Estrogen dominance is one of the more common hormone imbalances your clients may face, but what exactly is estrogen dominance, how does it differ from estrogen excess, and what can you do to holistically support your clients with this imbalance?
Both estrogen dominance and estrogen excess can contribute to many uncomfortable symptoms your female clients may face. Such as PMS, period pain, irregular or heavy periods, weight gain, acne, cravings, fatigue, and in more serious cases; fibroids, cysts, endometriosis, and/or infertility.
Supporting the body to maintain a healthy balance of estrogen by promoting estrogen elimination and progesterone production is imperative to supporting hormonal health and resiliency. Before we get into discussing how to go about supporting healthy estrogen levels, let’s cover some of the basics.
What is Estrogen?
Estrogen is a group of estrogenic steroid sex hormones that are produced primarily by the ovaries, but also by the adrenals and fat cells. The three main estrogen hormones are Estrone (E1), Estradiol (E2), and Estriol (E3).
Each of these estrogens play different roles within the body throughout the course of a woman’s reproductive life.
Estradiol (E2) is the most potent estrogen and is the primary estrogen in charge during a woman’s fertile years.
Estrone (E1) is also quite abundant and a potent estrogen as well.
Estriol (E3) is the weakest of estrogens and is typically highest only during pregnancy. Although when not pregnant, E3 is still a valuable player contributing anti-inflammatory & anti-oxidative properties that support bone health, heart health & more. When not pregnant, E3 can be made via the liver from the conversion of E2, and the conversion of the estrone metabolite, 16OH.
The Primary Roles of Estrogen:
Estrogen’s main role within the female reproductive system is to be proliferative, in other words, to promote growth. One of the proliferative jobs estrogen has is to stimulate the cells of the uterine lining to deposit a thick layer of nutritious blood in preparation for an embryo (it is this uterine lining that sheds resulting in a woman’s monthly period).
Estrogen also stimulates the proliferation of follicles in the ovaries, which leads to a mature egg that will eventually ovulate. When it comes to our reproductive health, estrogen plays a critical role in supporting female fertility by promoting ovulation and a healthy uterine endometrial lining for an embryo to implant.
Outside of fertility and reproductive health, estrogen:
- Supports healthy insulin sensitivity and blood sugar balance (1)
- Promotes healthy levels of inflammation within the brain (2)
- Supports the production and regulation of serotonin & dopamine (3)(4)
- Supports bone mineral density and remodeling (5)
- Maintains skin health & elasticity (6)
- Maintains vaginal tissue health and repair (7)
- And more
With all this being said, estrogen is important for many aspects beyond reproductive health and although in excess it may be problematic, not having enough of it may be just as concerning.
What is Estrogen Excess?
Estrogen excess occurs when there is too much estrogen in the system in relation to that which is being eliminated, leading to a build-up of estrogen and an increase of estrogen’s proliferative effects.
Too much estrogen in the system can be triggered by either endogenous (internal) or exogenous (external) sources, or a mixture of both.
Excess endogenous estrogen
It is not common for the body to naturally produce estrogen in excessive quantities. Rather, estrogen buildup can occur when the body is not eliminating estrogens properly. This can be due to poor liver function and impaired estrogen metabolism.
Excess exogenous estrogen
This occurs when the body is subjected to a high amount of estrogen-mimicking substances called xenoestrogens which can be found within endocrine disrupting chemicals. These substances can act as estrogen in the system, increasing proliferation and symptoms of estrogen excess, and may also impair endogenous estrogen elimination by taking a higher priority by the liver to process, and down-regulating more protective estrogen elimination pathways.
What is Estrogen Dominance?
Estrogen dominance occurs when there is excess estrogen in relation to the hormone progesterone.
Progesterone is produced in sufficient amounts only after a successful ovulation. Its primary role is to oppose the proliferative effects of estrogen within the luteal phase (following ovulation).
Estrogen dominance is often confused with estrogen excess because when progesterone is deficient, leaving estrogen unopposed, estrogenic symptoms can occur.
This is one of the reasons why a person may experience estrogenic symptoms while demonstrating low quantitative values of estrogen on lab tests, and is a great example of why functional hormone testing, such as with the DUTCH test, is so important when assessing hormone health and patterns.
