Article review of Hearn-Yates et al. (2024)
If you have endometriosis, chances are you’ve come across advice on diet and lifestyle changes. Whether it be low-FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides and polyols) diets, gluten or lactose-free diets, supplements or increasing fibre intake, the list goes on. The idea that changing the gut microbiome could improve endometriosis symptoms is gaining attention.
But what role does the gut microbiome actually play in inflammatory conditions such as endometriosis, and can altering your gut bacteria really reduce your symptoms? How much of this narrative is actually backed by research?
A 2024 narrative review by Hearn-Yates et al. explores this question through the microbiota-gut-brain (MGB) axis, investigating its potential role in endometriosis-associated symptoms and whether targeting the gut microbiome could offer opportunities for personalised management.
So what is the MGB Axis?
The MGB axis is the two-way communication pathway connecting the gut to the brain. The gut contains trillions of microorganisms that not only contribute to gut health, but also interact with many different systems around the body. Gut bacteria produce metabolites that can interact with the immune, hormonal and nervous systems, potentially influencing processes such as inflammation, pain perception and mood. These connections are particularly relevant to endometriosis, where inflammation, chronic pain and mood-related symptoms can all contribute to the burden of the condition.
This is particularly interesting because endometriosis extends far beyond just pelvic pain, including gastrointestinal symptoms as well as higher rates of IBS, anxiety and depression. Interestingly, the severity of endometriosis-associated pain does not necessarily correspond with the number, type or location of lesions.
So is the gut involved in endometriosis symptoms?
What did the researchers find?
Hearn-Yates et al. explored several pathways through which the microbiome could be linked to endometriosis-associated symptoms, including inflammation, pain processing, gastrointestinal symptoms and mood. Endometriosis is associated with altered immune and inflammatory responses, which may contribute to the establishment and growth of lesions.
The review also discusses evidence that the hypothalamic–pituitary–adrenal (HPA) axis, which helps regulate the body’s stress response and cortisol release, may be altered in chronic pain and endometriosis. The gut microbiome may interact with this stress response through the MGB axis, providing another possible link between the gut, brain and endometriosis-associated symptoms.
Lastly, when the gut microbiome is unbalanced, this is called dysbiosis. Dysbiosis has been associated with altered inflammatory signalling and visceral hypersensitivity, while gut bacteria may also influence how oestrogen is metabolised. These provide possible mechanisms through which the microbiome could interact with endometriosis.
Importantly, much of the evidence comes from animal models or other chronic conditions rather than people with endometriosis. Human endometriosis studies remain small and inconsistent, making it difficult to determine whether microbiome changes contribute to the condition or are a consequence of it.
What about endometriosis self-management?
The review also explored whether strategies that alter the gut microbiota could help manage endometriosis-associated symptoms. These included dietary changes, supplements, probiotics and antibiotics.
Low-FODMAP diets were one approach explored in the review. Although they are well studied in IBS, evidence specific to endometriosis remains limited, with preliminary research suggesting they may help gastrointestinal symptoms in people with both conditions.
Probiotics have also shown preliminary results. Small human trials reported reductions in pain following Lactobacillus supplementation, while findings suggesting that L. gasseri may reduce lesion growth and influence immune activity came from animal models.
Lastly, the review explored whether antibiotics could influence endometriosis progression. One study detected Fusobacterium more frequently in endometrial samples from patients with ovarian endometriosis than controls, before investigating antibiotic treatment in mice. Antibiotics produced promising results in some animal models, including reductions in lesion growth and inflammation. However, the only human clinical trial discussed in the review found that six months of clarithromycin was no more effective than placebo at reducing pain following endometriosis surgery.
However, these findings should be interpreted cautiously. Endometriosis-specific studies had small and heterogeneous populations (largely variable populations which can increase bias), used differing methodologies (to evaluate symptoms and pain), while much of the wider evidence came from animal models or related conditions such as IBS. This makes it difficult to compare findings and draw firm conclusions.
So what does this mean for endometriosis treatment?
Ultimately, the review suggests that the gut microbiome is a promising area of endometriosis research, but the evidence is not yet strong enough to translate these findings into established treatments. The authors suggest that better understanding the gut microbiome could eventually help develop microbial or biomarker profiles to guide more personalised management strategies, such as targeted dietary or probiotic approaches alongside existing medical and surgical treatments. They also suggest that antibiotics may warrant further investigation if the proposed role of bacteria in endometriosis progression can be replicated in larger and more diverse populations. For now, larger, well-controlled studies using standardised methodologies are needed before these approaches can be translated into clinical practice.
References
Hearn-Yates, F., Horne, A.W., O’Mahony, S.M. and Saunders, P.T.K. (2024). The impact of the microbiota-gut-brain axis on endometriosis-associated symptoms: mechanisms and opportunities for personalised management strategies. Reproduction and Fertility, 5(2). doi:10.1530/raf-23-0085.