Feminizing hormone therapy
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Feminizing hormone therapy, also known as transfeminine hormone therapy, is
The purpose of the therapy is to cause the development of the secondary sex characteristics of the desired
Feminizing hormone therapy has been empirically shown to reduce the distress and discomfort associated with gender dysphoria in transfeminine individuals.[7][8][9]
Requirements
Many physicians operate by the
Medications used in transgender hormone therapy are also sold without a prescription on the
The accessibility of transgender hormone therapy differs throughout the world and throughout individual countries.[2]
Medications
Medication | Brand name | Type | Route | Dosage[b] |
---|---|---|---|---|
Estradiol | Various | Estrogen | Oral | 2–10 mg/day |
Various | Estrogen | Sublingual | 1–8 mg/day | |
Climara[c] | Estrogen | TD patch | 25–400 μg/day | |
Divigel[c] | Estrogen | TD gel | 0.5–5 mg/day | |
Various | Estrogen | SC implant | 50–200 mg every 6–24 mos | |
Estradiol valerate | Progynova | Estrogen | Oral | 2–10 mg/day |
Progynova | Estrogen | Sublingual | 1–8 mg/day | |
Delestrogen[c] | Estrogen | IM, SC | 2–10 mg/wk or 5–20 mg every 2 wks | |
Estradiol cypionate | Depo-Estradiol | Estrogen | IM, SC | 2–10 mg/wk or 5–20 mg every 2 wks |
Estradiol dipropionate | Agofollin | Estrogen | IM, SC | 2–10 mg/wk or 5–20 mg every 2 wks |
Estradiol benzoate | Progynon-B | Estrogen | IM, SC | 0.5–1.5 mg every 2–3 days |
Estriol | Ovestin[c] | Estrogen | Oral | 4–6 mg/day |
Spironolactone | Aldactone | Antiandrogen | Oral | 100–400 mg/day |
Cyproterone acetate | Androcur | Antiandrogen; Progestogen |
Oral | 5–100 mg/day |
Androcur Depot | IM | 300 mg/month | ||
Bicalutamide | Casodex | Antiandrogen | Oral | 25–50 mg/day |
Enzalutamide | Xtandi | Antiandrogen | Oral | 160 mg/day |
GnRH analogue
|
Various | GnRH modulator | Various | Variable |
Elagolix | Orilissa | GnRH antagonist | Oral | 150 mg/day or 200 mg twice daily |
Finasteride | Propecia | 5αR inhibitor | Oral | 1–5 mg/day |
Dutasteride | Avodart | 5αR inhibitor | Oral | 0.25–0.5 mg/day |
Progesterone | Prometrium[c] | Progestogen | Oral | 100–400 mg/day |
Medroxyprogesterone acetate | Provera | Progestogen | Oral | 2.5–40 mg/day |
Depo-Provera | Progestogen | IM | 150 mg every 3 mos | |
Depo-SubQ Provera 104 | Progestogen | SC | 104 mg every 3 mos | |
Hydroxyprogesterone caproate | Proluton | Progestogen | IM | 250 mg/wk |
Dydrogesterone | Duphaston | Progestogen | Oral | 20 mg/day |
Drospirenone | Slynd | Progestogen | Oral | 3 mg/day |
Domperidone[d] | Motilium | Prolactin releaser | Oral | 30–80 mg/day[e] |
|
A variety of different
Estrogens
In addition to producing feminization, estrogens have
Prior to
Antiandrogens
Antiandrogens that directly block the androgen receptor are known as
Steroidal antiandrogens
Steroidal antiandrogens are antiandrogens that resemble steroid hormones like testosterone and progesterone in chemical structure.[83] They are the most commonly used antiandrogens in transgender women.[2] Spironolactone (Aldactone), which is relatively safe and inexpensive, is the most frequently used antiandrogen in the United States.[84][85] Cyproterone acetate (Androcur), which is unavailable in the United States, is widely used in Europe, Canada, and the rest of the world.[2][68][84][86] Medroxyprogesterone acetate (Provera, Depo-Provera), a similar medication, is sometimes used in place of cyproterone acetate in the United States.[87][88]
Spironolactone is an
Cyproterone acetate is an antiandrogen and progestin which is used in the treatment of numerous
