Commentary and Fact Check of Dr. Jerilynn Prior’s 2019 Review on Progesterone for Transfeminine People
By Aly W. | First published March 23, 2019 | Last modified December 20, 2020
In 2019, Dr. Jerilynn Prior, who among other things was responsible for the adoption of spironolactone in transfeminine hormone therapy in the 1980s, published a literature review arguing for the use of progesterone in transfeminine people. She based her claims on research from other research areas such as progesterone in cisgender women. However, many of Prior’s claims in the review are poorly supported or obviously incorrect. Accordingly, a letter to the editor by seven researchers including major figures in transgender medicine was published in response to Prior’s review and was critical of her claims. The purpose of this article is to serve as a commentary and fact check on some of the problematic claims made in Prior’s review. It is concluded that Prior’s review on progesterone for transfeminine people should be considered with a great deal of caution and skepticism.
In early 2019, a literature review on progesterone in transfeminine people was published by a researcher known as Dr. Jerilynn C. Prior (some biography below).
- Prior, J. C. (2019). Progesterone is Important for Transwomen’s Therapy—Applying Evidence for the Benefits of Progesterone in Ciswomen. The Journal of Clinical Endocrinology & Metabolism, 104(4): 1181–1186, [DOI:10.1210/jc.2018-01777]
Prior is notable in that she prioneered the use of spironolactone in transfeminine people in the 1980s (Prior et al., 1986 [PDF]; Prior et al., 1989). She has also been a longtime researcher into and advocate for use of progesterone in hormone therapy for cisgender women.
In her 2019 review, Prior argues that progesterone has many beneficial effects and should be used in all transfeminine people. Reading through it however, it quickly became clear to me that there were a lot of problematic claims in the review. Indeed, a letter to the editor against the review (see below), coauthored by seven researchers in the field of transgender medicine—including major and well-known experts like Guy T’Sjoen and Joshua Safer—was published in response to the review.
Some of Prior’s points regarding progesterone are extrapolated from studies on ovulation in cisgender women. I’m not well-acquainted with the lierature on the health effects of ovulation in cisgender women, so I can’t speak for what Prior says in this regard. But I can say that a number of her statements in the paper stood out to me as clearly incorrect. As evidenced by the letter to the editor below, other researchers had qualms with her paper as well. I’d like to highlight some of the problems with her review in this article so that others can be aware of them and maintain skepticism. The title of this paper and its content are likely to be attractive to many transfeminine people, and we don’t want people to unknowingly accept incorrect information.
The format as follows is excerpts from the paper followed by responses.
It is important to add progesterone to estradiol and an antiandrogen in transgender women’s CHT. Progesterone may add the following: (i) more rapid feminization, […] (iii) optimal breast maturation to Tanner stages 4/5 […]
In my clinical experience, feminization occurred more rapidly with E2 and antiandrogens plus progesterone than with E2 and antiandrogens alone.
There is also clinical evidence that breast maturation occurs on progesterone in men (7).
Progesterone plus E2 leads to optimal breast maturation and size. Along with elimination of facial and male pattern body hair, one of the important goals of transgender women is to develop mature and physiological breasts (that are classified as Tanner stage 5) (26). However, currently, the majority seeks breast augmentation surgery (3), because E/E2 plus antiandrogen therapy means the areola stays small (≤2.5 cm, ≤1 inch) and masculine, and breasts remain Tanner stage 3 (27). P4 is necessary for the ductal branching within the breast (and hence, for lactation) (28) and eventual maturation leading to the enlargement of the normal ciswoman’s areola diameter of ≥3 cm (7). Currently reviewed evidence (29, 30) is inadequate to assess the breast effects of transgender women’s CHT, because breast size, not areolar diameter (the primary difference between Tanner 3 and 5 stages) (26), has so far gone unreported except by one research group (7).
Also this, from another (2011) paper by Prior (Prior, 2011):
E2 stimulates breast glandular development in puberty (Tanner stages I-III) while P4 (plus E2) is required for final breast maturation to Tanner stages IV-V as the areolar diameter expands and the ductal system and nipple mature (Prior et al., 1989); […]
There is no evidence at present that progesterone is involved in feminization in either cisgender women or transfeminine people (Wiki; Wiki). Prior’s clinical experience is anecdotal and isn’t admissible as evidence. Likewise, there is no evidence that progesterone is involved in morphological pubertal breast development in cisgender girls or transfeminine people (Aly W., 2018; Wiki). That is, there is no evidence that progesterone is involved in breast development when it comes to size and shape at any other time besides pregnancy/lactation. As I’ve described elsewhere, cisgender women with complete androgen insensitivity syndrome (CAIS) have negligible levels of progesterone (<1 ng/mL) yet are perfectly phenotypically female, including having well-developed breasts and even breasts that are reportedly above average in size (Aly W., 2020). Hence, progesterone would appear to not be needed for complete feminization nor morphological pubertal breast development.
