain and discomfort 4. Because the cells are derived from the uterus, they are sensitive to oestrogen signalling, meaning that pain can be worse during menstruation. As well as chronic pelvic or abdominal pain, symptoms include pain during intercourse, gastrointestinal bloating, changes in bowel habits, and fatigue 2.
The connection between the reproductive system and gut health was, until recently, largely underexplored. However, research now points towards a two-way communication system, described by a framework called the gut-reproductive axis 7–9. Gut microbiota and the intestinal barrier can influence oestrogen metabolism, immune function, metabolism, and neuroendocrine signalling, all of which play an important role in female reproductive health. Conversely, reproductive hormones, particularly oestrogens, can alter the gut microbiome.
While the concept is still evolving, it has been proposed that the gut microbiota could influence the peritoneal environment in which endometriotic lesions are established and grow. Importantly, the gut microbiome helps set an inflammatory baseline for the body. This dictates how the body responds to everyday stimuli and whether it tends towards inflammatory or regulatory responses 10. Gut dysbiosis, an imbalance of the microorganisms in the digestive tract, can increase exposure of other tissues to lipopolysaccharide (LPS), which triggers pro-inflammatory signalling. In an inflammatory environment, immune cells shift towards a form that promotes cell growth, rather than clearing damaging or abnormal cells, potentially worsening the development of endometriosis 11.
Microbial metabolites, the small molecules produced by microorganisms in the gut, may also contribute. Short-chain fatty acids (SCFAs) are produced when bacteria in the gut ferment fibre and have anti-inflammatory and immunoregulatory effects. Research using mice found that those with endometriosis had less of one type of SCFA, n-butyrate. Furthermore, treatment with n-butyrate reduced the growth of endometriotic lesions in mice, with similar effects observed in laboratory studies using human endometriotic cells 12.
There is also evidence in humans for an endometriosis gut microbiome, but there isn’t currently a consistent, diagnostic pattern in these changes. In a Turkish case-control study of 14 women with stage 3/4 endometriosis, advanced forms of the condition, and 14 healthy controls, stool profiles dominated by Shigella/Escherichia were more common in the endometriosis group 13. A larger study in Sweden of 66 women with endometriosis found that they had lower gut microbial diversity than healthy controls 14.
These observed changes are not consistently reproduced across different cohorts in different studies. A recent meta-analysis pooled the data from 11 studies, including a total of 433 women, and found differences in endometriosis gut microbiome diversity, as well as some specific gut bacteria, including Bifidobacterium and Lachnospira. However, the authors highlighted substantial variation between studies, small sample sizes and inconsistent methods between studies, which makes it difficult to define a consistent microbial profile 15.
As we’ve seen, endometriosis is an oestrogen-dependent condition: endometrial lesions respond to oestrogen signalling, which can increase their growth. This means that other aspects of physiology that impact oestrogen activity can impact the disease. Oestrogens are inactivated in the liver when they are attached to molecules of glucuronic acid, after which they are excreted. One enzyme that regulates the binding of oestrogens to glucuronic acid is called β-glucuronidase, an enzyme produced in the gut. β-glucuronidase detaches oestrogens from glucuronic acid, preventing their excretion, meaning that more of the enzyme typically means more oestrogen 21,22. The collection of gut bacterial genes able to metabolise oestrogens is known as the oestrobolome 23.
In theory, an oestrobolome with greater β-glucuronidase activity could increase circulating oestrogen and cause lesion growth. However, human data supporting this link in endometriosis are limited. In a Taiwanese study of 27 women with endometriosis and 24 controls, faecal β-glucuronidase activity did not differ significantly between groups, although several faecal oestrogen metabolites were higher in women with endometriosis 24. A second study found higher serum β-glucuronidase in 35 women with endometriosis than in 30 controls. In mice, β-glucuronidase can promote growth and pro-endometriosis immune activity 24.
The intestinal barrier is formed by a layer of epithelial cells covered by protective mucus. Normally, it plays an important role in immunity by limiting the passage of bacteria into circulation. However, gut dysbiosis can weaken the barrier and increase its permeability, often described as “leaky gut”, although this isn’t a formal clinical diagnosis 25.
When the barrier is compromised, bacteria and their metabolites, such as LPS, can reach the blood, where they have pro-inflammatory effects. Sustained, chronic inflammation is associated with endometriosis, and some small studies have assessed whether intestinal permeability can impact disease development. One study found more frequent bacterial contamination in menstrual blood in women with endometriosis, along with higher toxin levels 26.
Diet is one of the strongest influences on the gut microbiome, and changes in diet can alter its composition in a matter of days 17. In one large study, higher fruit intake was associated with lower risk of endometriosis diagnosis, while higher intake of cruciferous vegetables, such as broccoli and cauliflower, was associated with a higher risk 27. However, the study was purely observational and cannot establish cause-and-effect relationships.
There is some evidence that changing diet can impact endometriosis symptoms. In a randomised controlled trial (RCT) of 35 women with endometriosis, 60% responded to a 28-day low-FODMAP diet, an elimination diet used to manage IBS-type symptoms, compared with 26% on a control diet 28. However, the low-FODMAP diet is restrictive and is intended to be short-term and followed by structured reintroduction. Many women with endometriosis change their diet to manage symptoms, including removing gluten or dairy. However, unsupervised exclusion diets can risk nutritional inadequacy and may reduce plant diversity and fibre intake, which could negatively affect the endometriosis gut microbiome. A personalised approach, guided by individual tolerance rather than unnecessary restriction, is likely to be most appropriate.
As more is understood about the gut-reproductive axis, interest in probiotics for endometriosis is increasing. Potential mechanisms include:
Most of the evidence for probiotic interventions comes from preclinical studies, but there have been promising results from small trials in humans. Two separate RCTs have found that Lactobacillus strains improved menstrual pain compared with placebo over 8 to 12 weeks 29,30. A more recent study also reported improvements in quality of life and changes in oestrogen levels in women with endometriosis taking a probiotic 31.
Probiotic effects are strain-specific, so findings from one product cannot be generalised to others. As such, larger trials are required to determine which probiotics may be best suited for alleviating endometriosis symptoms. At present, they may be considered as a possible addition to standard of care.
Emerging research suggests the endometriosis gut microbiome may differ from that of people without the condition. Proposed links include inflammation, immune signalling, oestrogen metabolism and gut barrier function. However, most human studies are small and observational, and it is not yet clear whether microbial changes contribute to endometriosis or result from it.
In practice, GI symptoms in people with endometriosis should be taken seriously, and endometriosis should be considered in patients presenting with IBS-type symptoms alongside pelvic pain. Supporting gut health in endometriosis currently centres on a varied, fibre-rich diet where tolerated. Probiotics for endometriosis remains an emerging area with small, strain-specific studies suggesting potential benefits in alleviating symptoms.
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