Medroxyprogesterone acetate is a progestin that is related to cyproterone acetate and is sometimes used as an alternative to it.[87][88] It is specifically used as an alternative to cyproterone acetate in the United States, where cyproterone acetate is not approved for medical use and is unavailable.[87][88] Medroxyprogesterone acetate suppresses testosterone levels in transgender women similarly to cyproterone acetate.[88][47] Oral medroxyprogesterone acetate has been found to suppress testosterone levels in men by about 30 to 75% across a dosage range of 20 to 100 mg/day.[120][121][122][123][124] In contrast to cyproterone acetate however, medroxyprogesterone acetate is not also an androgen receptor antagonist.[48][125] Medroxyprogesterone acetate has similar side effects and risks as cyproterone acetate, but is not associated with liver problems.[126][99]
Numerous other progestogens and by extension antigonadotropins have been used to suppress testosterone levels in men and are likely useful for such purposes in transgender women as well.[127][128][129][130][131][132][133] Progestogens alone are in general able to suppress testosterone levels in men by a maximum of about 70 to 80%, or to just above female/castrate levels when used at sufficiently high doses.[134][135][136] The combination of a sufficient dosage of a progestogen with very small doses of an estrogen (e.g., as little as 0.5–1.5 mg/day oral estradiol) is synergistic in terms of antigonadotropic effect and is able to fully suppress gonadal testosterone production, reducing testosterone levels to the female/castrate range.[137][138]
Nonsteroidal antiandrogens
Nonsteroidal antiandrogens are antiandrogens which are nonsteroidal and hence unrelated to steroid hormones in terms of chemical structure.[83][139] These medications are primarily used in the treatment of prostate cancer,[139] but are also used for other purposes such as the treatment of acne, excessive facial/body hair growth, and high androgen levels in women.[15][140][141][142] Unlike steroidal antiandrogens, nonsteroidal antiandrogens are highly selective for the androgen receptor and act as pure androgen receptor antagonists.[139][143] Similarly to spironolactone however, they do not lower androgen levels, and instead work exclusively by preventing androgens from activating the androgen receptor.[139][143] Nonsteroidal antiandrogens are more efficacious androgen receptor antagonists than are steroidal antiandrogens,[83][144] and for this reason, in conjunction with GnRH modulators, have largely replaced steroidal antiandrogens in the treatment of prostate cancer.[139][145]
The nonsteroidal antiandrogens that have been used in transgender women include the first-generation medications
Nonsteroidal antiandrogens like bicalutamide may be a particularly favorable option for transgender women who wish to preserve
GnRH modulators
There are two types of GnRH modulators:
GnRH modulators are highly effective for testosterone suppression in transgender women and have few or no side effects when
In adolescents of either sex, GnRH modulators can be used to suppress puberty. The eighth edition of the World Professional Association for Transgender Health's Standards of Care permit its use from Tanner stage 2 and recommends GnRH agonists as the preferred method of puberty blocking.[183]
5α-Reductase inhibitors
5α-Reductase inhibitors include
5α-Reductase inhibitors are sometimes used as a component of feminizing hormone therapy for transgender women in combination with estrogens and/or other antiandrogens.[4][209][64] They may have beneficial effects limited to improvement of scalp hair loss, body hair growth, and possibly skin symptoms such as acne.[210][2][211][64] However, little clinical research on 5α-reductase inhibitors in transgender women has been conducted, and evidence of their efficacy and safety in this group is limited.[209][212] Moreover, 5α-reductase inhibitors have only mild and specific antiandrogenic activity, and are not recommended as general antiandrogens.[212]
5α-Reductase inhibitors have minimal side effects and are well tolerated in both men and women.