Checking Prior’s cited source (“(7)” or “Prior et al., 1989”) for her claims about progestogens and breast development, the study used medroxyprogesterone acetate, not progesterone, and there was no actual mention of enhanced breast development or movement to Tanner stage 4/5 due to progestogens. I emailed Prior about this and other issues and she didn’t respond (despite responding to an earlier email I sent her asking about her 1986 paper she published—which she declined to provide). The study cited was actually her own 1989 publication however, and in her response to the letter to the editor to her 2019 review (which also challenged her on this), she claimed the following:
I appreciate that we currently have no systematic assessments of transgender women’s lobular breast maturation as likely reflected by differences in areolar size. A testable hypothesis is that that the areola will enlarge with estrogen-progesterone therapy; we showed this in early photo-documented clinical observations.3
However, Prior observed areolar enlargement with combined estrogen and medroxyprogesterone acetate therapy. She didn’t compare estrogen alone versus the combination. As estrogens are already known to cause areolar enlargement, it’s not possible to conclude to what extent estrogen versus the progestogen was involved in the breast changes and there’s no way to know whether medroxyprogesterone acetate provided any additional benefit over estrogen alone.
It may also be inadvisable to take progesterone too early (before Tanner breast stage 4 or 5), as progesterone induces lobuloalveolar maturation and hypothetically might interfere with normal pubertal breast development (Kay C. & Aly W., 2019).
The recent Endocrine Society clinical practice guidelines for “gender dysphoric/gender incongruous persons” advise clinicians to “maintain sex hormone levels within the normal range for the person’s affirmed gender” (1). Every normal, fertile, menstrual cycle in cisgendered women (whose gender identity as women aligns with their female sex assigned at birth) ideally produces progesterone, as well as estradiol (E2). Therefore, rather than being treated with daily E2 and an antiandrogen, as is the current clinical practice, to follow guidelines, we need to prescribe oral micronized progesterone (referred to in this article as progesterone) as an at least cyclic component of treatment of all transgender women (gender dysphoric men to women).
The 300-mg progesterone dose maintains the P4 blood level in the ciswoman’s luteal phase range (the desired goal) for the full 24 hours (38).
Prior advocates for the use of oral micronized progesterone in all transfeminine people. She furthermore claims that 300 mg/day oral progesterone maintains progesterone levels in the luteal range. However, in actuality, oral progesterone has very poor bioavailability, achieves low levels of progesterone that are far below normal luteal phase levels, and has weak progestogenic effects (Aly W., 2018; Wiki; Wiki-Graphs). Pharmacokinetic findings of high, luteal-phase progesterone levels with oral progesterone were from old studies that used flawed blood-analytic techniques. As such, while oral progesterone is effective for preventing endometrial hyperplasia in cisgender women, it likely has little effectiveness as a progestogen in transfeminine people.
When E or E2 treatments are prescribed for transgender women, I believe it is important to use physiological dose E2, delivered transdermally (either as a gel or patch). […] transdermal E2 carries less increased risk for venous thromboembolism (VTE) (21). Knowing what we now know about risks for VTE in transgender women (5), I believe that E2 should not be given orally.
I agree with Prior that estradiol should be used non-orally instead of orally. It’s well-established based on large observational studies that oral estradiol poses a significantly greater risk of blood clots than does transdermal estradiol (Aly W., 2020). There is no reason, aside from the critical issues of cost and convenience, for oral estradiol to be used in transfeminine people over non-oral forms of estradiol. In any case, the absolute risk of blood clots is very low even with oral estradiol (Arnold et al., 2016; Vinogradova, Coupland, & Hippisley-Cox, 2019).
