Hormone replacement therapy (male-to-female)
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Hormone replacement therapy (HRT) of the masculine-to-feminine (MTF) type is a form of hormone therapy and sex reassignment therapy that is used to change the secondary sexual characteristics of transgender and transsexual people from masculine (or androgynous) to feminine. It is one of two types of HRT for transgender and transsexual people (the other being hormone replacement therapy (feminine-to-masculine), and is predominantly used to treat transgender women. Some intersex people also receive this form of HRT, either starting in childhood to confirm the assigned sex or later if the assignment proves to be incorrect.
The purpose of this form of HRT is to cause the development of the secondary sex characteristics of the desired sex, such as breasts and a feminine pattern of hair, fat, and muscle distribution. It cannot undo many of the changes produced by naturally occurring puberty, which may necessitate surgery and other treatments (see below). The medications used in HRT of the MTF type include estrogens, antiandrogens, and progestogens.
While HRT cannot undo the effects of a person's first puberty, developing secondary sex characteristics associated with a different gender can relieve some or all of the distress and discomfort associated with gender dysphoria, and can help the person to "pass" or be seen as the gender they identify with. Introducing exogenous hormones into the body impacts it at every level and many patients report changes in energy levels, mood, appetite, etc. The goal of HRT, and indeed all somatic treatments, is to provide patients with a more satisfying body that is more congruent with their gender identity.
Requirements and accessibilityEdit
Some medical conditions may be a reason to withhold hormone replacement therapy because of the harm it could cause to the patient. Such interfering factors are described in medicine as contraindications.
Absolute contraindications – those that can cause life-threatening complications, and in which hormone replacement therapy should never be used – include histories of estrogen-sensitive cancer (e.g., breast cancer), thrombosis or embolism (unless the patient receives concurrent anticoagulants), or macroprolactinoma. In such cases, the patient should be monitored by an oncologist, hematologist or cardiologist, or neurologist, respectively.
Relative contraindications – in which the benefits of HRT may outweigh the risks, but caution should be used – include:
- Liver disease, kidney disease, heart disease, or stroke
- Risk factors for heart disease, such as high cholesterol, diabetes, obesity, or smoking
- Family history of breast cancer or thromboembolic disease
- Gallbladder disease
- Circulation or clotting conditions, such as peripheral vascular disease, polycythemia vera, sickle-cell anemia, paroxysmal nocturnal hemoglobinuria, hyperlipidemia, hypertension, factor V Leiden, prothrombin mutation, antiphospholipid antibodies, anticardiolipin antibodies, lupus anticoagulants, plasminogen or fibrinolysis disorders, protein C deficiency, protein S deficiency, or antithrombin III deficiency.
As dosages increase, risks increase as well. Therefore, patients with relative contraindications may start at low dosages and increase gradually.
Hormone therapy for transgender individuals has been shown in medical literature to be safe when supervised by a qualified medical professional.
Types of therapyEdit
Estrogen is one of the two major sex hormones in XX chromosomed individuals (the other being progesterone), and is responsible for the development and maintenance of feminine secondary sexual characteristics, such as breasts, wide hips, and a feminine pattern of fat distribution. Estrogens act by binding to and activating the estrogen receptor (ER), their biological target in the body. A variety of different forms of estrogen are available and used medically. The most common estrogens used in transgender women include estradiol (which is the predominant natural estrogen in women) and estradiol esters such as estradiol valerate and estradiol cypionate (which are prodrugs of estradiol). Conjugated equine estrogens (CEEs), marketed as Premarin, and ethinylestradiol are also sometimes used, but this is becoming less common. Estrogens may be administered orally, sublingually, transdermally (via patch), topically (via gel), by intramuscular or subcutaneous injection, or by an implant.
Prior to gender confirmation surgery, dosages of estrogen for transgender people are often higher than replacement dosages used for cisgender women. Hembree et al. (2009) recommend "maintain[ing] sex hormone levels within the normal range for the person’s desired gender". Dosages are typically reduced after an orchiectomy (removal of the testes) or sex reassignment surgery. However, that practice has been carried over from an era in which very high doses of estrogen were required to decrease testosterone, since antiandrogens were not used concurrently. Today, high doses of a less potent estrogen – estradiol, which is endogenous to the human body, rather than the riskier ethinylestradiol and conjugated estrogens used in the past – are recommended during the first ten or so years of HRT, with or without an orchiectomy or genital reassignment. After that period, dosages can be reduced.
Androgens, such as testosterone and dihydrotestosterone (DHT), are the major sex hormones in XY chromosomed individuals, and are responsible for the development and maintenance of masculine secondary sexual characteristics, such as a deep voice, broad shoulders, and a masculine pattern of hair, muscle, and fat distribution. In addition, they stimulate sex drive and the frequency of spontaneous erections and are responsible for acne, body odor, and masculine-pattern scalp hair loss. Androgens act by binding to and activating the androgen receptor (AR), their biological target in the body. In contrast to androgens, antiandrogens are drugs that prevent the effects of androgens in the body. They do this by preventing androgens from binding to the AR or by preventing the production of androgens. The most commonly used antiandrogens in transgender women are cyproterone acetate, spironolactone, and GnRH analogues.
The most commonly used antiandrogens for transgender women are steroidal: spironolactone and cyproterone acetate. Spironolactone, which is relatively safe and inexpensive, is the most frequently used antiandrogen in the United States. Cyproterone acetate, which is unavailable in the United States, is more commonly used in the rest of the world.
Spironolactone is a potassium-sparing diuretic that is mainly used to treat low-renin hypertension, edema, hyperaldosteronism, and low potassium levels caused by other diuretics. It can cause high potassium levels (hyperkalemia) and is therefore contraindicated in people who have renal failure or already-elevated potassium levels. Spironolactone prevents the formation of androgens in the testes (though not in the adrenal glands) by inhibiting enzymes involved in androgen production. It is also an androgen receptor antagonist (that is, it prevents androgens from binding to and activating the androgen receptor).
Cyproterone acetate is a powerful antiandrogen and progestin that suppresses gonadotropin levels (which in turn reduces androgen levels), blocks androgens from binding to and activating the androgen receptor, and inhibits enzymes in the androgen biosynthesis pathway. It has been used as a means of androgen deprivation therapy to treat prostate cancer. If used long-term in dosages of 150 mg or higher, it can cause liver damage or failure.