Progestogens
There are two types of progestogens: progesterone, which is the
Clinical research on the use of progestogens in transgender women is very limited.[2][226] Some patients and clinicians believe, on the basis of anecdotal and subjective claims, that progestogens may provide benefits such as improved breast and/or nipple development, mood, and libido in transgender women.[4][3][226] There are no clinical studies to support such reports at present.[2][4][226] No clinical study has assessed the use of progesterone in transgender women, and only a couple of studies have compared the use of progestins (specifically cyproterone acetate and medroxyprogesterone acetate) versus the use of no progestogen in transgender women.[226][235][176] These studies, albeit limited in the quality of their findings, reported no benefit of progestogens on breast development in transgender women.[226][176][210] This has also been the case in limited clinical experience.[236]
Progestogens have some
In terms of the effects of progestogens on sex drive, one study assessed the use of dydrogesterone to improve sexual desire in transgender women and found no benefit.[233] Another study likewise found that oral progesterone did not improve sexual function in cisgender women.[251]
Progestogens can have
Progesterone is most commonly taken orally.[48][256] However, oral progesterone has very low bioavailability, and produces relatively weak progestogenic effects even at high doses.[259][260][256][261][262] In accordance, and in contrast to progestins, oral progesterone has no antigonadotropic effects in men even at high doses.[253][263] Progesterone can also be taken by various parenteral (non-oral) routes, including sublingually, rectally, and by intramuscular or subcutaneous injection.[48][243][264] These routes do not have the bioavailability and efficacy issues of oral progesterone, and accordingly, can produce considerable antigonadotropic and other progestogenic effects.[48][261][265] Transdermal progesterone is poorly effective, owing to absorption issues.[48][243][262] Progestins are usually taken orally.[48] In contrast to progesterone, most progestins have high oral bioavailability, and can produce full progestogenic effects with oral administration.[48] Some progestins, such as medroxyprogesterone acetate and hydroxyprogesterone caproate, are or can be used by intramuscular or subcutaneous injection instead.[266][243] Almost all progestins, with the exception of dydrogesterone, have antigonadotropic effects.[48]
Miscellaneous
The
Interactions
Many of the medications used in feminizing hormone therapy, such as
Effects
The spectrum of effects of hormone therapy in transfeminine people depend on the specific medications and dosages used. In any case, the main effects of hormone therapy in transfeminine people are
Effect | Time to expected onset of effect[a] |
Time to expected maximum effect[a][b] |
Permanency if hormone therapy is stopped |
---|---|---|---|
Breast development and nipple/areolar enlargement | 2–6 months | 1–5 years | Surgically reversible |
Thinning/slowed | 4–12 months | >3 years[c] | Reversible |
Cessation/reversal of male-pattern scalp hair loss |
1–3 months | 1–2 years[d] | Reversible |
Softening of oiliness and acne |
3–6 months | Unknown | Reversible |
Redistribution of body fat in a feminine pattern | 3–6 months | 2–5 years | Reversible |
Decreased muscle mass/strength | 3–6 months | 1–2 years[e] | Reversible |
Widening and rounding of the pelvis[f] |
Unspecified | Unspecified | Permanent |
Changes in mood, emotionality, and behavior | Unspecified | Unspecified | Reversible |
Decreased sex drive |
1–3 months | Temporary[274] | Reversible |
Decreased morning erections |
1–3 months | 3–6 months | Reversible |
decreased ejaculate volume |
1–3 months | Variable | Reversible |
Decreased fertility |
Unknown | >3 years | Reversible or permanent[g] |
Decreased testicle size | 3–6 months | 2–3 years | Unknown |
Decreased penis size | None[h] | Not applicable | Not applicable |
Decreased prostate gland size |
Unspecified | Unspecified | Unspecified |
Voice changes | None[i] | Not applicable | Not applicable |
Footnotes and sources
Footnotes:
|
Breast development
Breast, nipple, and areolar development varies considerably depending on genetics, body composition, age of HRT initiation, and many other factors. Development can take a couple years to nearly a decade for some. However, many transgender women report there is often a "stall" in breast growth during transition, or significant breast asymmetry. Transgender women on HRT often experience less breast development than cisgender women (especially if started after young adulthood). For this reason, many seek breast augmentation. Transgender patients opting for breast reduction are rare. Shoulder width and the size of the rib cage also play a role in the perceivable size of the breasts; both are usually larger in transgender women, causing the breasts to appear proportionally smaller. Thus, when a transgender woman opts to have breast augmentation, the implants used tend to be larger than those used by cisgender women.[285]