I also believe that higher E2 doses (arbitrarily, more than double physiological) carry increased risks (note that the mean dose in the large Goodman study was 4 mg of oral E2, where a physiological ciswoman dose is 0.5 to 1.0 mg/d) (5). […] Both oral E/E2 and higher doses are associated with an increased risk of VTE and pulmonary embolism in transgender women (2, 5, 23), and the recent paper also showed increased ischemic stroke (5). These are life-threatening, adverse effects that can be devastating for a transgender woman and therefore, when possible, using transdermal E2 and lower doses, should be avoided.
[Progesterone] may also facilitate transgender women’s acceptance of physiological (rather than high) E2 doses ideally delivered transdermally.
While higher oral estradiol doses (e.g., 2 to 8 mg/day) likely do pose a higher risk of blood clots than the lower doses that Prior proposes, and while transdermal estradiol is certainly preferable, the absolute risk of blood clots with even high doses of oral estradiol is likely to be very low in most transfeminine people and is likely specific to those with risk factors like older age, smoking, obesity, concomitant progestin use, and others (Aly W., 2020). Hence, I take issue with Prior’s statements here; while oral estradiol does have greater risk than non-oral estradiol, I feel that her tone is exaggerated. Oral estradiol is widely used in both cisgender women and transfeminine people and is considered to be reasonably safe (e.g., Stuenkel et al., 2015; Hembree et al., 2017).
Also, 0.5 to 1.0 mg/day estradiol is not a physiological dosage of oral estradiol, at least for premenopausal-age cisgender women. This dosage results in very low menopausal replacement levels of estradiol that are well under 50 pg/mL (Aly W., 2020). For transfeminine people who have undergone gonadectomy and are in the age range of a premenopausal woman (i.e., less than 50 years of age), estradiol levels should be in the normal physiological range for premenopausal women. This range is about 50 to 200 pg/mL generally with an integrated average of around 100 pg/mL (Aly W., 2018). Only doses of oral estradiol of 4 to 8 mg/day (and sometimes not even then) are typically able to achieve such levels. (This is additional support for the use of non-oral estradiol, which can more easily achieve such levels, and then some, plus with lower risks.)
High oral estradiol doses also are not arbitrary, as they are needed for adequate testosterone suppression in transfeminine people (see immediately below).
Progesterone suppresses LH and T in men (17), […]
Progesterone feeds back to the hypothalamus slowing the pulsatility of LH and lowering average LH levels (25), thus decreasing gonadal T production. Again, this is an action of P4/progesterone to assist antiandrogen therapy in achieving a feminine shape and secondary sexual characteristics.
For metabolic and antiandrogen effects [to suppress LH and gonadal testosterone (T) and inhibit the conversion of T to dihydro-T (DHT)], I suggest that transgender women’s progesterone be given daily rather than cyclically, […]
Prior says that progesterone suppresses luteinizing hormone and testosterone levels. But checking her source, it was for medroxyprogesterone acetate. She advocates for the use of oral micronized progesterone (rather than non-oral progesterone or a progestin), yet oral micronized progesterone has been shown to have no effect on testosterone levels in cisgender men even at high doses (400 mg/day) (Wiki). Conversely, non-oral progesterone, including for example rectal administration and intramuscular injection, shows strong testosterone suppression (Wiki; Aly W., 2019). Progestogens in general can maximally suppress testosterone levels by about 50 to 70% (Aly W., 2019; Wiki). Hence, progesterone and other progestogens can be very useful for testosterone suppression, but in the case of progesterone, only if it is taken non-orally; oral progesterone is likely to be ineffective for such purposes.
Given the recent evidence that “low doses” of conjugated equine E (0.625 to 1.25 mg/d), with or without cyproterone acetate, lowered androgen, LH, and follicle-stimulating hormone levels into ciswoman ranges (22), it is not clear why higher E/E2 doses are commonly used for transgender women’s cross-sex hormone therapy (CHT).
The findings of Cunha and colleagues (Cunha et al., 2018) are very surprising and warrant skepticism. The study is contradicted by many other studies on the antigonadotropic effectiveness of estrogens (Wiki). Studies have generally found that estradiol levels of at least 200 pg/mL are needed to suppress testosterone levels to 50 ng/dL or less (Wiki). Cunha and colleagues found that 0.625 to 1.25 mg/day oral conjugated estrogens suppressed testosterone levels by 98% (732 ng/dL to 18 ng/dL), while estradiol levels were, surprisingly, unchanged (went from 45 to 38 pg/mL) (Cunha et al., 2018):
The estrogen levels before and after cross-sex hormone treatment were not significantly different (p=0.6) (Table 1). […] In our cohort, the estrogen levels before and after cross-sex hormone treatment were not significantly different. The conversion of male levels of T to estrogen before treatment was similar to that achieved by the low-dose estrogen treatment (30).