Nonsteroidal antiandrogens (NSAAs) used in HRT for transgender women include flutamide, nilutamide, and bicalutamide, all three of which are primarily used in the treatment of prostate cancer in cisgender men. Unlike steroidal antiandrogens such as spironolactone and cyproterone acetate, these drugs are pure androgen receptor antagonists. They do not lower androgen levels; rather, they act solely by preventing the binding of androgens to the androgen receptor. However, they do so very strongly, and are highly effective antiandrogens. Bicalutamide has improved tolerability and safety profiles relative to cyproterone acetate, as well as to flutamide and nilutamide, and has largely replaced the latter two in clinical practice for this reason. Enzalutamide is a more recently introduced NSAA with even greater potency and efficacy as an antiandrogen than bicalutamide, but it is still under patent protection and in relation to this is currently (and for the foreseeable future) extremely expensive. Moreover, enzalutamide has been found to act as a negative allosteric modulator of the GABA receptor and has been associated with central side effects such as anxiety, insomnia, and, most notably, seizures (in ≈1% of patients), properties that it does not share with bicalutamide.
NSAAs may be an appealing option for those who wish to preserve sex drive and function and/or fertility, as well as for those who desire more selective action with fewer side effects than spironolactone and cyproterone acetate (which increase the risk of depressive symptoms, among other adverse effects). Bicalutamide specifically may also be a safer drug than cyproterone acetate or spironolactone, as it has a much lower risk of hepatotoxicity relative to cyproterone acetate and, unlike spironolactone, has no risk of hyperkalemia or other antimineralocorticoid-associated adverse reactions. However, bicalutamide does have a very small risk of hepatotoxicity itself, as well as of interstitial pneumonitis.
In both sexes, the hypothalamus produces gonadotropin-releasing hormone (GnRH) to stimulate the pituitary gland to produce luteinizing hormone (LH) and follicle-stimulating hormone (FSH). This in turn cause the gonads to produce sex steroids such as androgens and estrogens. In adolescents of either sex with relevant indicators, GnRH analogues such as goserelin acetate can be used to stop undesired pubertal changes for a period without inducing any changes toward the sex with which the patient currently identifies. GnRH agonists work by initially overstimulating the pituitary gland, then rapidly desensitizing it to the effects of GnRH. After an initial surge, over a period of weeks, gonadal androgen production is greatly reduced. Conversely, GnRH antagonists act by blocking the action of GnRH in the pituitary gland.
There is considerable controversy over the earliest age at which it is clinically, morally, and legally safe to use GnRH analogues, and for how long. The sixth edition of the World Professional Association for Transgender Health's Standards of Care permit it from Tanner stage 2 but do not allow the addition of hormones until age 16, which could be five or more years later. Sex steroids have important functions in addition to their role in puberty, and some skeletal changes (such as increased height) that may be considered masculine are not hindered by GnRH analogues.
GnRH analogues are often prescribed to prevent the reactivation of testicular function when surgeons require the cessation of estrogens prior to surgery.
The high cost of GnRH analogues is a significant factor in their relative lack of use in transgender people. However, they are prescribed as standard practice in the United Kingdom.
Certain antiandrogens do not reduce testosterone or prevent its action upon tissues, but instead prevent its metabolite, dihydrotestosterone (DHT), from forming. These medications can be used when the patient has male-pattern hair loss and/or an enlarged prostate (benign prostatic hyperplasia), both of which DHT exacerbates. Two medications are currently available to prevent the creation of DHT: finasteride and dutasteride. DHT levels can be lowered up to 60–75% with the former, and up to 93–94% with the latter. These medications have also been found to be effective in the treatment of hirsutism in women.
Progesterone, a progestogen, is the other of the two major sex hormones in women. Unlike estrogen, progesterone is not overtly involved in the development of female secondary sexual characteristics, and is instead involved mainly in the menstrual cycle and pregnancy. For this reason, progestogens are not commonly prescribed for transgender women. However, there may be a role of progestogens in breast development (though controversial and disputed) and in regulation of skin and hair, and progesterone specifically may have positive effects on sex drive, sleep, and levels of anxiety. Moreover, due to their antigonadotropic and/or antiandrogen effects, progestogens can be useful in helping to suppress the effects of androgens in the body. The most common progestogens used in transgender women include progesterone and progestins (synthetic progestogens) like CPA and medroxyprogesterone acetate (MPA). These drugs are usually taken orally, but may also be administered by intramuscular injection.
Antiandrogenic and androgenic effectsEdit
High doses of progestogens exert negative feedback on the hypothalamic-pituitary-gonadal axis by activating the progesterone receptor. As a result, they have antigonadotropic effects – that is, they suppress the gonadal production of sex hormones such as androgens. As such, sufficient dosages of progestogens, such as cyproterone acetate, gestonorone caproate, hydroxyprogesterone caproate, megestrol acetate, and MPA, can considerably lower androgen levels. In addition, certain other progestogens, such as cyproterone acetate, megestrol acetate, drospirenone, and nomegestrol acetate, bind to and block the activation of the androgen receptor. On the other hand, certain other progestogens, including 19-nortestosterone derivatives like levonorgestrel, norgestrel, norethisterone, and norethisterone acetate, as well as, to a lesser extent, the 17α-hydroxyprogesterone derivative MPA, have weak androgenic activity because they bind to and activate the androgen receptor similarly to testosterone, and may produce androgenic effects such as acne, hirsutism, and increased sex drive.
Role in breast developmentEdit
Progestogens, in conjunction with the hormone prolactin, are involved in the maturation of the lobules, acini, and areola during pregnancy: mammary structures that estrogen has little to no direct effect on. However, there is no clinical evidence that progestogens enhance breast size, shape, or appearance in either transgender women or cisgender women, and one study found no benefit to breast hemicircumference over estrogen alone in a small sample of transgender women given both an estrogen and an oral progestogen (usually 10 mg/day medroxyprogesterone acetate). However, the authors of the paper stated that the sample size was too small to make any definitive conclusions, and that further studies should be carried out to confirm whether progestogens significantly affect breast size and/or shape in transgender women. As of 2014, no additional study had looked at the issue. Anecdotal evidence from transgender women suggests that those who take progesterone supplements may experience more full breast development, including stage IV on the Tanner scale (many transgender women do not develop Tanner stage V breasts). However, there have been no formal studies with sufficiently large sample sizes to confirm this.
