In this article we explore five of the most common causes of endometriosis and key hormonal imbalances that can exacerbate your symptoms.
What is endometriosis?
Endometriosis is an estrogen dependent inflammatory and immune disease in which there is a growth of endometrial-like tissue that grows outside of the uterus. It impacts about 10% of women in their reproductive years and some of the common symptoms include extreme pelvic pain, heavy periods and infertility.
Read more about the symptoms of endometriosis.
There is a lot of research that attempts to pinpoint the root cause or main drivers of endometriosis, although there is still more research needed in this area. There are many theories as to why endometriosis develops, including retrograde menstruation, genetics, environmental toxins, bacteria, hormones and more.
1. Dysfunctional immune activity and inflammation
There is much research and evidence that the immune system is not acting appropriately in those with endometriosis. Essentially the innate immune system (the body’s first line of defense against pathogens, viruses and bacteria etc) does not clear up the endometrial tissue as it should and allows for gram-negative bacteria to flourish.
To understand this in more detail we need to look more closely at how the innate immune system works.
The innate immune system has many tools to support the body such as physical barriers like the skin, mucus membranes and it also has an inflammatory response to pathogens. There are many cells involved in the innate immune system including mast cells, natural killer cells, neutrophils and macrophages. This is important to understand as in endometriosis there is an abnormal innate immune system response in terms of increased inflammatory responses and there are also a lower number of natural killer cells to fight the pathogens and mop up the endometrial tissue.
We also have an immune system called the adaptive immune system which is an acquired immune system that involves specialised immune cells and antibodies that fight off pathogens such as T-cells and B-cells. In endometriosis there are abnormalities with the T-cell and B-cells which research is now linking this abnormal functioning of T and B- cells to being one of the key drivers of endometriosis.
To put it simply, those with endometriosis seem to have a dysregulated immune response, especially in the peritoneal cavity. This dysregulated immune activity results in increased inflammation and the proliferation of the growth of endometriosis. Research is still being conducted in this area to understand what is driving these immune changes, some research suggests that endometriosis may be an autoimmune disease, and some research concluded there may be an abnormal response to hormones such as progesterone in the immune system, but more research is required.
Understanding that there is dysregulated immune activity and increased inflammation driving endometriosis is vital as there are many ways that we at FUTURE WOMAN can work to regulate your immune system and reduce inflammation through diet and supplementation. For example, we recommend all clients with endometriosis remove gluten and A1 casein dairy for a period of at least three months to reduce inflammation and avoid these immune-disrupting proteins to allow the body a chance to regulate immune activity and reduce inflammation.
2. Toxin exposure
The latest research suggests that toxin exposure may be an important factor in the immune dysregulation and inflammatory response of endometriosis. In particular research has highlighted the role of dioxins in the development of endometriosis.
Dioxins are environmental toxins or pollutants that are found in the food chain, particularly in meats and dairy. Dioxins can be found in household chemicals, air pollution, tampons and more. These dioxins can accumulate in the body and can negatively affect physiological processes within the body. Research has connected dioxins to reproductive dysfunction, immunological and thyroid disorders, as well as to endometriosis. In particular research has found that women with endometriosis have higher dioxin levels in their menstrual fluid compared to those without endometriosis.
Dioxins can alter normal endometrial and immune cell physiology which can then allow the development of endometrial tissue within the peritoneal cavity. This would otherwise normally be cleared by immune system cells, but in endometriosis this does not occur. Although more research is required in this area, some research has shown that the presence of dioxins can increase not only the incidence but also the severity of endometriosis too.
One of our favorite ways to reduce exposure to environmental toxins is to remove all fragrances from the house. This includes perfume, household cleaners, body washes, body creams and candles. We also advocate for eating a mainly organic diet where possible to reduce pesticides and excess toxins .
3. Gut bacteria (LPS toxins and gram negative)
Recent research has hypothesized that one of the main drivers of endometriosis may be bacteria imbalance and the presence of endotoxins in the gut and pelvic environment.
The research states that those with endometriosis have a higher level of gram negative bacteria, concluding that the menstrual blood of those with endometriosis was very high in the bacteria Escherichea coli, in comparison to those without endometriosis. Higher levels of the bacterias Gardnerella and Enterococci were also found in those with endometriosis.
Gram negative bacteria is a type of bacteria that is increasingly antibiotic and drug resistant, therefore it is an increasing problem for many people. The presence of this gram-negative bacteria in the peritoneal cavity has been suggested to trigger a change in certain genes that then increase the likelihood of endometriosis for that person.
Very interestingly research has shown that women with a previous gynaecological infection are actually more likely (in fact up to 50% more likely) to develop endometriosis. So how does this work? Well gram-negative bacteria releases something called LPS which stands for lipopolysaccharides which are bacterial toxins. These LPS toxins can trigger a pro-inflammatory response in the pelvis and in turn trigger the growth of endometriosis. Therefore addressing the gut bacteria, underlying infections and gram-negative bacteria is a vital part of addressing endometriosis. There is much research on how certain supplements such as berberine may be able to help in this area but seeking supervised, 1:1 support is highly recommended.
Purchase a 1-1 consultation with a FUTURE WOMAN practitioner.