Regardless, estrogen dominance, like estrogen excess, is not a condition to take lightly as it can lead to more serious complications if not controlled once diagnosed.
Although estrogen dominance and estrogen excess are inherently different, we may often see these two situations presenting together, where a person has both an over-abundance of estrogen due to poor elimination and low progesterone due to impaired ovulatory health.
As you may have gathered by now, although estrogen has many important roles within the body, it needs to be the right kind and in the right amount in order for it to contribute to healthful outcomes.
When there is too much estrogen in the system, it can wreak havoc and lead to a host of uncomfortable (and potentially dangerous) situations. If there is too little, it can lead to other issues like weight gain, loss of menses, and a low libido.
To keep this state of estrogen balance, the body has to be able to eliminate excess estrogen properly. The estrogen elimination process can be a lengthy one and is often where many women experience issues leading to their estrogen-dominant symptoms.
Phase 1 of Estrogen Metabolism:
Once estrogen is shuttled to the liver for elimination, it gets broken down into 1 of 3 different estrogen metabolite pathways: 2-hydroxyestrone (2OH), 4-hydroxyestrone (4OH), or 16-hydroxyestrone (16OH).
2OH is the most protective pathway, as it can lead to many beneficial aspects such as heart protection, bone health, breast health, and a healthy functioning reproductive system.
Whereas the 4OH and 16OH metabolite pathways tend to be more problematic, leading to free radical production and oxidative stress, contributing to estrogenic symptoms and conditions such as fibroids, cysts, endometriosis, autoimmunity, obesity, and in some cases estrogen-related cancers.
Regardless, the over-abundance of estrogen metabolites, despite the metabolite type, can contribute to estrogen excess symptoms and conditions if they do not continue to phase 2 of the estrogen elimination process.
Phase 2 of Estrogen Metabolism:
After the estrogen has been metabolized and gone through one of the 3 pathways listed above, it then goes through an additional step by the liver to transform the estrogen from a fat-soluble compound to a water-soluble compound. These processes include Sulfation, Glucuronidation, and Methylation.
With sulfation, estrogen is conjugated via sulfate by the hepatic phase II enzymes into their inactive, sulfated versions which are then either eliminated via the urine or converted back into estrogen compounds & recirculated. (8)
With glucuronidation, estrogen is conjugated via glucuronic acid by the hepatic phase II enzymes to be eliminated through the bowels.
Finally, the process of methylation attaches a methyl group to the estrogens via the COMT enzyme, creating 2-methoxy and 4-methoxy metabolites to be eliminated through the urine (observed on DUTCH tests).
Those with methylation problems or the MTHFR gene may have issues methylating estrogen metabolites properly and may depend more on the other two pathways for their estrogen elimination.
Phase 3 of estrogen metabolism:
After the estrogen metabolites are conjugated into water-soluble compounds and are ready to be eliminated, they are either transferred to the kidneys to be eliminated via urine or are transferred into the biliary system, into the digestive tract to be eliminated via feces.
For many, this is the last step of estrogen metabolism and is where estrogen is finally able to be eliminated from the body. However, for some, especially those with kidney issues, biliary insufficiency, or digestive dysfunction, this part of the process of estrogen elimination may also be impaired, resulting in more estrogen buildup.
Within the gut microbiome is a certain subset of bacteria that produce the enzyme beta-glucuronidase, which has the potential to inhibit the elimination of estrogen by initiating enterohepatic circulation – that is, the reactivation and recirculation of estrogen metabolites back through the bloodstream. (10)
Although this may seem like a bad thing, there is actually some benefit to this enzymatic process. In a healthy microbiome, you would ideally see some bacteria with beta-glucuronidase activity, as it can help to recirculate moderate amounts of estrogen back through the system, maintaining estrogen levels and reducing the need for estrogen synthesis.
However, in cases of dysbiosis where these bacteria are overgrown, it may lead to an overabundance of beta-glucuronidase activity, and an increase in estrogen recirculation. This is one reason why gut health is so important for estrogen balance, and digestive issues such as constipation may exacerbate estrogen excess or estrogen dominant conditions.