Progestogens reportedly alter fat distribution (e.g., by increasing fat in the buttocks and thighs), increase sex drive (specifically progesterone, via its active metabolite allopregnanolone; this does not occur through activation of the progesterone receptor), cause increased appetite and weight gain (only in combination with estrogen), produce a sense of calm (i.e., anxiolysis), and promote sleep (i.e., sedative and hypnotic effects).
Progesterone specifically is essential for bone health and seems to have a role in skin elasticity and nervous system function. Other effects seen with progesterone include reducing spasms and relaxing smooth muscle tone; reducing gallbladder activity; widening bronchi, which helps respiration; reducing inflammation and immune response; and normalizing blood clotting and vascular tone, zinc and copper levels, cell oxygen levels, and use of fat stores for energy. Progesterone also assists in thyroid function and bone building by osteoblasts.
The main effects of HRT of the MTF type are as follows:
- Breast development and enlargement
- Softening and thinning of the skin
- Decreased body hair growth and density
- Redistribution of body fat in a feminine pattern
- Decreased muscle mass and strength
- Widening of the hips (if epiphyseal closure has not yet occurred; see below)
- Decreased acne, skin oiliness, scalp hair loss, and body odor
- Decreased size of the penis, scrotum, testicles, and prostate
- Suppressed or abolished spermatogenesis and fertility
- Decreased semen production/ejaculate volume
- Changes in mood, emotionality, and behavior
- Decreased sex drive and incidence of spontaneous erections
The psychological effects of hormone replacement therapy are harder to define than physical changes. Because HRT 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.
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.
In transgender women on HRT, as in cisgender women during puberty, breast ducts and Cooper's ligaments develop under the influence of estrogen. Progesterone causes the milk sacs (mammary alveoli) to develop, and with the right stimuli, a transgender woman may lactate. Additionally, HRT often makes the nipples more sensitive to stimulation.
The uppermost layer of skin, the stratum corneum, becomes thinner and more translucent. Spider veins may appear or be more noticeable as a result. Collagen decreases, and tactile sensation increases. The skin becomes softer, more susceptible to tearing and irritation from scratching or shaving, and slightly lighter in color because of a slight decrease in melanin.
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. The pores become smaller because of the lower quantities of oil being produced. Many apocrine glands – a type of sweat gland – become inactive, and body odor decreases. Remaining body odor becomes less metallic, sharp, or acrid, and more sweet and musky.
As subcutaneous fat accumulates, dimpling, or cellulite, becomes more apparent on the thighs and buttocks. Stretch marks (striae distensae) may appear on the skin in these areas. Susceptibility to sunburn increases, possibly because the skin is thinner and less pigmented.
Antiandrogens affect existing facial hair only slightly; patients may see slower growth and some reduction in density and coverage. Those who are less than a decade past puberty and/or whose race generally lacks a significant amount of facial hair may have better results. Patients taking antiandrogens tend to have better results with electrolysis and laser hair removal than those who are not. In patients in their teens or early twenties, antiandrogens prevent new facial hair from developing if testosterone levels are within the normal female range.
Body hair (on the chest, shoulders, back, abdomen, buttocks, thighs, tops of hands, and tops of feet) turns, over time, from terminal ("normal") hairs to tiny, blonde vellus hairs. Arm, perianal, and perineal hair is reduced but may not turn to vellus hair on the latter two regions (some cisgender women also have hair in these areas). Underarm hair changes slightly in texture and length, and pubic hair becomes more typically female in pattern. Lower leg hair becomes less dense. All of these changes depend to some degree on genetics.
Head hair may change slightly in texture, curl, and color. This is especially likely with hair growth from previously bald areas. Eyebrows do not change because they are not androgenic.
The lens of the eye changes in curvature. Because of decreased androgen levels, the meibomian glands (the sebaceous glands on the upper and lower eyelids that open up at the edges) produce less oil. Because oil prevents the tear film from evaporating, this change may cause dry eyes.
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. (Fat on the hips, thighs, and buttocks has a higher concentration of omega-3 fatty acids and is meant to be used for lactation.) The body begins to burn old adipose tissue in the waist, shoulders, and back, making those areas smaller.
Male-to-female hormone therapy causes the hips to rotate slightly forward because of changes in the tendons. Hip discomfort is not uncommon.
If estrogen therapy is begun prior to pelvis ossification, which occurs around the age of 25, the pelvic outlet and inlet open slightly. The femora also widen, because they are connected to the pelvis. The pelvis retains some masculine characteristics, but the end result of HRT is wider hips than a cisgender man and closer to those of a cisgender woman.
HRT does not reverse bone changes that have already been established by puberty. Consequently, it does not affect height; the length of the arms, legs, hands, and feet; or the width of the shoulders and rib cage. However, details of bone shape change throughout life, with bones becoming heavier and more deeply sculptured under the influence of androgens, and HRT does prevent such changes from progressing further.
The width of the hips is not affected in individuals for whom epiphyseal closure (fusion and closure of the ends of bones, which prevents any further lengthening) has taken place. This occurs in most people between 18 and 25 years of age. Already-established changes to the shape of the hips cannot be reversed by HRT whether epiphyseal closure has taken place or not.
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. Also unaffected is the prominence of the thyroid cartilage (Adam's apple). These changes may be reversed by surgery (facial feminization surgery and tracheal shave, respectively).
During puberty, the voice deepens in pitch and becomes more resonant. These changes are permanent and are not affected by HRT. Voice therapy and/or surgery may be used instead to achieve a more female-sounding voice.
Mood changes, including depression, can occur with hormone replacement therapy. However, many transgender women report significant mood-lifting effects as well. The risk of depressive side effects is more common in patients who take progestins. Medroxyprogesterone acetate, in particular, has been shown to cause depression in certain individuals, perhaps by affecting dopamine levels.
Some transgender women report a significant reduction in libido, depending on the dosage of antiandrogens. A small number of post-operative transgender women take low doses of testosterone to boost their libido. Many pre-operative transgender women wait until after reassignment surgery to begin an active sex life. Raising the dosage of estrogen or adding a progestogen raises the libido of some transgender women.
Spontaneous and morning erections decrease significantly in frequency, although some patients who have had an orchiectomy still experience morning erections. Voluntary erections may or may not be possible, depending on the amount of hormones and/or antiandrogens being taken.
All aforementioned physical changes can, and reportedly do, change the experience of sensation compared to prior to HRT. Areas affected include, but aren't limited to, the basic senses, erogenous stimulus, perception of emotion, perception of social interaction, and processing of feelings and experiences.
