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The Link Between Endometriosis and the Gut Microbiome

  • Dr. Kyla Stewart
  • 11 minutes ago
  • 5 min read

Endometriosis and the gut microbiome

Severe period pain is never normal. Pain so intense it feels like you’re being stabbed with a knife, pain that radiates through your body like a bolt of hot lighting, leaving you sweating, nauseous, and sometimes even fainting. This is not something you should have to endure. Sadly, many women’s experiences are dismissed with phrases like “it’s just your period” or “it can’t be that bad.” But when your menstrual pain causes you to miss work, cancel plans, or struggle with everyday tasks, it’s time to look deeper—this could be endometriosis.


Endometriosis is when endometrial (uterine tissue) grows outside the uterus— this could be the pelvic lining, ovaries, and the tissues behind the uterus, but, while less common, they can also affect the bladder, intestines, or other nearby organs.


What causes endometriosis still remains unclear, however the most widely accepted theory is retrograde menstruation— when period blood that has flown backwards into the pelvic cavity, carrying endometrial cells that can implant and grow outside of the uterus. These cells can produce their own estrogen, which stimulates their growth leading to chronic pelvic pain. Because of this, the conventional first-line treatments for endometriosis often involve hormonal therapies such as oral contraceptives or IUDs that suppress estrogen production. Because of this, the conventional first-line treatments for endometriosis often involve hormonal therapies such as oral contraceptives or IUDs that suppress estrogen production. It is a complex chronic inflammatory disease influenced by multiple factors, including immune system dysfunction, hormonal imbalances, environmental toxins, and—more recently—the health of the gut microbiome.


The Gut Connection


Endometriosis is increasingly being recognized as a systemic, inflammatory disease. One of the most compelling areas of research focuses on the gut immune axis—specifically how the make up of an endometriosis patient’s gut microbiome is directly influencing estrogen metabolism and immune signalling, which in turn continues to drive inflammation.

The gut microbiome is disrupted, leading to an imbalance in the amount of beneficial and potentially harmful species of bacteria, this is called dysbiosis. This imbalance can lead to a weakened gut integrity, increase gut permeability, triggers immune activation and inflammation. Over time, this can fuel systemic inflammation and worsen endometriosis symptoms.


Diet and Inflammation


Because endometriosis is fundamentally inflammatory, removing certain pro-inflammatory foods can be a powerful first step toward reducing symptoms.


• Gluten is one of the most researched triggers. Studies show that a gluten-free diet can improve symptoms in up to 75% of endometriosis patients. Immunologist Dr. Jeffrey Braverman notes that a genetic haplotype linked to autoimmune conditions and celiac disease also appears in endometriosis, which may explain why avoiding gluten brings relief.

• Dairy, particularly A1 casein from cow’s milk, can trigger gut inflammation and increase intestinal permeability, further promoting dysbiosis.

• Eggs may be problematic for certain individuals, especially those with a history of eczema, due to heightened immune reactivity.

• High-histamine foods—such as aged cheeses, fermented products, and certain cured meats—can raise estrogen levels, which may worsen endometriosis by stimulating tissue growth.


Gut Dysbiosis - SIBO & Lipopolysaccharide


Emerging research shows that women with endometriosis often have a distinctly altered gut microbiome compared to women without the condition. The alteration in gut microbes is called SIBO (small intestinal bacterial overgrowth)—a condition where bacteria that normally live in the large intestine migrate into the small intestine. A 2025 study by the International Federation of Gynaecology and Obstetrics found that over 90% of women with endometriosis who underwent lactulose breath testing had significant small intestine bacterial overgrowth. (Halfon, 2025) This could be due to the chronic inflammation or adhesions created by endometriosis, which disrupts motility and impairs the migratory motor complex, the MMC, which creates a favourable environment for bacteria to overgrow. These microbes tends to ferment foods in the small intestine leading to symptoms of bloating, gas, constipation, diarrhea, and abdominal pain, which often overlap with endometriosis symptoms. Some women may find temporary relief from a low FODMAP diet, which limits fermentable foods like garlic, onions, broccoli, and Brussels sprouts. However, low-FODMAP eating is generally not a long-term solution. Testing for and treating SIBO can significantly reduce digestive and pelvic symptoms.


