Of all the hormone-related topics that I have tried to understand, estrogen dominance has been one of the most confusing. The misconception for me was that if you have “estrogen dominance” then your ovaries must be producing too much estrogen. Outside of puberty and perimenopause, this is very rarely the case. The term estrogen dominance does not mean producing too much estrogen but rather that there is too much estrogen in relation to progesterone. It is entirely possible and in fact very common to have low estrogen but have estrogen dominance at the same time. Estrogen dominance does not necessarily mean that estrogen levels are too high, but rather that they are too high in relation to progesterone. This can take many forms including:
- no ovulation: some level of estrogen, but no progesterone
- high estrogen, normal progesterone
- high estrogen, low progesterone
- normal estrogen, low progesterone
- low estrogen, lower progesterone
Women who do not ovulate regularly (eg. PCOS) are by default estrogen dominant. This is not because they produce too much estrogen, this is simply because a failure to ovulate means a failure to produce progesterone so by default there is more estrogen in relation to progesterone when there is no ovulation. Things become more confusing in cases of hypothalamic ammenorrhea as this is not a state of estrogen excess, but rather an estrogen deficiency. It’s important to get the right diagnosis in order to avoid inappropriate treatment.
For women who do ovulate regularly and have regular periods, estrogen dominance is rarely an issue of overproduction of estrogen from the ovaries but rather an issue with how much estrogen is retained in the body. In order to understand this, it is important to understand the pathway of estrogen throughout the body:
How it all works:
The pituitary gland in the brain sends a signal to the ovary to produce estrogen. Once estrogen is released it is moved out to affect its target tissue (eg. the uterus, the brain, the bones, the heart). Once estrogen has completed its important work it is then moved to the liver to be metabolised. The liver will then move the estrogen to the gall bladder. It then moves to the intestines/gut for excretion out of the body. Estrogen also gets excreted in the urine via the kidneys. If the liver, gall bladder or gut are overburdened or unbalanced this often leads to an inability of the body to successfully break down and eliminate estrogen. Estrogen then recirculates or re-enter the system leading to symptoms of estrogen excess. It does this through enterohepatic circulation which describes the circulation of substances from the liver to the gut and back to the liver. Furthermore, the liver can choose to metabolise estrogen into less favourable estrogen metabolites. These metabolites are more potent and toxic and are associated with increase risk of estrogenic conditions including breast cancer. Common symptoms of estrogen dominance are fibrocystic breasts, heavy and painful periods, PMS symptoms and cyclical mood swings, ovarian cysts, uterine fibroids and estrogenic cancers.
The Liver
The liver’s job is to process fat soluble estrogen into a water soluble form to make it inactive in the body and ready for excretion. It does this through phase I and phases II liver detoxification pathways. Phase I liver detoxification converts estrogen into “intermediary metabolites.” These metabolites can be more or less toxic depending on the type of metabolite produced. Hyrdoxy 2, 4 and 16 are the main estrogen metabolites produced by the liver. Hydroxy 2 is considered safe but hydroxy 4 and 16 are considered more estrogenic. The aim then becomes helping the liver choose the safest pathway for estrogen metabolism. There are three main obstacles that can get in the way of efficient metabolism of estrogen in the liver:
1. Toxins
2. Nutrient deficiencies
3. Stress
Toxins: Alcohol, medications and recreational drugs are highly toxic to the body. Other environmental toxins that can burden the liver include chemical food additives, herbicides & pesticides, cosmetics, plastics and cleaning products. In the presence of more threatening toxins, estrogen is deemed lower priority for metabolism and so a potential build up of estrogen can occur.
Nutrient deficiencies: Liver function is highly nutrient dependant. The liver needs nutrients including protein, fat-soluble vitamins A D E and K, magnesium, zinc, selenium, all B vitamins and many other phytochemicals like DIM, sulforaphane and betalain in order to function optimally. For women, nutrient deficiencies may be caused by inadequate diet or low calorie intake (including excessive intermittent fasting) but often they are also caused by nutrient depletion following hormonal contraception, various medications and periods of stress, illness and trauma. This includes periods of intense nutrient demand such as pregnancy, breastfeeding or intense physical exercise.