The most significant cardiovascular risk for transgender women is the pro-thrombotic effect (increased blood clotting) of estrogens. This manifests most significantly as an increased risk for thromboembolic disease: deep vein thrombosis (DVT) and pulmonary embolism, which occurs when blood clots from DVT break off and migrate to the lungs. Symptoms of DVT include pain or swelling of one leg, especially the calf. Symptoms of pulmonary embolism include chest pain, shortness of breath, fainting, and heart palpitations, sometimes without leg pain or swelling.
Deep vein thrombosis occurs more frequently in the first year of treatment with estrogens. The risk is higher with oral estrogens (particularly ethinylestradiol and conjugated estrogens) than with injectable, transdermal, implantable, and nasal formulations. DVT risk also increases with age and in patients who smoke, so many clinicians advise using the safer estrogen formulations in smokers and patients older than 40.
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, pro-thrombotic mutations (such as factor V Leiden, antithrombin III, and protein C or S deficiency) are not absolute contraindications for hormonal therapy.
Estrogens may increase the risk of gallbladder disease, especially in older and obese people. They may also increase transaminase levels, indicating liver toxicity, especially when taken in oral form.
A patient's metabolic rate may change, causing an increase or decrease in weight and energy levels, changes to sleep patterns, and temperature sensitivity. Androgen deprivation leads to slower metabolism and a loss of muscle tone. Building muscle takes more work. The addition of a progestogen may increase energy, although it may increase appetite as well.
Both estrogens and androgens are necessary in all humans for bone health. Young, healthy women produce about 10 mg of testosterone monthly, and higher bone mineral density in males is associated with higher serum estrogen. Both estrogen and testosterone help to stimulate bone formation, especially during puberty. Estrogen is the predominant sex hormone that slows bone loss, even in men.
Risk of hormone-sensitive cancersEdit
In spite of the induction of breast development, transwomen who undergo HRT do not have an increased risk of breast cancer, as cissexual women do. Only a handful of cases of breast cancer have ever been described in transsexual women who have undergone male-to-female HRT. This is in accordance with research in cissexual men in which gynecomastia has been found not to be associated with an increased risk of breast cancer, suggesting a protective role of the male sex-determination chromosome. On the other hand, men with Klinefelter's syndrome (two X chromosomes and one Y chromosome), which causes hypoandrogenism, hyperestrogenism, and a very high incidence of gynecomastia (80%), have a dramatically (20- to 58-fold) increased risk of breast cancer compared to men with one X chromosome, closer to the rate of homogametic females. The incidences of breast cancer in karyotypical men (46,XY karyotype), men with Klinefelter's syndrome (47,XXY karyotype), and karyotypical women (46,XX karyotype) are approximately 0.1%, 3%, and 12.5%, respectively. Individuals with the 46,XY karyotype affected by complete androgen insensitivity syndrome never develop male sex characteristics and have normal and complete female morphology, and accelerated breast growth during puberty, but appear to have little (or possibly even no) incidence of breast cancer. The risk of breast cancer in women with Turner syndrome (45,XO karyotype) also appears to be significantly decreased, though this may be related to ovarian failure/hypogonadism rather necessarily than to genetics.
Prostate cancer is extremely rare in orchidectomised transgender women who have been treated with oestrogens for a prolonged period of time. Whereas as many as 70% of men show prostate cancer by their 80's, only a handful of cases of prostate cancer in transgender women have been reported in the literature. As such, and in accordance with the fact that androgens are responsible for the development of prostate cancer, HRT appears to be highly protective against prostate cancer in transgender women.
Estrogens can also cause prolactinomas. Milk discharge from the nipples can be a sign of elevated prolactin levels. If a prolactinoma becomes large enough, it can cause visual changes (especially decreased peripheral vision), headaches, depression or other mood changes, dizziness, nausea, vomiting, and symptoms of pituitary failure, like hypothyroidism.
Especially in the early stages of hormone replacement 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 2–3 months in the first year. The optimal ranges for estradiol and testosterone are not limited to but include the following:
|Hormone||Endocrine Society||Royal College of Psychiatry|
|Estradiol||Less than 200 pg/ml||80–140 pg/ml|
|Testosterone||Less than 55 ng/dl||"Well below normal male range"|
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., CEEs or ethinylestradiol).
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.
- "Weinand J, Safer J. Feb 2015. “Hormone therapy in transgender adults is safe with provider supervision; A review of hormone therapy sequelae for transgender individuals.” Journal of Clinical & Translational Endocrinology (2015).".
- Hembree, W. C.; Cohen-Kettenis, P.; Delemarre-van de Waal, H. A.; Gooren, L. J.; Meyer, W. J.; Spack, N. P.; Tangpricha, V.; Montori, V. M. (2009-09-01). "Endocrine Treatment of Transsexual Persons: An Endocrine Society Clinical Practice Guideline" (PDF). Journal of Clinical Endocrinology & Metabolism. 94 (9): 3132–3154. PMID 19509099. doi:10.1210/jc.2009-0345. Retrieved 31 October 2013.
- Stripp B, Taylor AA, Bartter FC, et al. (October 1975). "Effect of spironolactone on sex hormones in man". The Journal of Clinical Endocrinology and Metabolism. 41 (4): 777–81. PMID 1176584. doi:10.1210/jcem-41-4-777.
- Pozzi AG, Ceballos NR (August 2000). "Human chorionic gonadotropin-induced spermiation in Bufo arenarum is not mediated by steroid biosynthesis". General and Comparative Endocrinology. 119 (2): 164–71. PMID 10936036. doi:10.1006/gcen.2000.7509.
- Canosa LF, Ceballos NR (August 2001). "Effects of different steroid-biosynthesis inhibitors on the testicular steroidogenesis of the toad Bufo arenarum". Journal of Comparative Physiology B. 171 (6): 519–26. PMID 11585264. doi:10.1007/s003600100203.
- Boisselle A, Dionne FT, Tremblay RR (July 1979). "Interaction of spironolactone with rat skin androgen receptor". Canadian Journal of Biochemistry. 57 (7): 1042–6. PMID 487244. doi:10.1139/o79-131.
- Tremblay RR. (May 1986). "Treatment of hirsutism with spironolactone". Clinics in Endocrinology and Metabolism. 15 (2): 363–371. PMID 2941190. doi:10.1016/S0300-595X(86)80030-5.
- Biffignandi P, Molinatti GM (1987). "Antiandrogens and hirsutism". Hormone Research. 28 (2–4): 242–249. PMID 2969862. doi:10.1159/000180949.