Breast development in transgender women begins within two to three months of the start of hormone therapy and continues for up to two years.[286][211] Breast development seems to be better in transgender women who have a higher body mass index.[286][211] As a result, it may be beneficial to breast development for thin transgender women to gain some weight in the early phases of hormone therapy.[286][211] Different estrogens, such as estradiol valerate, conjugated estrogens, and ethinylestradiol, appear to produce equivalent results in terms of breast sizes in transgender women.[286][235][176] The sudden discontinuation of estrogen therapy has been associated with onset of galactorrhea (lactation).[286][211]
Skin changes
Estrogens cause the accumulation of
Sebaceous gland activity (which is triggered by androgens) lessens, reducing oil production on the skin and scalp. Consequently, the skin becomes less prone to acne. It also becomes drier, and lotions or oils may be necessary.[285][289]
Hair changes
Antiandrogens affect existing facial hair only slightly; patients may see slower growth and some reduction in density and coverage. This reduction of density is due to the decreasing hair diameter and slower terminal growth rate. Effects on hair size and density were noticeable in the first four months following the start of hormone therapy, but later subsided, with measurements staying constant.[288] In patients in their teens or early twenties, antiandrogens prevent new facial hair from developing if testosterone levels are within the normal female range.[285][289]
Eye changes
The
Fat changes
The distribution of adipose (fat) tissue changes slowly over months and years. HRT causes the body to accumulate new fat in a typically feminine pattern, including in the hips, thighs, buttocks, pubis, upper arms, and breasts. The body begins to burn old adipose tissue in the waist, shoulders, and back, making those areas smaller.[285]
Bone/skeletal changes
Sex hormones play an important role in bone growth and maintenance. The effects of hormone therapy on bone health are not fully understood, and may depend on whether hormone therapy is started before or after puberty.[299] Significant changes to bone structure have been observed,[300][301][302] and transgender women have statistically poorer bone health even before beginning the transition process, possibly due to a lack of physical exercise[303] or other risk factors such as low vitamin D, eating disorders, and substance abuse.[304]
Approximately 14% of transgender women suffer from osteoporosis.[304] Transgender women below the age of 50 show increased fracture risk compared to age-matched cisgender women, equal to the risk to cisgender men of equivalent age. Transgender women above the age of 50 have a similar fracture risk to post-menopausal women — higher than that of age-matched cis men. In both cases, trans women's fracture patterns follow that of cis women, suffering long-term stress fractures concentrated in the hip, spine, and arms, typical of chronic low bone mineral density, rather than the fracture patterns typical of external injury suffered by cis men.[305] Current clinical guidelines are for bone health to be monitored regularly throughout the transition process, particularly if risk factors are present.[299] Transgender individuals are encouraged to ingest at least 1g of Calcium and 1000 IU of Vitamin D daily, engage regularly in weight-bearing physical activity, and reduce alcohol and smoking consumption.[306]
The effects of hormone therapy on bone health are reversible should treatment be interrupted. However, withdrawing hormone therapy after
Mental changes
The psychological effects of feminizing hormone therapy are harder to define than physical changes. Because hormone therapy is usually the first physical step taken to transition, the act of beginning it has a significant psychological effect, which is difficult to distinguish from hormonally induced changes.
Changes in mood and well-being occur with hormone therapy in transgender women.[309]
Side effects of hormone therapy have the ability to significantly impact sexual functioning, either directly or indirectly through the various side effects, such as cerebrovascular disorders, obesity, and mood fluctuations.[310] Some transgender women report a significant reduction in libido, depending on the dosage of antiandrogens.[311] The effects of long-term hormonal regimens have not been conclusively studied and are difficult to estimate because research on the long-term use of hormonal therapy has not been noted.[255] One study found that sex drive returned to baseline after three years of hormone therapy. [274] It is possible to approximate outcomes of these therapies on transgender people based on their observed effect in cisgender men and women.[310] Firstly, if one is to decrease testosterone in feminizing gender transition, it is likely that sexual desire and arousal would be inhibited; alternatively, if high doses of estrogen negatively impact sexual desire, which has been found in some research with cisgender women, it is hypothesized that combining androgens with high levels of estrogen would intensify this outcome.[310] To date there have not been any randomized clinical trials looking at the relationship between type and dose of transgender hormone therapy, so the relationship between them remains unclear.[310] Typically, the estrogens given for feminizing gender transition are 2 to 3 times higher than the recommended dose for HRT in postmenopausal women.[255] Pharmacokinetic studies indicate taking these increased doses may lead to a higher boost in plasma estradiol levels; however, the long-term side effects have not been studied and the safety of this route is unclear.[255]