Stress: Cortisol and adrenalin (stress hormones) must also be broken down in the liver for elimination. In the presence of too much cortisol and adrenalin, the liver struggles to also process estrogen. Cortisol lowers the ovarian output of estrogen and progesterone while simultaneously raising circulating estrogen levels. The solution to improving estrogen dominance by optimising liver function is to reduce external toxin exposure, correct any nutritional deficiencies and lower stress.
Gall bladder
The main role of the gall bladder is to process fat. The exact role of the gall bladder in processing estrogen is not well understood however we know that periods of high estrogen exposure such as in pregnancy, using synthetic estrogens in hormonal birth control as well as hormone replacement therapy (HRT) increase cholesterol production in the liver which can burden the gall bladder and lead to gallstones. At the same time, high-fat diets have been shown in studies to increase estrogen in the body. High fat leads to high estrogen and high estrogen leads to high cholesterol. Studies show fat greatly increases the reabsorption of estrogen from bile secretions leading to estrogen dominance. Conversely, removal of the gall bladder leads to a sharp increase in estrogen dominance symptoms shortly after surgery. Gall bladder issues that relate to estrogen dominance are more likely to occur in the perimenopause period when estrogen levels are fluctuating and varying changes in metabolism occur.
Improving gall bladder function is dependent on improving liver function, taking care not to overeat or consume overly fatty or greasy foods and avoiding exposure to external estrogens from hormonal birth control and HRT if possible and appropriate. Improving gall bladder function may improve both liver and gut function which can help minimise symptoms of estrogen dominance.
Intestines/Gut
The role of the gut is to safely remove metabolised estrogens from the body. Constipation can lead to the reabsorption of estrogen in the body. Regular bowel movements (1-3 times a day) are needed for adequate excretion of estrogen from the body. A good microbiome is also needed to help move estrogen out of the body. Various unfavourable bacterial strands have been shown to excrete an enzyme called beta-glucuronidase that can reactivate the inactive forms of estrogen which have been metabolised by the liver. This estrogen can then re-enter the bloodstream and recirculate in the body via enterohepatic circulation. You can read more about estrogen dominance and beta-glucaronidase here
Improving gut function can be complex and may need professional attention especially in cases of IBS or SIBO however a good place to start is increasing fibre intake through a wider diversity of plant foods. Fibre helps to trap estrogen in the stool while also helping to build a diverse and robust microbiome. Women consuming high-fibre diets show significant increased excretion of estrogen in the stool (up to 3x more than woman consuming low fibre diets).
External Estrogen
Toxic chemicals found in everyday cosmetics, cleaning products, as well as herbicides and pesticides, contain chemicals known as “xenoestrogens” which can mimic the action of estrogen and further increase the load of estrogen in the body. Animal products contain real estrogens produced in the body of the animals, even if the animals are not treated with added hormones. Environmental toxins such as pesticides are stored and concentrated within animal fat. This toxicity and high fat intake will simultaneously “clog” up liver cells and burden the gall bladder. Animal-based saturated fat is also shown to negatively impact the microbiome in the gut.
Congested Lymph
Little is understood about the role of lymph in hormone balance, however many traditional cultures around the world attribute many of the common hormone imbalance symptoms to a congested lymph and not to the hormones themselves. The lymph can help hormones flow more efficiently through the body, help break up the accumulation of hormones in various tissues including the breasts and uterus and speed up the removal of unwanted hormones out of the body. The lymphatic tissue needs mechanical stimulation in order to function. Appropriate exercise is needed to help move the lymph and therefore sedentary lifestyles may prove to be problematic for women with estrogen dominance. Lymph can also be moved through massage and lymphatic drainage techniques and adequate hydration. Castor oil packs are also beneficial for lymph in women. Read my article on castor oil for women here
Body Fat
There is a strong relationship between fat and estrogen. Too little body fat can lower estrogen produced by the ovary leading to a lack of ovulation and loss of periods (this is partially why many women with eating disorders lose their periods). Conversely, having too much body fat can lead to estrogen dominance. This is because fat cells create estrogen and the more fat cells there are the more estrogen is produced. Excess body fat can lead to estrogen-dominance symptoms as mentioned above.
References:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5580118/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756670/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2656650/
https://pubmed.ncbi.nlm.nih.gov/3628202/
https://pubmed.ncbi.nlm.nih.gov/30655101/
https://cebp.aacrjournals.org/content/27/5/585