- Loy R, Seibel MM (December 1988). "Evaluation and therapy of polycystic ovarian syndrome". Endocrinology and Metabolism Clinics of North America. 17 (4): 785–813. PMID 3143568.
- Yamasaki K, Sawaki M, Noda S, et al. (February 2004). "Comparison of the Hershberger assay and androgen receptor binding assay of twelve chemicals". Toxicology. 195 (2–3): 177–86. PMID 14751673. doi:10.1016/j.tox.2003.09.012.
- Kaiser E, Gruner HS (1987). "Liver structure and function during long-term treatment with cyproterone acetate". Archives of Gynecology. 240 (4): 217–23. PMID 2955749. doi:10.1007/BF02134071.
- Willemse PH, Dikkeschei LD, Mulder NH, van der Ploeg E, Sleijfer DT, de Vries EG (March 1988). "Clinical and endocrine effects of cyproterone acetate in postmenopausal patients with advanced breast cancer". European Journal of Cancer & Clinical Oncology. 24 (3): 417–21. PMID 2968261. doi:10.1016/S0277-5379(98)90011-6.
- Hinkel A, Berges RR, Pannek J, Schulze H, Senge T (1996). "Cyproterone acetate in the treatment of advanced prostatic cancer: retrospective analysis of liver toxicity in the long-term follow-up of 89 patients". European Urology. 30 (4): 464–70. PMID 8977068.
- Watanabe S, Cui Y, Tanae A, et al. (September 1997). "Follow-up study of children with precocious puberty treated with cyproterone acetate. Ad hoc Committee for CPA". Journal of Epidemiology. 7 (3): 173–8. PMID 9337516. doi:10.2188/jea.7.173.
- Migliari R, Muscas G, Murru M, Verdacchi T, De Benedetto G, De Angelis M (December 1999). "Antiandrogens: a summary review of pharmacodynamic properties and tolerability in prostate cancer therapy". Archivio Italiano Di Urologia, Andrologia. 71 (5): 293–302. PMID 10673793.
- Laron Z, Kauli R (July 2000). "Experience with cyproterone acetate in the treatment of precocious puberty". Journal of Pediatric Endocrinology & Metabolism. 13 Suppl 1: 805–10. PMID 10969925. doi:10.1515/JPEM.2000.13.S1.805.
- Giordano N, Nardi P, Santacroce C, Geraci S, Gennari C (September 2001). "Acute hepatitis induced by cyproterone acetate". The Annals of Pharmacotherapy. 35 (9): 1053–5. PMID 11573856. doi:10.1345/aph.10426.
- Lin AD, Chen KK, Lin AT, et al. (December 2003). "Antiandrogen-associated hepatotoxicity in the management of advanced prostate cancer". Journal of the Chinese Medical Association. 66 (12): 735–40. PMID 15015823.
- Savidou I, Deutsch M, Soultati AS, Koudouras D, Kafiri G, Dourakis SP (December 2006). "Hepatotoxicity induced by cyproterone acetate: a report of three cases". World Journal of Gastroenterology. 12 (46): 7551–5. PMC . PMID 17167851. doi:10.3748/wjg.v12.i46.7551.
- Gooren LJ. "Clinical practice. Care of transsexual persons". N Engl J Med. 364: 1251–7. PMID 21449788. doi:10.1056/NEJMcp1008161.
- Ho CK (Dec 2011). "Testosterone testing in adult males". The Malaysian Journal of Pathology. 33 (2): 71–81. PMID 22299206.
- Iversen P, Melezinek I, Schmidt A (Jan 2001). "Nonsteroidal antiandrogens: a therapeutic option for patients with advanced prostate cancer who wish to retain sexual interest and function". BJU International. 87 (1): 47–56. PMID 11121992. doi:10.1046/j.1464-410x.2001.00988.x.
- Morgante, E; Gradini, R; Realacci, M; Sale, P; D'eramo, G; Perrone, G A; Cardillo, M R; Petrangeli, E; Russo, Ma; Di Silverio, F (2001). "Effects of long-term treatment with the anti-androgen bicalutamide on human testis: an ultrastructural and morphometric study". Histopathology. 38 (3): 195–201. ISSN 0309-0167. PMID 11260298. doi:10.1046/j.1365-2559.2001.01077.x.
- Seal, L. J.; Franklin, S.; Richards, C.; Shishkareva, A.; Sinclaire, C.; Barrett, J. (2012). "Predictive Markers for Mammoplasty and a Comparison of Side Effect Profiles in Transwomen Taking Various Hormonal Regimens". The Journal of Clinical Endocrinology & Metabolism. 97 (12): 4422–4428. ISSN 0021-972X. PMID 23055547. doi:10.1210/jc.2012-2030.
- Raudrant D, Rabe T (2003). "Progestogens with antiandrogenic properties". Drugs. 63 (5): 463–92. PMID 12600226. doi:10.2165/00003495-200363050-00003.
- Georg Wick; Cecilia Grundtman (3 December 2011). Inflammation and Atherosclerosis. Springer Science & Business Media. pp. 560–. ISBN 978-3-7091-0338-8.
- Armen H. Tashjian; Ehrin J. Armstrong (21 July 2011). Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy. Lippincott Williams & Wilkins. pp. 523–. ISBN 978-1-4511-1805-6.
- Kenneth Hugdahl; René Westerhausen (2010). The Two Halves of the Brain: Information Processing in the Cerebral Hemispheres. MIT Press. pp. 272–. ISBN 978-0-262-01413-7.
- *Orentreich N, Durr NP (July 1974). "Mammogenesis in transsexuals". Journal of Investigative Dermatology. 63 (1): 142–6. PMID 4365991. doi:10.1111/1523-1747.ep12678272.
- Mauvais-Jarvis P, Kuttenn F, Gompel A, Malet C, Fournier S (1986). "[Estradiol-progesterone interaction in normal and pathological human breast cells]". Ann. Endocrinol. (in French). Paris. 47 (3): 179–87. PMID 3535636.
- Mauvais-Jarvis P, Kuttenn F, Gompel A (1986). "Antiestrogen action of progesterone in breast tissue.". Breast Cancer Research and Treatment. 8 (3): 179–188. PMID 3297211. doi:10.1007/BF01807330.
- Cooke BA, King RJ, van der Molen HJ, eds. (1988). New Comprehensive Biochemistry: Hormones and Their Actions, Part I. vol. 18a. Amsterdam: Elsevier.