Several studies have found that hormone therapy in transgender women causes the structure of the brain to change in the direction of female proportions.[312][313][314][315][316] In addition, studies have found that hormone therapy in transgender women causes performance in cognitive tasks, including visuospatial, verbal memory, and verbal fluency, to shift in a more female direction.[312][309]
Cardiovascular effects
The most significant cardiovascular risk for transgender women is the prothrombotic effect (increased
VTE occurs more frequently in the first year of treatment with estrogens. The risk of VTE is higher with oral non-bioidentical estrogens such as ethinylestradiol and conjugated estrogens than with parenteral formulations of estradiol such as injectable, transdermal, implantable, and intranasal.[317][163][55] Increased risk of VTE with estrogens is thought to be due to their influence on
Because the risks of warfarin – which is used to treat blood clots – in a relatively young and otherwise healthy population are low, while the risk of adverse physical and psychological outcomes for untreated transgender patients is high, prothrombotic mutations (such as factor V Leiden, antithrombin III, and protein C or S deficiency) are not absolute contraindications for hormonal therapy.[211]
A 2018 cohort study of 2842 transfeminine individuals in the
A 2019
In a 2016 study that specifically assessed oral estradiol, the incidence of VTE in 676 transgender women who were treated for an average of 1.9 years each was only one individual, or 0.15% of the group, with an incidence of 7.8 events per 10,000 person-years.[323][324] The dosage of oral estradiol used was 2 to 8 mg/day.[324] Almost all of the transgender women were also taking spironolactone (94%), a subset were also taking finasteride (17%), and fewer than 5% were also taking a progestogen (usually oral progesterone).[324] The findings of this study suggest that the incidence of VTE is low in transgender women taking oral estradiol.[323][324]
Cardiovascular health in transgender women has been reviewed in recent publications.[325][53]
Gastrointestinal effects
Estrogens may increase the risk of gallbladder disease, especially in older and obese people.[287]
Metabolic changes
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Cancer risk
Studies are mixed on whether the risk of breast cancer is increased with hormone therapy in transgender women.[326][327][328][329] Two cohort studies found no increase in risk relative to cisgender men,[327][328] whereas another cohort study found an almost 50-fold increase in risk such that the incidence of breast cancer was between that of cisgender men and cisgender women.[329][326] There is no evidence that breast cancer risk in transgender women is greater than in cisgender women.[330] Twenty cases of breast cancer in transgender women have been reported as of 2019.[326][331]
Cisgender men with
The risks of certain types of
Estrogens and progestogens can cause
Unaffected characteristics
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Established changes to the bone structure of the face are also unaffected by HRT. A significant majority of craniofacial changes occur during adolescence. Post-adolescent growth is considerably slower and minimal by comparison.[343]
Facial hair develops during puberty and is only slightly affected by HRT.[289]
A person's voice is unaffected by feminizing hormone therapy. Transgender individuals who have undergone male puberty often opt for
Monitoring
Especially in the early stages of feminizing hormone therapy, blood work is done frequently to assess hormone levels and liver function. The Endocrine Society recommends that patients have blood tests every three months in the first year of HRT for estradiol and testosterone, and that spironolactone, if used, be monitored every two to three months in the first year.[1] Recommended ranges for total estradiol and total testosterone levels include but are not limited to the following:
Source | Place | Estradiol, total | Testosterone, total | |
---|---|---|---|---|
Endocrine Society | United States | 100–200 pg/mL | <50 ng/dL | |
World Professional Association for Transgender Health (WPATH) | United States | "[T]estosterone levels [...] below the upper limit of the normal female range and estradiol levels within a premenopausal female range but well below supraphysiologic levels." "[M]aintain levels within physiologic ranges for a patient's desired gender expression (based on goals of full feminization/masculinization)." | ||
