When you think of endometriosis, what comes to mind? Do you think of pain, hormones, and burnout? What about the bacteria, viruses and other microbes living within you? Most women with endometriosis struggle with digestive symptoms, and recent research has been shedding light on how microbes might be involved. Are you unsure of how these little bugs are contributing to endo? Let’s break it down.
Women with endometriosis have a higher rate of upper and lower genital tract and pelvic infections. A history of pelvic inflammatory disease, which is commonly sexually transmitted but can involve a combination of bacteria and viruses, has a 3-fold increased risk of developing endometriosis within 10 years. Microbes in the uterus have been shown to affect implantation during in-vitro fertilization (IVF). Among viruses, the association between endometriosis and human papillomavirus (HPV) is the most well-researched. You can carry certain strains of HPV even if you’ve been vaccinated against HPV, since not all strains are covered. A variety of other viruses may also be able to change gene expression and behaviour of endometrial cells to allow them to form patches where they shouldn’t, including herpes simplex viruses, retroviruses, Epstein-Barr virus and cytomegalovirus. It’s been shown that enough genetic changes can make certain cells form endometriosis. Beyond viruses, radiation, chemical pollutants, oxidative stress, infections and other influences can also cause genetic changes.
What about bacteria? Researchers have compared microbes from the large intestine and genital tract in women with endometriosis versus non-endo cases. Higher E. coli, Shigella, Enterococcus, Proteobacteria, Streptococcus, Eubacteria, Gardnerella and Ureaplasma have been seen in the vaginal and intestinal microbiomes, and these can contribute to local inflammation. In particular, E. coli and Shigella are consistent in the research. These bacteria both have toxins (endotoxins) that are potent triggers for the immune system. Women with endometriosis also tend to carry more mollicutes in their pelvis – these are bacteria without a cell wall, mainly different kinds of Mycoplasma and Ureaplasma, and they can have a sleeper effect on the immune system by changing gene expression in immune cells. This is the “bacterial contamination theory” of endometriosis, where bugs can be a trigger for the inflammatory response, or perpetuate it.
Surprisingly, there’s even evidence that the bugs in our mouth are involved! Researchers have found higher Fusobacterium in moderate-to-severe endometriosis (gum disease, anyone?) and high Cardiobacterium in mild cases. Previous research has shown higher Fusobacterium associated with endo patches, in fecal and vaginal samples. Fusobacterium has even been shown to drive endometrial implant growth in animal studies.
Did you know that some bacteria can increase estrogen levels in our body? They’re part of the “estrobolome” and are an important piece to consider when we’re working on hormone balance in endometriosis or other hormonal concerns.
After this little biology lesson, here are the takeaways: women with moderate-to-severe endometriosis may have less gut microbial diversity compared to “healthy” women, and addressing dysbiosis (imbalances in our gut microbes) is vital to addressing endo symptoms.
Be aware that bacteria release toxins when they die, and these toxins are also inflammatory triggers in endometriosis. This can be challenging to navigate on your own, and we recommend addressing this with a knowledgeable naturopathic doctor. We’re here to help you put the pieces together and build a plan that really works for you.
- Oral, Vaginal, and Stool Microbial Signatures in Patients With Endometriosis as Potential Diagnostic Non-Invasive Biomarkers: A Prospective Cohort Study. Hicks et al. Oct 2024. https://doi.org/10.1111/1471-0528.17979
- Shan J, Ni Z, Cheng W, Zhou L, Zhai D, Sun S, et al. Gut microbiota imbalance and its correlations with hormone and inflammatory factors in patients with stage 3/4 endometriosis. Arch Gynecol Obstet. 2021;304:1363–73. doi: 10.1007/s00404-021-06057-z.
- Ata B, Yildiz S, Turkgeldi E, Brocal VP, Dinleyici EC, Moya A, et al. The Endobiota Study: Comparison of Vaginal, Cervical and Gut Microbiota Between Women with Stage 3/4 Endometriosis and Healthy Controls. Sci Rep. 2019;9:2204. doi: 10.1038/s41598-019-39700-6.
- Koninckx PR, Ussia A, Tahlak M, Adamyan L, Wattiez A, Martin DC, Gomel V. Infection as a potential cofactor in the genetic-epigenetic pathophysiology of endometriosis: a systematic review. Facts Views Vis Obgyn. 2019 Sep;11(3):209-216. PMID: 32082526; PMCID: PMC7020943.
- Koninckx PR, Ussia A, Adamyan L, et al. Pathogenesis of endometriosis: the genetic/epigenetic theory. Fertil Steril. 2019;111:327–340. doi: 10.1016/j.fertnstert.2018.10.013.
- de Ziegler D, Pirtea P, Galliano D, et al. Optimal uterine anatomy and physiology necessary for normal implantation and placentation. Fertil Steril. 2016;105:844–854. doi: 10.1016/j.fertnstert.2016.02.023.
- Tai FW, Chang CY, Chiang JH, et al. Association of Pelvic Inflammatory Disease with Risk of Endometriosis: A Nationwide Cohort Study Involving 141,460 Individuals. J Clin Med. 2018;7:379. doi: 10.3390/jcm7110379.