Other studies have found that a dosage of 7.5 mg/day oral conjugated estrogens is needed to consistently suppress testosterone levels into the castrate range (<50 ng/dL) in men with prostate cancer (Shearer et al., 1973; Wiki-Graph; Scott, Menon, & Walsh, 1980). Moreover, oral estradiol at up to 8 mg/day, with or without spironolactone, fails to suppress testosterone levels into the female range in many transfeminine people (Leinung, 2014; Liang et al., 2018; Leinung, Feustel, & Joseph, 2018; Cheung et al., 2018). (Note that in Leinung et al. (2018), mean estradiol levels ranged from about 50 to 150 pg/mL across a dosage range of 1 to 8 mg/day oral estradiol in transfeminine people. This is fairly consistent with other studies.) As such, we should be quite skeptical of the findings of Cunha and colleagues. Their results were probably due to flawed blood tests or some other methodological problem—particularly considering the lack of increase in estradiol levels.
Prior made no mention of the various other recent studies, which clearly show that even high (8 mg/day) doses of oral estradiol are often insufficient for suppressing testosterone levels into the female range. In addition, Prior herself showed in the 1980s that high doses of oral conjugated estrogens (e.g., 7.5 mg/day) were insufficient for adequate suppression of testosterone levels in transfeminine people (Prior et al., 1986; Prior et al., 1989). In fact, this was the reason for her advocacy of the use of spironolactone in transfeminine people (Prior et al., 1986; Prior et al., 1989).
[Progesterone] inhibits conversion of T to DHT in men (18), […]
Progesterone competes for the 5-alpha reductase enzyme that converts T into DHT (18), the hormone that masculinizes skin and hair follicles. Thus, progesterone decreases the masculinizing effects of DHT on unwanted male-pattern hair.
Progesterone is a 5α-reductase inhibitor in vitro, but this is almost certainly clinically insignificant even at pregnancy levels of progesterone (Wiki). Only topical progesterone locally in the skin is likely to have any meaningful inhibitory effects on 5α-reductase.
Progesterone and breast cancer risk. E (E or E2) with MPA increased the risks for breast cell proliferation and breast cancer, but there is increasing evidence that the opposite may occur with progesterone (15, 46). The large French E3N Prospective Cohort Study of menopausal therapy in ciswomen by its component characteristics showed no increased risk for breast cancer in women on E/E2 with progesterone, although the same study showed a significantly elevated risk with ET or EPT (14). The combined evidence suggested that progesterone would protect against the rare risk of breast cancer in transgender women treated with E.
Progesterone and cardiovascular effects. The assumption that progesterone causes adverse cardiovascular effects is primarily because of CVD related to androgenic progestins. However, there are no long-term RCT data on progesterone and cardiovascular effects and no progesterone therapy studies in which the primary outcomes are acute myocardial infarction, stroke, VTE, or heart failure. In part, at least, this is because oral micronized progesterone has only been available for a couple of decades. However, progesterone shows no signal for increased coagulation (21, 24). Progesterone has substantial random-ordered, positive endothelial effects compared with vehicle and E2 (20), but similar results did not reach significance in a 3-month RCT in menopausal ciswomen for which the endothelial function data were underpowered (42). In that same 3-month RCT, progesterone caused no changes in weight, waist circumference, blood pressure, inflammation, coagulation, or lipids (except a substantial but clinically unimportant lowering of high-density lipoprotein cholesterol) (42).
Decades ago, many researchers thought that progestogens might protect against breast cancer similarly to how they protect against estrogen-induced endometrial hyperplasia and endometrial cancer. However, numerous large observational studies, as well as the Women’s Health Initiative (a large randomized controlled trial), have since shown that progestins are associated with a significantly greater risk of breast cancer, as well as risk of blood clots and cardiovascular issues. Conversely, oral progesterone has been associated with no change in the risk of breast cancer, blood clots, and cardiovascular issues relative to estrogens alone. As a result, many researchers assumed that, for some reason, oral progesterone was different from progestins.