Center of Excellence for Transgender Health (UCSF ) | United States | "The interpretation of hormone levels for transgender individuals is not yet evidence based; physiologic hormone levels in non-transgender people are used as reference ranges." "Providers are encouraged to consult with their local lab(s) to obtain hormone level reference ranges for both 'male' and 'female' norms, [which can vary,] and then apply the correct range when interpreting results based on the current hormonal sex, rather than the sex of registration." | ||
Fenway Health | United States | 100–200 pg/mL | <55 ng/dL | |
Callen-Lorde | United States | "Some guidelines recommend checking estradiol and testosterone levels at baseline and throughout the monitoring of estrogen therapy. We have not found a clinical use for routine hormone levels that justifies the expense. However, we recognize that individual providers may adjust their prescribing and monitoring practices as needed to comply with guidelines or when guided by patient need." | ||
International Planned Parenthood Federation (IPPF) | United Kingdom | <200 pg/mL | 30–100 ng/dL | |
Foundation Trusts |
United Kingdom | 55–160 pg/mL | 30–85 ng/dL | |
Royal College of Psychiatry (RCP) |
United Kingdom | 80–140 pg/mL | "Well below normal male range" | |
Vancouver Coastal Health (VCH) | Canada | ND | <1.5 nmol/L | |
Sources: See template. |
The optimal ranges for estrogen apply only to individuals taking estradiol (or an ester of estradiol), and not to those taking synthetic or other non-bioidentical preparations (e.g., conjugated estrogens or ethinylestradiol).[1]
Physicians also recommend broader medical monitoring, including complete blood counts; tests of renal function, liver function, and lipid and glucose metabolism; and monitoring of prolactin levels, body weight, and blood pressure.[1][347]
If prolactin levels are greater than 100 ng/mL, estrogen therapy should be stopped and prolactin levels should be rechecked after 6 to 8 weeks.[347] If prolactin levels remain high, an MRI scan of the pituitary gland to check for the presence of a prolactinoma should be ordered.[347] Otherwise, estrogen therapy may be restarted at a lower dosage.[347] Cyproterone acetate is particularly associated with elevated prolactin levels, and discontinuation of cyproterone acetate lowers prolactin levels.[342][258][348] In contrast to cyproterone acetate, estrogen and spironolactone therapy is not associated with increased prolactin levels.[348][349]
History
Effective pharmaceutical female sex-hormonal medications, including androgens, estrogens, and progestogens, first became available in the 1920s and 1930s.
One of the first transgender health clinics was opened in the mid-1960s at the
Hormone therapy for transgender women was initially done using
In modern times, hormone therapy in transgender women is usually done with the combination of an estrogen and an antiandrogen.[381] In some places however, such as Japan, use of antiandrogens is uncommon, and estrogen monotherapy, for instance with high-dose injectable estradiol esters, is still frequently used.[382]
See also
- Menopausal hormone therapy
- Androgen replacement therapy
- Masculinizing hormone therapy
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CPA, as mentioned earlier, leads to an incomplete suppression of plasma testosterone levels, which decrease by about 70% and remain at about three times castration values. [Rennie et al.] found that the combination of CPA with an extremely low dose (0.1 mg/d) of DES led to a very effective withdrawal of androgens in terms of plasma testosterone and tissue dihydrotestosterone. [...] this regimen combines the testosterone-reducing effects of two compounds, therefore, only small amounts of estrogen are required to bring down plasma testosterone to approximately castrate levels.
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[Megestrol acetate] produces a transient reduction in plasma testosterone to levels somewhat higher than those in castrated men. When used in a dose of 40 mg tid, in combination with estradiol 0.5–1.5 mg/d, it acts synergistically to suppress pituitary gonadotropins and maintain plasma testosterone at castration levels for periods up to one year.
- ^ ISBN 978-0-7817-6879-5.
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Non-steroidal antiandrogens include flutamide, nilutamide, and bicalutamide, which do not lower androgen levels and may be favorable for individuals who want to preserve sex drive and fertility [9].
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Traditionally, patients have been advised to cryopreserve sperm prior to starting cross-sex hormone therapy as there is a potential for a decline in sperm motility with high-dose estrogen therapy over time (Lubbert et al., 1992). However, this decline in fertility due to estrogen therapy is controversial due to limited studies.
- ISBN 978-1-59745-453-7.
Estrogens are highly efficient inhibitors of the hypothalamic-hypophyseal-testicular axis (212–214). Aside from their negative feedback action at the level of the hypothalamus and pituitary, direct inhibitory effects on the testis are likely (215,216). [...] The histology of the testes [with estrogen treatment] showed disorganization of the seminiferous tubules, vacuolization and absence of lumen, and compartmentalization of spermatogenesis.
- ^ ISBN 978-1-58112-412-5.