How to holistically support your clients with estrogen dominance
If you suspect that your client’s symptoms are related to estrogen excess and/or estrogen dominance, it is best you suggest they get their hormones tested via a comprehensive hormone test such as the DUTCH test. However, as a starting point, here are a few simple things you can suggest to help support your client’s estrogen metabolism and elimination:
- Evaluate your client’s product quality and usage. Opting for non-toxic household & beauty products can be a great first step in reducing their exogenous xenoestrogen exposure. For support with learning more about endocrine-disrupting chemicals, check out the Environmental Working Group’s website here.
- Support your clients to choose organic food & filtered water. Many conventionally-produced foods such as conventional animal products and non-organic produce can be laden with xenoestrogens. (9) Unfiltered tap water can also be hiding many of these endocrine disrupting chemicals. Having your clients opt for naturally-raised animal products, organic produce and clean, filtered or spring water will minimize their overall hormone-disrupting chemical exposure.
- Support your client’s digestive health and ensure they are having a daily bowel movement. Although working on the foundations of digestive health is important for addressing the root of constipation and other digestive symptoms, if your client experiences constipation, sometimes strategic support is necessary to move the needle and calm more serious estrogen-related issues. For constipation support, you may consider suggesting they increase their intake of water & electrolytes, dietary fiber, magnesium citrate, and natural laxatives such as senna or psyllium husk. However, just using supplements to get your client to poop isn’t going to solve the main problem at hand if they are chronically constipated. If your client suffers from daily constipation, it will be important to dial in the root of their gut health issues to effectively support their estrogen health and balance.
- Support your client in reducing their sugar and alcohol consumption to decrease the burden that is placed on their liver. The liver does over 500 enzymatic processes in the body, each another straw on the camel’s back. In order to see results in estrogen metabolism, you need to make sure your client’s liver isn’t overburdened with unnecessary stressors. Suggesting your client limits their added sugar & alcohol consumption can ensure that their liver has enough energy & tools to be able to eliminate excess estrogens properly.
- Cruciferous vegetables (broccoli, cabbage, cauliflower, etc.) can be very powerful tools for supporting estrogen balance. These foods contain compounds called indols that help support estrogen metabolism down the 2OH pathway rather than 4OH or 16OH pathways. Indols must be activated via stomach acid into the active form, DIM (diindolylmethane) before it has this supportive effect on estrogen metabolism. For many, eating cruciferous vegetables daily can provide general support, however, DIM may have more of an impact on estrogen metabolism when taken in supplement form. A couple of notes of precaution. For one, DIM has the potential to lower estrogen levels, so it is not recommended to take in those with lower quantitative estrogen, and two, DIM is not recommended for those who have an impairment in phase 2 of estrogen metabolism. For example, if your client has issues with methylation, DIM would not be recommended as it may up-regulate estrogen metabolite production, contributing to more oxidative stress and damage. Before supplementing with DIM, it is recommended to test your client’s hormone health via a DUTCH test so you can assess the metabolism of their estrogen.
- Broccoli sprouts, also a part of the cruciferous family, are very rich in glucoraphanin, which is a precursor to sulforaphane, a powerful molecule that promotes the elimination of estrogen via sulfation. To support the activation of glucoraphanin into sulforaphane, it must first be activated by myrosinase, an enzyme that is also found within broccoli sprouts. This activation process occurs once the compounds are masticated (chopped or chewed) together. Heating and cooking deactivates the myrosinase enzyme, inhibiting the conversion to sulforaphane. Suggesting your clients incorporate raw broccoli sprouts into their daily or weekly diet may help to support estrogen elimination and can be a great alternative for those who experience methylation complications.
- Address stress management and sleep optimization. High stress levels and insufficient sleep patterns can contribute to ovulatory dysfunction, progesterone deficiency, and estrogen dominance. Supporting your client’s ovulatory health by promoting nervous system regulation, adrenal health, and decreasing their overall allostatic load, is a great way to support them in producing their own endogenous progesterone in sufficient amounts to avoid estrogen dominance from occurring.
Looking for more resources on estrogen dominance?
Want more tools and strategies for holistically supporting your clients with impaired estrogen metabolism and poor ovulatory health? Be sure to check out our practitioner training, the IAFHH Functional Hormone Specialist Certification Program.