Lipopolysaccharide(LPS)


LPS is a molecule found on the outer surface of Gram-negative bacteria. While under healthy gut conditions, these bacteria are maintained at low and balanced levels, when there is an imbalance in the gut these gram-negative bacteria can multiply excessively and causing permeability of the gut wall. The LPS component of these bacteria is highly immunogenic, meaning the immune system reacts strongly to it. LPS binds to a receptor on immune cells called Toll-like receptor 4 (TLR4). This receptor acts like an alarm system, recognizing bacterial toxins and triggering inflammation. With TLR4 activated, it causes a signalling cascade that it turns on genes that promote inflammation, immune activation, and tissue growth


Microbiome–Estrogen Metabolism Link


Gut dysbiosis can also affects how the body detoxes and eliminates estrogen, a key driver in endometrial lesion growth and inflammation.


Estrogen, produced by the ovaries, adrenal glands and fat tissues, enters the bloodstream to completed its bodily function then travels to the liver to be processed in to a water-soluble form (called conjugated estrogen) so it can be safely excreted through urine and stool.


When the gut microbiome is imbalanced, this allows for certain bacteria to produce more of an enzymes called β-glucuronidase. When β-glucuronidase levels are elevated—a common finding in dysbiosis—it can cause previously detoxified (conjugated) estrogen to become reabsorbed into the bloodstream, instead of being eliminated. Higher circulating estrogen levels means more growth of endometrial tissues and worsening of symptoms of pain, inflammation and heavy period bleeds. Studies have shown that certain bacterial families, such as Clostridia and Ruminococcaceae, can increase active estrogen levels. While beneficial bacteria like Lactobacillus and Bifidobacterium may help reduce β-glucuronidase activity and lower estrogen reabsorption, offering potential support for hormonal balance.


Gut health is an overlooked factor in the management of endometriosis. Given how much it can affect one’s fertility, immune status, and impact hormone metabolism this needs to be an area of treatment focus. By targeting gut dysbiosis, reducing endotoxin load, and supporting gut barrier repair this can help break the chronic inflammatory cycle, offering a more integrated and root cause approach to endometriosis care.


If you are struggling with severe period pain or have been diagnosed with endometriosis, book an initial visit with Dr. Kyla Stewart to discuss your symptoms further.


Medical Disclaimer: This content is for educational and informational purposes only and is not intended as medical advice, diagnosis, or treatment. It should not be used as a substitute for professional medical guidance. Always consult a qualified healthcare provider for any medical concerns.


Reference

1. Marziali, M., Venza, M., Lazzaro, S., Lazzaro, A., Micossi, C., & Stolfi, V. M. (2012). Gluten-free diet: a new strategy for management of painful endometriosis related symptoms?. Minerva chirurgica, 67(6), 499–504.

2. Stephansson, O., Falconer, H., & Ludvigsson, J. F. (2011). Risk of endometriosis in 11,000 women with celiac disease. Human reproduction (Oxford, England), 26(10), 2896–2901. https://doi.org/10.1093/humrep/der263

3. Porpora, M. G., Scaramuzzino, S., Sangiuliano, C., Piacenti, I., Bonanni, V., Piccioni, M. G., Ostuni, R., Masciullo, L., & Benedetti Panici, P. L. (2020). High prevalence of autoimmune diseases in women with endometriosis: a case-control study. Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology, 36(4), 356–359. https://doi.org/10.1080/09513590.2019.1655727

4. Halfon, P., Estrade, J. P., Penaranda, G., Choucroun, N., Bouaziz, J., Nicolas-Boluda, A., Retornaz, F., Gurriet, B., & Plauzolles, A. (2025). High prevalence of small intestinal bacterial overgrowth and intestinal methanogen overgrowth in endometriosis patients: A case-control study. International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics, 170(1), 284–291. https://doi.org/10.1002/ijgo.70005

5. Khan, K. N., Kitajima, M., Inoue, T., Fujishita, A., Nakashima, M., & Masuzaki, H. (2015). 17β-estradiol and lipopolysaccharide additively promote pelvic inflammation and growth of endometriosis. Reproductive sciences (Thousand Oaks, Calif.), 22(5), 585–594. https://doi.org/10.1177/1933719114556487

6. Guo C, Zhang C. Role of the gut microbiota in the pathogenesis of endometriosis: a review. Frontiers in Microbiology. 2024;15. doi:10.3389/fmicb.2024.1363455.

 
 
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