Estrogens act primarily through negative feedback at the hypothalamic-pituitary level to reduce LH secretion and testicular androgen synthesis. [...] Interestingly, if the treatment with estrogens is discontinued after 3 yr. of uninterrupted exposure, serum testosterone may remain at castration levels for up to another 3 yr. This prolonged suppression is thought to result from a direct effect of estrogens on the Leydig cells.
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[...] estrogen or antiandrogen treatment prior to the first leuprolide injection may reduce [the risk of symptoms caused by the testosterone "flare" at the initiation of treatment] (16).
- ^ PMID 16320157.
- ^ ISBN 978-0-323-61075-9.
- ISBN 978-1-4511-5406-1. Archivedfrom the original on 16 May 2016.
Therapy with GnRH analogs is expensive and requires intramuscular injections of depot formulations, the insert of a subcutaneous implant yearly, or, much less commonly, daily subcutaneous injections.
- ISBN 978-1-118-53857-9.
Treatment is expensive, with costs typically in the range of $10,000–$15,000 per year.
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[...] caution is recommended while prescribing oral finasteride to male-to-female transsexuals, as the drug has been associated with inducing depression, anxiety and suicidal ideation, symptoms that are particularly common in patients with gender dysphoria, who are already at a high risk.[9]
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It has been suggested that progestins be added during the last week of each cycle of estrogen therapy in order to develop more rounded breasts rather than the conical breasts many of these patients develop, but we have been unable to detect any difference in breast contour with or without progestins.
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Experimentally I have been able to induce lactogenesis in a male transvestite whose testes had been removed some years before and whose breasts had been well developed over a long period with stilbestrol and ethisterone.9 In July, 1955, 600 mg. of estradiol was implanted subcutaneously and weekly injections of 50 mg. of progesterone were given for four months. For the next month daily injections of 10 mg. estradiol dipropionate and 50 mg. progesterone were given. These injections were continued for another month, increasing progesterone to 100 mg. daily. Both hormones were then withdrawn, and daily injections of increasing doses of prolactin and somatotropin were given for four days; at the same time, the patient used a breast bump four times daily for 5 minutes on both sides. During this time the mammary veins were visibly enlarged and on the sixth and seventh days 1 to 2 cc. of milky fluid was collected.
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[...] castration and feminizing plastic surgery of the external genitalia was performed [...] Some time after the operation, the patient developed a renewed interest in life. After the surgical and hormonal correction, the patient irresistibly developed maternal instincts. Unmarried, the patient obtained permission for the adoption of a child, simulated pregnancy, and was discharged from the maternity hospital with a son. From the first days after the "birth", galactorrhea sharply increased, and spontaneous outflow of milk appeared, with galactorrhea (+++). The baby was breastfed up to 6 months of age. [...] Our message is the second in the world literature describing galactorrhea in a male patient with transsexualism. The first description of this kind was made in 1983 by R. [Flückiger] et al. (6). This observation demonstrates the independence of the mechanism of lactation development from one's genetic sex and is alarming with regard to the possibility of drug-induced galactorrhea development in men.
- ^ Foss GL (January 1956). "Abnormalities of form and function of the human breast". Journal of Endocrinology. 14 (1): R6–R9.
Based on the theories of lactogenesis and stimulated by the success of Lyons, Li, Johnson & Cole [1955], who succeeded in producing lactation in male rats, an attempt was made to initiate lactogenesis in a male transvestist. Six years ago this patient had been given oestrogens. Both testes and penis were then removed and an artificial vagina was constructed by plastic surgery. The patient was implanted with 500 mg oestradiol in September 1954, and 600 mg in July 1955. The breasts were then developed more intensively with daily injections of oestradiol dipropionate and progesterone for 6 weeks. Immediately following withdrawal of this treatment, prolactin 22·9 mg was injected daily for 3 days without effect. After a second month on oestradiol and progesterone daily, combined injections of prolactin and somatotrophin were given for 4 days and suction was applied by a breast pump-four times daily. On the 4th and 5th days a few drops of colostrum were expressed from the right nipple.
- ^ Gardiner-Hill H (1958). Modern Trends in Endocrinology. Butterworth. p. 192.