As we have mentioned above, there is a lot of research around the genetic link of endometriosis. There is research that confirms that there is a relationship between environmental toxins and the permanent changes in certain gene expression which can increase the risk of endometriosis. Not only have toxins from the environment been linked to changing gene expression, but toxins from the gut such as LPS toxins have also been linked to changing gene expression in those with endometriosis.
Research concludes that epigenetic changes seem to be attributable for both the immune and the hormonal changes that occur in endometriosis. There needs to be more research into this are to understand which genes in particular may be contributing to the development of endometriosis and therefore what possible interventions may be available to change the expression of these genes.
5. Estrogen - does it really ‘cause’ endometriosis?
We cannot talk about endometriosis without discussing the role estrogen has to play. But is it a driver of endometriosis? Firstly, it is important to reiterate that endometriosis is an immune and inflammatory disease that is influenced by estrogen. Therefore it is not a hormonal condition and estrogen does not cause the actual growth or proliferation of endometriosis.
Estrogen can act as a driver of the inflammation and pain in endometriosis, but it does not cause the endometrial like tissue to grow outside of the uterus.
Estrogen plays a very important role in how endometrial tissue grows, it essentially causes it to thicken which in turn can increase the pain and inflammation that a person with endometriosis might experience. Those who have endometriosis typically have high estrogen (in particular estradiol) levels, and therefore it is important to address estrogen when looking at treatment. High estrogen can also lead to the increase of histamine being released from mast cells which can in turn increase pain and inflammation even more. This inflammation from the increase in mast cell activation and release of histamine may contribute to the proliferation of endometrial like tissue growing outside the uterus.
Read more about high or unopposed estrogen.
Therefore an important part of addressing endometriosis is testing your estrogen levels. It is not only important to assess the overall levels of estrogen, but also the ratio of estrogen in comparison to progesterone too. It is also vital to test the estrogen metabolites to see which pathways your estrogen is moving through to assess if this may be contributing to the pain and inflammation in endometriosis.
Read more about testing and endometriosis.
Based on your test results our practitioners will suggest supplementation (for example DIM or sulforaphane) that helps to clear estrogen from the body and modulate your estrogen pathways. All FUTURE WOMAN recommendations are personalised based on your symptoms and results so we never recommend trying a supplement that can alter hormone levels without testing first. .
At FUTURE WOMAN when we address endometriosis we take all of the possible driving factors into account, including these five mentioned and ensure that your health plans include support for hormone imbalance, inflammation and the immune system.
Birnbaum LS, Cummings AM. Dioxins and endometriosis: a plausible hypothesis. Environ Health Perspect. 2002 Jan;110(1):15-21. doi: 10.1289/ehp.0211015. PMID: 11781160; PMCID: PMC1240688.
Giampaolino P, Della Corte L, Foreste V, Barra F, Ferrero S, Bifulco G. Dioxin and endometriosis: a new possible relation based on epigenetic theory. Gynecol Endocrinol. 2020 Apr;36(4):279-284. doi: 10.1080/09513590.2019.1698024. Epub 2019 Dec 5. PMID: 31805795.
Guo SW. Epigenetics of endometriosis. Mol Hum Reprod. 2009 Oct;15(10):587-607. doi: 10.1093/molehr/gap064. Epub 2009 Aug 3. PMID: 19651637.
Khan KN, Fujishita A, Kitajima M, Hiraki K, Nakashima M, Masuzaki H. Intra-uterine microbial colonization and occurrence of endometritis in women with endometriosis†. Hum Reprod. 2014 Nov;29(11):2446-56. doi: 10.1093/humrep/deu222. Epub 2014 Sep 8. PMID: 25205755.
Khan KN, Fujishita A, Hiraki K, Kitajima M, Nakashima M, Fushiki S, Kitawaki J. Bacterial contamination hypothesis: a new concept in endometriosis. Reprod Med Biol. 2018 Jan 18;17(2):125-133. doi: 10.1002/rmb2.12083. PMID: 29692669; PMCID: PMC5902457.
Khan KN, Kitajima M, Inoue T, Tateishi S, Fujishita A, Nakashima M, Masuzaki H. Additive effects of inflammation and stress reaction on Toll-like receptor 4-mediated growth of endometriotic stromal cells. Hum Reprod. 2013 Oct;28(10):2794-803. doi: 10.1093/humrep/det280. Epub 2013 Jul 9. PMID: 23842561.
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.
Lin WC, Chang CY, Hsu YA, Chiang JH, Wan L. Increased Risk of Endometriosis in Patients With Lower Genital Tract Infection: A Nationwide Cohort Study. Medicine (Baltimore). 2016 Mar;95(10):e2773. doi: 10.1097/MD.0000000000002773. PMID: 26962775; PMCID: PMC4998856.
Soave I, Caserta D, Wenger JM, Dessole S, Perino A, Marci R. Environment and Endometriosis: a toxic relationship. Eur Rev Med Pharmacol Sci. 2015;19(11):1964-72. PMID: 26125255.
Zhang T, De Carolis C, Man GCW, Wang CC. The link between immunity, autoimmunity and endometriosis: a literature update. Autoimmun Rev. 2018 Oct;17(10):945-955. doi: 10.1016/j.autrev.2018.03.017. Epub 2018 Aug 11. PMID: 30107265.