- Cyrlak D, Wong CH (December 1993). "Mammographic changes in postmenopausal women undergoing hormonal replacement therapy". American Journal of Roentgenology. 161 (6): 1177–83. PMID 8249722. doi:10.2214/ajr.161.6.8249722.
- Gorins A, Denis C (1995). "Effects of progesterone and progestational hormones on the mammary gland". Archives d'anatomie et de cytologie pathologiques. 43 (1–2): 28–35. PMID 7794024.
- Futterweit W (April 1998). "Endocrine therapy of transsexualism and potential complications of long-term treatment". Archives of Sexual Behavior. 27 (2): 209–26. PMID 9562902. doi:10.1023/A:1018638715498.
- edited by Dallas Denny. (1998). "17. Hormonal Therapy in Gender Dysphoria: The Male-to-Female Transsexual". In Denny D (ed.). Current Concepts in Transgender Identity. chap. by Basson R, Prior JC. New York: Garland Publishing. ISBN 0-8153-1793-X. OCLC 37156496.
- Colin, Claude. "Hormone Dependence of the Mammary Tissue". Retrieved June 14, 2008.
- Shyamala G (January 1999). "Progesterone signaling and mammary gland morphogenesis". Journal of Mammary Gland Biology and Neoplasia. 4 (1): 89–104. PMID 10219909. doi:10.1023/A:1018760721173.
- Kanhai RC, Hage JJ, van Diest PJ, Bloemena E, Mulder JW (January 2000). "Short-term and long-term histologic effects of castration and estrogen treatment on breast tissue of 14 male-to-female transsexuals in comparison with two chemically castrated men". The American Journal of Surgical Pathology. 24 (1): 74–80. PMID 10632490. doi:10.1097/00000478-200001000-00009.
- Schams D, Kohlenberg S, Amselgruber W, Berisha B, Pfaffl MW, Sinowatz F (May 2003). "Expression and localisation of oestrogen and progesterone receptors in the bovine mammary gland during development, function and involution". The Journal of Endocrinology. 177 (2): 305–17. PMID 12740019. doi:10.1677/joe.0.1770305.
- Lamote I, Meyer E, Massart-Leën AM, Burvenich C (March 2004). "Sex steroids and growth factors in the regulation of mammary gland proliferation, differentiation, and involution". Steroids. 69 (3): 145–59. PMID 15072917. doi:10.1016/j.steroids.2003.12.008.
- Swerdloff RS, Ng J, Palomeno GE (March 2004). "Gynecomastia: Etiology, Diagnosis, and Treatment". Archived from the original on April 14, 2008. Retrieved June 14, 2008.
- Baltzell K, Eder S, Wrensch M (January 2005). "Breast carcinogenesis: can the examination of ductal fluid enhance our understanding?". Oncology Nursing Forum. 32 (1): 33–9. PMID 15660141. doi:10.1188/05.ONF.33-39.
- Brisken C. "Genetic dissection of signaling pathways important in breast development and breast cancer". Retrieved June 14, 2008.
- Macias, Hector; Hinck, Lindsay (2012). "Mammary gland development". Wiley Interdisciplinary Reviews: Developmental Biology. 1 (4): 533–557. ISSN 1759-7684. PMC . PMID 22844349. doi:10.1002/wdev.35.
- Meyer WJ, Webb A, Stuart CA, Finkelstein JW, Lawrence B, Walker PA (April 1986). "Physical and hormonal evaluation of transsexual patients: a longitudinal study". Archives of Sexual Behavior. 15 (2): 121–38. PMID 3013122. doi:10.1007/bf01542220.
- Wierckx K, Gooren L, T'Sjoen G (2014). "Clinical review: Breast development in trans women receiving cross-sex hormones". J Sex Med. 11 (5): 1240–7. PMID 24618412. doi:10.1111/jsm.12487.
- Stelmanska, Ewa; Kmiec, Zbigniew; Swierczynski, Julian (2012). "The gender- and fat depot-specific regulation of leptin, resistin and adiponectin genes expression by progesterone in rat". The Journal of Steroid Biochemistry and Molecular Biology. 132 (1–2): 160–167. ISSN 0960-0760. PMID 22634476. doi:10.1016/j.jsbmb.2012.05.005.
- Hirschberg AL (2012). "Sex hormones, appetite and eating behaviour in women". Maturitas. 71 (3): 248–56. PMID 22281161. doi:10.1016/j.maturitas.2011.12.016.
- Pfaus JG (1999). "Neurobiology of sexual behavior". Curr. Opin. Neurobiol. 9 (6): 751–8. PMID 10607643. doi:10.1016/s0959-4388(99)00034-3.
- Frye CA, Bayon LE, Pursnani NK, Purdy RH (1998). "The neurosteroids, progesterone and 3alpha,5alpha-THP, enhance sexual motivation, receptivity, and proceptivity in female rats". Brain Res. 808 (1): 72–83. PMID 9795145. doi:10.1016/s0006-8993(98)00764-1.
- Friess E, Tagaya H, Trachsel L, Holsboer F, Rupprecht R (May 1997). "Progesterone-induced changes in sleep in male subjects". The American Journal of Physiology. 272 (5 Pt 1): E885–91. PMID 9176190.
- Montplaisir J, Lorrain J, Denesle R, Petit D (2001). "Sleep in menopause: differential effects of two forms of hormone replacement therapy". Menopause. 8 (1): 10–6. PMID 11201509. doi:10.1097/00042192-200101000-00004.
- Söderpalm AH, Lindsey S, Purdy RH, Hauger R, Wit de H (April 2004). "Administration of progesterone produces mild sedative-like effects in men and women". Psychoneuroendocrinology. 29 (3): 339–54. PMID 14644065. doi:10.1016/S0306-4530(03)00033-7.
- van Broekhoven F, Bäckström T, Verkes RJ (November 2006). "Oral progesterone decreases saccadic eye velocity and increases sedation in women". Psychoneuroendocrinology. 31 (10): 1190–9. PMID 17034954. doi:10.1016/j.psyneuen.2006.08.007.
- Schumacher M, Guennoun R, Ghoumari A, et al. (June 2007). "Novel perspectives for progesterone in hormone replacement therapy, with special reference to the nervous system". Endocrine Reviews. 28 (4): 387–439. PMID 17431228. doi:10.1210/er.2006-0050.
- Golparvar M, Ahmadi F, Saghaei M (January 2005). "Effects of progesterone on the ventilatory performance in adult trauma patients during partial support mechanical ventilation" (PDF). Archives of Iranian Medicine. 8 (1): 27–31.