By receiving the cutting-edge research and specialized education available in our program, you will quickly excel in your private practice and become the go-to hormone health expert in your community. In this program, we support you with all the tools, resources & information you need to expand your expertise in functional hormone health, get your female clients to achieve real & lasting results, and excel in your women’s health practice.
About the Author
Ashe Milkovic, NTP, IC-FHS, FBCS
Ashe is the founder and CEO of The International Association for Functional Hormone Health. She has a passion for spreading awareness about the power of functional nutrition for optimizing hormones & fertility, and her mission is to build community and safe space for other practitioners and aspiring learners to expand their knowledge and expertise in functional hormone health.
- Hui Yan, Wangbao Yang, Fenghua Zhou, Xiaopeng Li, Quan Pan, Zheng Shen, Guichun Han, Annie Newell-Fugate, Yanan Tian, Ravikumar Majeti, Wenshe Liu, Yong Xu, Chaodong Wu, Kimberly Allred, Clinton Allred, Yuxiang Sun, Shaodong Guo; Estrogen Improves Insulin Sensitivity and Suppresses Gluconeogenesis via the Transcription Factor Foxo1. Diabetes 1 February 2019; 68 (2): 291–304. https://doi.org/10.2337/db18-0638
- Vegeto E, Benedusi V, Maggi A. Estrogen anti-inflammatory activity in brain: a therapeutic opportunity for menopause and neurodegenerative diseases. Front Neuroendocrinol. 2008 Oct;29(4):507-19. doi: 10.1016/j.yfrne.2008.04.001. Epub 2008 Apr 29. PMID: 18522863; PMCID: PMC2630539.
- Lokuge S, Frey BN, Foster JA, Soares CN, Steiner M. Depression in women: windows of vulnerability and new insights into the link between estrogen and serotonin. J Clin Psychiatry. 2011 Nov;72(11):e1563-9. doi: 10.4088/JCP.11com07089. PMID: 22127200.
- Del Río, J. P., Alliende, M. I., Molina, N., Serrano, F. G., Molina, S., & Vigil, P. (1AD, January 1). Steroid hormones and their action in women’s brains: The importance of hormonal balance. Frontiers. Retrieved August 10, 2022, from https://doi.org/10.3389/fpubh.2018.00141
- Väänänen HK, Härkönen PL. Estrogen and bone metabolism. Maturitas. 1996 May;23 Suppl:S65-9. doi: 10.1016/0378-5122(96)01015-8. PMID: 8865143.
- Shah MG, Maibach HI. Estrogen and skin. An overview. Am J Clin Dermatol. 2001;2(3):143-50. doi: 10.2165/00128071-200102030-00003. PMID: 11705091.
- Lena Secky, Martin Svoboda, Lukas Klameth, Erika Bajna, Gerhard Hamilton, Robert Zeillinger, Walter Jäger, Theresia Thalhammer, “The Sulfatase Pathway for Estrogen Formation: Targets for the Treatment and Diagnosis of Hormone-Associated Tumors”, Journal of Drug Delivery, vol. 2013, Article ID 957605, 13 pages, 2013. https://doi.org/10.1155/2013/957605
- Miyagawa S, Iguchi T. Epithelial estrogen receptor 1 intrinsically mediates squamous differentiation in the mouse vagina. Proc Natl Acad Sci U S A. 2015 Oct 20;112(42):12986-91. doi: 10.1073/pnas.1513550112. Epub 2015 Oct 5. PMID: 26438838; PMCID: PMC4620905.
- Kwa M, Plottel CS, Blaser MJ, Adams S. The Intestinal Microbiome and Estrogen Receptor-Positive Female Breast Cancer. J Natl Cancer Inst. 2016 Apr 22;108(8):djw029. doi: 10.1093/jnci/djw029. PMID: 27107051; PMCID: PMC5017946.
- Paterni I, Granchi C, Minutolo F. Risks and benefits related to alimentary exposure to xenoestrogens. Crit Rev Food Sci Nutr. 2017 Nov 2;57(16):3384-3404. doi: 10.1080/10408398.2015.1126547. PMID: 26744831; PMCID: PMC6104637.