However, there is a problem in that this perception has come from studies that have used oral progesterone. As described above, oral progesterone has major bioavailability issues and weak progestogenic effects, which the biomedical community was originally not aware of. There have been no sufficiently powered studies using non-oral progesterone (e.g., vaginal, injected) that have shown that progesterone does not in fact have a risk of breast cancer, blood clots, or cardiovascular issues. As a result, assuming that progesterone does not have such risks is premature and non-oral progesterone may actually share similar risks as progestins (Kuhl & Schneider, 2013; Davey, 2018). This notion makes sense considering that both progesterone and progestins share the common action of progesterone receptor agonism and that this action is thought to underly much of the said risks (though not all; androgenic and/or glucocorticoid activities of certain progestins may contribute some to certain risks as well). With that said however, similarly to the case of oral estradiol, the risks are not marked, and apply largely to those with specific risk factors (e.g., old age). Progestins have been widely used in transfeminine people in the form of medroxyprogesterone acetate and cyproterone acetate and are reasonably safe.
Indeed, a large observational study found that long-term (10-year) treatment with oral progesterone was associated with a significantly increased risk of breast cancer, which has been said to be consistent with the low levels of progesterone achieved with oral progesterone having a weak proliferative effect on the breasts that requires a longer period of exposure to manifest as an increase in breast cancer risk (Kuhl & Schneider, 2013; Davey, 2018). Moreover, Prior’s claim that progesterone could decrease breast cancer risk is unfounded based on available clinical research (Aly W., 2020).
There is also clinical evidence that breast maturation occurs on progesterone in men (7).
The cited source indicates that the “men” Prior refers to here were in fact transgender women.
[…] we need to prescribe oral micronized progesterone (referred to in this article as progesterone) as an at least cyclic component of treatment of all transgender women (gender dysphoric men to women).
Gonadal steroids have sex-specific actions (16); thus, the application of data from progesterone actions in women to the care of those who were biological men before they became transgender women requires evidence.
The terminology used by Prior here, such as transgender women having been “gender dysphoric men” or “biological men” before they “became” transgender women, is outdated by modern standards and is likely to be insensitive and even offensive to many transfeminine people. Moreover, an argument can’t even be made that transfeminine children who transitioned young were ever “men”.
Terminology of the sort used by Prior is rarely seen in the literature on transgender health nowadays. I think that clinicians and researchers, including old-fashioned ones like Prior, should discard the disagreeable terminology of the past and become fully competent in more appropriate language. Much as how Prior previously referred to us as “male-to-female transsexuals” or “men” regardless of transition status (Prior et al., 1986; Prior et al., 1989; Basson & Prior, 1998)—but now no longer does so and instead (usually) refers to us as “transgender women”—she can change here as well.
The letter to the editor in response to Prior’s paper also challenged her claims that progesterone has beneficial effects on breast development, bone mineral density, breast cancer risk, and cardiovascular risk (see below). They criticized Prior’s extrapolation from clinical experience, preclinical research, and findings in cisgender women, calling instead for evidence-based recommendations based on rigorous and well-designed clinical studies in transfeminine people. They described Prior’s conclusions as “premature and potentially dangerous”. In her response, Prior claimed that they were conflating progesterone with progestins. This certainly may be true. But, as I described above, it may for the most part actually not be inappropriate to treat progesterone and progestins as a combined group, at least when the form of progesterone is not oral progesterone.
I should note that I am not opposed to the use of progesterone in transfeminine people. Rectal progesterone and progestins are very useful for suppressing testosterone levels in transfeminine people (Aly W., 2019; Aly W., 2019; Wiki). And, as pointed out by Madeline Deutsch—the editor of the University of California, San Francisco transgender health guidelines—the risks of progestogens are likely small in transfeminine people (Deutsch, 2016). While there are no certain benefits of progestogens aside from testosterone suppression, I think that if people want to, they should be able to try progesterone and other progestogens. Cisgender women have progesterone in their bodies, so it’s hard to make a case that transfeminine people absolutely should never have it in theirs.
On the issue of Prior and her review, I am simply interested in scientific accuracy and rigor, which I feel that her review falls quite short on. Moreover, I want to mention that my critique here is not comprehensive; I’ve largely only spoken on the issues that particularly stood out to me. As touched on by the letter to the editor, there are also other problems with the article.