- "Standards of Care for the Health of Transsexual, Transgender, and Gender Nonconforming People" (PDF). 7th version. World Professional Association for Transgender Health. p. 18. Archived from the original (PDF) on 2012-09-20. Retrieved 31 October 2013.
- Michael S. Baggish; Mickey M. Karram (18 August 2011). Atlas of Pelvic Anatomy and Gynecologic Surgery. Elsevier Health Sciences. pp. 1200–. ISBN 1-4557-1068-7.
- Asscheman H, Gooren LJ (1992). "Hormone Treatment in Transsexuals". Retrieved 13 June 2008.
- Meikle, James. "Breast regrowth procedure trialled for mastectomy patients". Retrieved 17 January 2015.
- Kirk, MD, Sheila (1999). Feminizing Hormonal Therapy For The Transgendered (1999 Edition). Pittsburgh, PA: Together Lifeworks. p. 38.
- Giltay EJ, Gooren LJ (August 2000). "Effects of sex steroid deprivation/administration on hair growth and skin sebum production in transsexual males and females". Journal of Clinical Endocrinology and Metabolism. 85 (8): 2913–21. PMID 10946903. doi:10.1210/jc.85.8.2913.
- Randall, V. A.; Hibberts, N. A.; Thornton, M. J.; Hamada, K.; Merrick, A. E.; Kato, S.; Jenner, T. J.; De Oliveira, I.; Messenger, A. G. (2000-01-01). "The hair follicle: a paradoxical androgen target organ". Hormone Research. 54 (5–6): 243–250. ISSN 0301-0163. PMID 11595812. doi:10.1159/000053266.
- Leach NE, Wallis NE, Lothringer LL, Olson JA (May 1971). "Corneal hydration changes during the normal menstrual cycle--a preliminary study". The Journal of Reproductive Medicine. 6 (5): 201–4. PMID 5094729.
- Kiely PM, Carney LG, Smith G (October 1983). "Menstrual cycle variations of corneal topography and thickness". American Journal of Optometry and Physiological Optics. 60 (10): 822–9. PMID 6650653. doi:10.1097/00006324-198310000-00003.
- Gurwood AS, Gurwood I, Gubman DT, Brzezicki LJ (January 1995). "Idiosyncratic ocular symptoms associated with the estradiol transdermal estrogen replacement patch system". Optometry and Vision Science. 72 (1): 29–33. PMID 7731653. doi:10.1097/00006324-199501000-00006.
- Kirk, MD, Sheila (1999). Feminizing Hormonal Therapy For The Transgendered (1999 Edition). Pittsburgh, PA: Together Lifeworks. p. 56.
- Krenzer KL, Dana MR, Ullman MD, et al. (December 2000). "Effect of androgen deficiency on the human meibomian gland and ocular surface". The Journal of Clinical Endocrinology and Metabolism. 85 (12): 4874–82. PMID 11134156. doi:10.1210/jcem.85.12.7072.
- Sullivan DA, Sullivan BD, Evans JE, et al. (June 2002). "Androgen deficiency, Meibomian gland dysfunction, and evaporative dry eye". Annals of the New York Academy of Sciences. 966: 211–22. PMID 12114274. doi:10.1111/j.1749-6632.2002.tb04217.x.
- Sullivan BD, Evans JE (December 2002). "Complete androgen insensitivity syndrome: effect on human meibomian gland secretions". Archives of Ophthalmology. 120 (12): 1689–1699. PMID 12470144. doi:10.1001/archopht.120.12.1689.
- Cermak JM, Krenzer KL, Sullivan RM, Dana MR, Sullivan DA (August 2003). "Is complete androgen insensitivity syndrome associated with alterations in the meibomian gland and ocular surface?". Cornea. 22 (6): 516–21. PMID 12883343. doi:10.1097/00003226-200308000-00006.
- Oprea L, Tiberghien A, Creuzot-Garcher C, Baudouin C (October 2004). "Influence des hormones sur le film lacrymal" [Hormonal regulatory influence in tear film]. Journal Français D'ophtalmologie (in French). 27 (8): 933–41. PMID 15547478. doi:10.1016/S0181-5512(04)96241-9.
- Peterson's Principles of Oral and Maxillofacial Surgery. PMPH-USA. 2012. pp. 1209–. ISBN 978-1-60795-111-7.
- Harel Z, Biro FM, Kollar LM (May 1995). "Depo-Provera in adolescents: effects of early second injection or prior oral contraception". The Journal of Adolescent Health. 16 (5): 379–84. PMID 7662688. doi:10.1016/S1054-139X(95)00094-9.
- Archer B, Irwin D, Jensen K, Johnson ME, Rorie J (1997). "Depot medroxyprogesterone. Management of side-effects commonly associated with its contraceptive use". Journal of Nurse-midwifery. 42 (2): 104–11. PMID 9107118. doi:10.1016/S0091-2182(96)00135-8.
- Civic D, Scholes D, Ichikawa L, et al. (June 2000). "Depressive symptoms in users and non-users of depot medroxyprogesterone acetate". Contraception. 61 (6): 385–90. PMID 10958882. doi:10.1016/S0010-7824(00)00122-0.
- Ott MA, Shew ML, Ofner S, Tu W, Fortenberry JD (August 2008). "The influence of hormonal contraception on mood and sexual interest among adolescents". Archives of Sexual Behavior. 37 (4): 605–13. PMC . PMID 18288601. doi:10.1007/s10508-007-9302-0.
- St-André M, Stikarovska I, Gascon S (February 2012). "Clinical Case Rounds in Child and Adolescent Psychiatry: De Novo Self-Mutilation and Depressive Symptoms in a 17-year-old Adolescent Girl Receiving Depot-Medroxyprogesterone Acetate". Journal of the Canadian Academy of Child and Adolescent Psychiatry. 21 (1): 59–62. PMC . PMID 22299016.
- Gupta ML, Tandon P, Barthwal JP, Gupta TK, Bhargava KP (November 1983). "Role of catecholamines in the central actions of medroxyprogesterone acetate". Experimental and Clinical Endocrinology. 82 (3): 380–3. PMID 6228435. doi:10.1055/s-0029-1210303.
- Hulshoff, Cohen-Kettenis; et al. (July 2006). "Changing your sex changes your brain: influences of testosterone and estrogen on adult human brain structure". European Journal of Endocrinology. 155 (Suppl 1): 107–114. ISSN 0804-4643. doi:10.1530/eje.1.02248.
