Yet another study pouring cold water on the recent attempts of Big Pharma to tarnish the findings of the WHI and con women back into estrogenic HRT. This time, the study is about endometriosis and it looks like this condition may have its beginnings during pregnancy when the female fetus is exposed to higher levels of estrogen in-utero. This exposure apparently imprints the female offspring for higher risk of endometrial cells proliferation and as such not only increases the risk of endometriosis, but also of endometrial cancer. In addition to exposing estrogen is a clear culprit in yet another conditions that Big Pharma claims would be “helped” by estrogenic HRT, the study also pours cold water on the claims that endometriosis is largely genetic in origin. In addition, the study busts yet another myth in regards to female reproductive health. Namely, that androgens, being strictly “male” hormones, are detrimental to female health. The study found that exposure to high estrogen and/or low androgens (e.g. testosterone, DHEA, DHEA-S, androstenedione) was linked to endometriosis later in the female offspring’s life. It is well-known in research (but not medical) circles that most androgens are an antagonist of the estrogen receptor. This fact was the reason testosterone was used as a therapy with high success rate for even terminal breast cancer in women up until the late 1960s, before more “advanced” (read: cytotoxic) therapies emerged. The beneficial effects of androgens in breast cancer led to the synthesis and FDA approval of the DHT-derived androgenic and non-aromatizable steroid known as Drostanolone/Masteron, which remains approved by FDA for breast cancer to this day, yet this fact is unknown to the vast majority of OBGYN doctors and breast oncologists. As corollary, this finding highlights an important, but obscure, physiological fact. Namely, it is not the absolute estrogen levels that the female fetus is exposed to that matter the most, but rather the estrogens/androgens ratio. When that ratio is high due to either high estrogen and/or low androgens, estrogen runs unopposed due to deficiency of endogenous antagonists (e.g. androgens) to mitigate estrogen’s effects. As such, the fetus develops in a state of relative estrogen excess even if blood tests show that the mother’s estrogen levels are normal. Since virtually no doctor cares to test a woman’s androgen levels, especially during pregnancy, the pre-conditions for offspring endometriosis would likely go unnoticed even in women with severe, relative estrogen dominance characterized by normal estrogen levels, but low androgen levels. Finally, this study once again underscores the importance of progesterone and progesterone therapy in pregnancy, as progesterone is the main endogenous estrogen antagonist in women, while androgens are the dominant one in males.
https://link.springer.com/article/10.1186/s12958-025-01467-z
Endometriosis Linked to Higher In Utero Estradiol Exposure in Female Offspring
“…To assess differences in umbilical cord estradiol (E2) and androgen levels among female offspring from women with and without endometriosis, investigators conducted a case-control study. Participants included women with no pre-existing health conditions delivering a female singleton at gestational age of more than 32 weeks. Endometriosis was confirmed before pregnancy by surgery or imaging; women in the control group had no previous endometriosis diagnosis, as well as a history of regular menstrual cycles. Among the total cohort of 160 women, 10.6% had endometriosis; propensity score matching (PSM) was 1:3 with 51 women in the control group without endometriosis. After PSM, factors known to influence the outcome measure were well-balanced between those with vs without endometriosis, including maternal age (35.8 vs 35.7 years) and gestational age at delivery (275.2 vs 277.7 days). Women with vs without endometriosis had higher median (IQR) levels of E2 before (6.8 [4.3-9.1] µg/L vs 3.6 [1.4-8.6] µg/L; P =.03) and after (6.8 [4.3-9.1] µg/L vs 2.4 [1.1-6.6] µg/L; P =.002) PSM, respectively. Compared with control individuals, women with endometriosis had a higher-estrogen, lower-androgen hormonal status, indicated by elevated ratios of:
- E2-to-testosterone (P <.001);
- E2-to-dehydroepiandrosterone (DHEA; P <.001);
- E2-to-DHEA sulfate (DHEAS; P <.001); and,
- E2-to-androstenedione (P =0.001).
Following PSM, the ratios were higher by factors of:
- 4.38 (95% CI, 2.28-6.49; E2-to-testosterone);
- 2.52 (95% CI, 1.32-3.72; E2-to-DHEA);
- 4.57 (95% CI, 1.86-7.27; E2-to-DHEAS); and,
- 3.28 (95% CI, 1.29-5.28; E2-to-androstenedione).
…”
“…“Our findings provide biological evidence supporting the hypothesis that endometriosis susceptibility originates from an imbalance of high estrogen and low testosterone during fetal development — a hormonal environment that ‘programs’ female reproductive traits and may drive in utero susceptibility to endometriosis,” the study authors concluded.”
