The Connection Between Estrogen and Endometriosis
For those unfamiliar with the underpinnings of endometriosis, many may be surprised to find out that the disease is often fueled by estrogen. Estrogen is the primary female sex hormone and is vital in the sexual and reproductive development of women. There are 4 types of estrogen: estrone (E1), estradiol (E2), estriol (E3), and estetrol (E4). Estriol is the most plentiful of these estrogens, but estradiol is the strongest, as well as the most active and prominent, during a woman’s reproductive years (from the time of her first period until she hits menopause).
So, if estrogen is a dominant hormone found in all people who menstruate, how come only a fraction of those who ovulate and menstruate suffer from endometriosis?
The role of estrogen dominance
Some researchers posit that people with endometriosis have a problem with estrogen dominance- that is, they have higher-than-usual amount of estrogen in their bodies as compared to others. This overabundance of estrogen is believed to proliferate the growth of endometrial lesions in the body. A study from 20 years ago supported this idea when researchers confirmed that prescribing treatments to endometriosis patients that reduced their estrogen levels also led to reductions (sometimes significant) in pelvic pain and other symptoms associated with the disease.1
Unfortunately, these treatments were on the extreme side. In particular, they included a bilateral oophorectomy- which is the surgical removal of both ovaries; or, as an alternative, the use of gonadotropin releasing hormone (GnRH) agonist treatment. An oophorectomy of both ovaries will effectively cease estrogen production (since ovaries are the organs responsible for releasing them) and cause the patient to go into immediate menopause. GnRH is the hormone responsible for the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH). Therefore, a GnRH agonist basically induces temporary menopause for the time one is taking it, so side effects are similar to menopause, and include hot flashes, mood swings, decreased libido, and dizziness. Yet, GnRH has the benefit of being reversible (at least for most), unlike the surgical removal of ovaries, which is permanent. Both treatments risk a long-term impact of developing osteoporosis since estrogen is vital for bone density. For this reason, sometimes a patient takes a low-dose estrogen supplement in an attempt to ward off this impact.
The role of estrogen exposure
Of course, this still doesn’t answer why some people seem to make more estrogen and so are more predisposed toward developing endo than others. Some researchers now believe those with endometriosis were exposed to an excess of estrogen while in their mothers’ wombs. Strangely, female babies who were exposed to excess estrogens in utero while fetuses, tend to have their genitals located close to their the anus than those who weren’t.
As such, a 2017 study from Spain discovered that they were able to predict not only endometriosis in those with these short distances in those anatomical features, but even certain subtypes of endo.2 For instance, those who suffer the most severe form of endo- known as deep-infiltrating endometriosis (which infiltrates into the bowels, bladder, and other pelvic organs)- tend to also have the shortest distance between their genitals and anus of all the study participants. This further supports the theory that exposure to surplus estrogens during fetal development increases risks for endometriosis. This excess in estrogen exposure could be be naturally occurring. They could also be due to exposure with environmental chemicals that mimic estrogens- also known as xenoestrogens, which are found in things like plastics and personal care products. Overexposure to plant estrogens, known as phytoestrogens, which are found in foods like soy, can also contribute to this anatomical difference and seems to be complicit in contributing to endo.
Have you heard about the new tampon technology currently being tested to detect endometriosis?