On another note, this excerpt, from the letter to the editor, was also notable:
We await the World Professional Association for Transgender Health’s commissioned systematic review on progesterone use for the upcoming Standards of Care, 8th Version. We propose that RCTs, as advocated in the 2017 Endocrine Society Clinical Practice Guidelines(8), investigate the addition of P4 to current GAHT regimens and the risks/benefits of GAHT in older trans women.
Here is the letter to the editor in opposition to Prior’s review on progesterone for transfeminine people:
- Iwamoto, S. J., T’Sjoen, G., Safer, J. D., Davidge-Pitts, C. J., Wierman, M. E., Glodowski, M. B., & Rothman, M. S. (2019). Letter to the Editor: “Progesterone is Important for Transwomen’s Therapy—Applying Evidence for the Benefits of Progesterone in Ciswomen”, The Journal of Clinical Endocrinology & Metabolism, 104(8), 3127–3128. [DOI:10.1210/jc.2019-00249]
Prior replied to the letter to the editor in the following response:
- Prior, J. C. (2019). Response to Letter to the Editor: “Progesterone is Important for Transwomen’s Therapy—Applying Evidence for the Benefits of Progesterone in Ciswomen”, The Journal of Clinical Endocrinology & Metabolism, 104(8), 3129–3130. [DOI:10.1210/jc.2019-00524]
Some biography on Prior can be found here. She is a professor of Endocrinology and Metabolism at the University of British Columbia in Vancouver, British Columbia, Canada. She has studied and published on reproductive endocrinology since the 1980s.
Prior worked at the Vancouver Gender Clinic in the 1980s and was responsible for the 1986 and 1989 publications that led to the use of spironolactone in transfeminine people. Before that, cyproterone acetate was not available in Canada or the United States and high-dose estrogen monotherapy with oral estrogens like conjugated estrogens and ethinylestradiol was mainly used in transfeminine people. Her publications reported that spironolactone could decrease testosterone levels in transfeminine people and reduce needed doses of estrogens (Prior et al., 1986; Prior et al., 1989).
However, as other researchers have since pointed out (Leinung, Feustel, & Joseph, 2018), Prior’s study was confounded because of the concomitant use of medroxyprogesterone acetate, a known antigonadotropin which reduces testosterone levels itself (Aly W., 2018). In actuality, spironolactone does not consistently decrease testosterone levels in cisgender men or transfeminine people (Aly W., 2018) nor in cisgender women (Aly W., 2020). In any case, spironolactone is still an effective antiandrogen due to its antagonistic activity at the androgen receptor.
- Baxter, S., & Prior, J. C. (2009). The Estrogen Errors: Why Progesterone is Better for Women’s Health. Praeger Pub Text. [Official website] [CeMCOR page] [Amazon] [Google Books]
Prior has written the following notable papers and book chapters, among many others (Google Scholar):
- Basson, R. & Prior, J. C. (1998). Hormonal Therapy of Gender Dysphoria: The Male-to-Female Transsexual. In Concepts in Transgender Identity. Garland Publishing Inc, New York. [Google Books]
- Prior, J. C. (2008–2010). Preventive Powers of Ovulation and Progesterone. Centre for Menstrual Cycle and Ovulation Research (CeMCOR). [Google Scholar] [PDF]
- Prior, J. C. (2011). Progesterone for Symptomatic Perimenopause Treatment—Progesterone Politics, Physiology and Potential for Perimenopause. Facts, Views & Vision in ObGyn, 3(2), 109–120. [PubMed] [PubMed Central]
- Prior, J. C. (2015). Progesterone or Progestin as Menopausal Ovarian Hormone Therapy: Recent Physiology-Based Clinical Evidence. Current Opinion in Endocrinology, Diabetes and Obesity, 22(6), 495–501. [DOI:10.1097/MED.0000000000000205]
- Prior, J. C. (2018). Progesterone for Treatment of Symptomatic Menopausal Women. Climacteric, 21(4), 358–365. [DOI:10.1080/13697137.2018.1472567]
- Prior, J. C. (2018). Progesterone for the Prevention and Treatment of Osteoporosis in Women. Climacteric, 21(4), 366–374. [DOI:10.1080/13697137.2018.1467400]
- Prior, J. C. (2020). Women’s Reproductive System as Balanced Estradiol and Progesterone Actions—A revolutionary, paradigm-shifting concept in women’s health. Drug Discovery Today: Disease Models, 30(20), 1–10. [DOI:10.1016/j.ddmod.2020.11.005]