Recently, an attempt has been made by Foss (1956) to initiate lactation in a castrated male transvestist. He was given an implant of 500 milligrams of oestradiol, and 10 months later, a further 600 milligrams of oestradiol, followed by daily injections of oestradiol dipropionate and progesterone for 6 weeks. Immediately after withdrawal of this treatment, 22·9 milligrams of prolactin were injected daily for 3 days but without effect. After a second month of treatment with oestradiol and progesterone daily, he was given combined injections of prolactin and somatotrophin for 4 days, suction with a breast-pump being employed 4 times daily. On the fourth and fifth days a few drops of colostrum were expressed from the right nipple. There is a possible application here of modern hormone knowledge to man, and further trials would be of interest.
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[...] An observation (Wyss and Del Pozo unpublished) in a male transsexual showed that induction of lactation can be similarly achieved in the human male. [...]
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Just 2 years later, Winfrey would feature another interview that elicited many of the same audience reactions. In this 2010 episode, lesbian partners Dr. Christine McGinn and Lisa Bortz beamed with joy as they held their infant twins. Again, audience members' jaws dropped when it was revealed that beautiful Christine was a male-to-female transsexual who used to be a handsome military officer Chris, and that Lisa had given birth to the couple's biological children using sperm Chris banked prior to gender confirmation surgeries.10 And it was Winfrey's chin that nearly hit the floor as she watched video of Christine breastfeeding the couples' children (the episode is referred to online as "The Mom Who Fathered Her Own Children"). [...]
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{{cite book}}
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- ^ a b c Benjamin H, Lal GB, Green R, Masters RE (1966). The Transsexual Phenomenon. Ace Publishing Company.
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- ^ "International Symposia - WPATH World Professional Association for Transgender Health".
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- ^ Benjamin H, Ihlenfeld CL (November 1970). "The nature and treatment of transsexualism". Medical Opinion and Review. 6 (11): 24–35.
Fortunately, the first medical textbook in this field, Transsexualism and Sex Reassignment, edited by Richard Green and John Money (Johns Hopkins Press, Baltimore, 1969), is now available
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Estrogen is given to MTF transsexuals orally as conjugated estrogens, or 17b-estradiol, as transdermal estrogen, or as parenteral estrogen esters to feminize the body.5 There is no evidence that progestin has beneficial effects on treatment with estrogen in MTF transsexuals; however, progestins were administered to some of MTF transsexuals. Because administration of antiandrogen to MTF transsexuals is not common in Japan, we could exclude the modification with antiandrogen in the present study.
Further reading
- Fabris B, Bernardi S, Trombetta C (March 2015). "Cross-sex hormone therapy for gender dysphoria". Journal of Endocrinological Investigation. 38 (3): 269–282. S2CID 207503049.
- Gooren LJ (March 2011). "Clinical practice. Care of transsexual persons". The New England Journal of Medicine. 364 (13): 1251–1257. PMID 21449788.
- Gooren LJ, Giltay EJ, Bunck MC (January 2008). "Long-term treatment of transsexuals with cross-sex hormones: extensive personal experience". The Journal of Clinical Endocrinology and Metabolism. 93 (1): 19–25. PMID 17986639.
- Tangpricha V, den Heijer M (April 2017). "Oestrogen and anti-androgen therapy for transgender women". The Lancet. Diabetes & Endocrinology. 5 (4): 291–300. PMID 27916515.
- Unger CA (December 2016). "Hormone therapy for transgender patients". Translational Andrology and Urology. 5 (6): 877–884. PMID 28078219.
- Wesp LM, Deutsch MB (March 2017). "Hormonal and Surgical Treatment Options for Transgender Women and Transfeminine Spectrum Persons". The Psychiatric Clinics of North America. 40 (1): 99–111. PMID 28159148.
- Wierckx K, Gooren L, T'Sjoen G (May 2014). "Clinical review: Breast development in trans women receiving cross-sex hormones". The Journal of Sexual Medicine. 11 (5): 1240–1247. PMID 24618412.
External links
- Deutsch M (17 June 2016). "Guidelines for the Primary and Gender-Affirming Care of Transgender and Gender Nonbinary People" (2nd ed.). University of California, San Francisco: Center of Excellence for Transgender Health. p. 28.
- Bourns A (2015). "Guidelines and Protocols for Comprehensive Primary Care for Trans Clients" (PDF). Sherbourne Health Centre. Retrieved 15 August 2018.
- Transgender HRT Research Repository