- Henriksson P, Eriksson A, Stege R, et al. (1988). "Cardiovascular follow-up of patients with prostatic cancer treated with single-drug polyestradiol phosphate". The Prostate. 13 (3): 257–61. PMID 3211807. doi:10.1002/pros.2990130308.
- von Schoultz B, Carlström K, Collste L, et al. (1989). "Estrogen therapy and liver function--metabolic effects of oral and parenteral administration". The Prostate. 14 (4): 389–95. PMID 2664738. doi:10.1002/pros.2990140410.
- Asscheman H, Gooren LJ, Eklund PL (September 1989). "Mortality and morbidity in transsexual patients with cross-gender hormone treatment". Metabolism: Clinical and Experimental. 38 (9): 869–873. PMID 2528051. doi:10.1016/0026-0495(89)90233-3.
- Aro J, Haapiainen R, Rasi V, Rannikko S, Alfthan O (1990). "The effect of parenteral estrogen versus orchiectomy on blood coagulation and fibrinolysis in prostatic cancer patients". European Urology. 17 (2): 161–5. PMID 2178941.
- Henriksson P, Blombäck M, Eriksson A, Stege R, Carlström K (March 1990). "Effect of parenteral oestrogen on the coagulation system in patients with prostatic carcinoma". British Journal of Urology. 65 (3): 282–5. PMID 2110842. doi:10.1111/j.1464-410X.1990.tb14728.x.
- Aro J (1991). "Cardiovascular and all-cause mortality in prostatic cancer patients treated with estrogens or orchiectomy as compared to the standard population". The Prostate. 18 (2): 131–7. PMID 2006119. doi:10.1002/pros.2990180205.
- Henriksson P, Stege R (1991). "Cost comparison of parenteral estrogen and conventional hormonal treatment in patients with prostatic cancer". International Journal of Technology Assessment in Health Care. 7 (2): 220–5. PMID 1907600. doi:10.1017/S0266462300005110.
- Henriksson P (Jan–Feb 1991). "Estrogen in patients with prostatic cancer. An assessment of the risks and benefits". Drug Safety. 6 (1): 47–53. PMID 2029353. doi:10.2165/00002018-199106010-00005.
- Caine YG, Bauer KA, Barzegar S, et al. (October 1992). "Coagulation activation following estrogen administration to postmenopausal women". Thrombosis and Haemostasis. 68 (4): 392–5. PMID 1333098.
- Stege R, Sander S (March 1993). "[Endocrine treatment of prostatic cancer. A renaissance for parenteral estrogen]". Tidsskrift for Den Norske Lægeforening (in Norwegian). 113 (7): 833–5. PMID 8480286.
- Stege R, Carlström K, Hedlund PO, Pousette A, von Schoultz B, Henriksson P (September 1995). "[Intramuscular depot estrogens (Estradurin) in treatment of patients with prostate carcinoma. Historical aspects, mechanism of action, results and current clinical status]". Der Urologe. Ausg. A (in German). 34 (5): 398–403. PMID 7483157.
- Cox RL, Crawford ED (December 1995). "Estrogens in the treatment of prostate cancer". Journal of Urology. 154 (6): 1991–8. PMID 7500443. doi:10.1016/S0022-5347(01)66670-9.
- Henriksson P, Carlström K, Pousette A, et al. (July 1999). "Time for revival of estrogens in the treatment of advanced prostatic carcinoma? Pharmacokinetics, and endocrine and clinical effects, of a parenteral estrogen regimen". The Prostate. 40 (2): 76–82. PMID 10386467. doi:10.1002/(SICI)1097-0045(19990701)40:2<76::AID-PROS2>3.0.CO;2-Q.
- Hedlund PO, Henriksson P (March 2000). "Parenteral estrogen versus total androgen ablation in the treatment of advanced prostate carcinoma: effects on overall survival and cardiovascular mortality. The Scandinavian Prostatic Cancer Group (SPCG)-5 Trial Study". Urology. 55 (3): 328–33. PMID 10699602. doi:10.1016/S0090-4295(99)00580-4.
- Hedlund PO, Ala-Opas M, Brekkan E, et al. (2002). "Parenteral estrogen versus combined androgen deprivation in the treatment of metastatic prostatic cancer -- Scandinavian Prostatic Cancer Group (SPCG) Study No. 5". Scandinavian Journal of Urology and Nephrology. 36 (6): 405–13. PMID 12623503. doi:10.1080/003655902762467549.
- Scarabin PY, Oger E, Plu-Bureau G (August 2003). "Differential association of oral and transdermal oestrogen-replacement therapy with venous thromboembolism risk". Lancet. 362 (9382): 428–32. PMID 12927428. doi:10.1016/S0140-6736(03)14066-4.
- Straczek C, Oger E, Yon de Jonage-Canonico MB, et al. (November 2005). "Prothrombotic mutations, hormone therapy, and venous thromboembolism among postmenopausal women: impact of the route of estrogen administration". Circulation. 112 (22): 3495–500. PMID 16301339. doi:10.1161/CIRCULATIONAHA.105.565556.
- Ockrim J; Lalani el-N; Abel P (October 2006). "Therapy Insight: parenteral estrogen treatment for prostate cancer--a new dawn for an old therapy". Nature Clinical Practice Oncology. 3 (10): 552–63. PMID 17019433. doi:10.1038/ncponc0602.
- Basurto L, Saucedo R, Zárate A, et al. (2006). "Effect of pulsed estrogen therapy on hemostatic markers in comparison with oral estrogen regimen in postmenopausal women". Gynecologic and Obstetric Investigation. 61 (2): 61–4. PMID 16192735. doi:10.1159/000088603.
- Hemelaar M, Rosing J, Kenemans P, Thomassen MC, Braat DD, van der Mooren MJ (July 2006). "Less effect of intranasal than oral hormone therapy on factors associated with venous thrombosis risk in healthy postmenopausal women". Arteriosclerosis, Thrombosis, and Vascular Biology. 26 (7): 1660–6. PMID 16645152. doi:10.1161/01.ATV.0000224325.96659.53.
- Hedlund PO, Damber JE, Hagerman I, et al. (2008). "Parenteral estrogen versus combined androgen deprivation in the treatment of metastatic prostatic cancer: part 2. Final evaluation of the Scandinavian Prostatic Cancer Group (SPCG) Study No. 5". Scandinavian Journal of Urology and Nephrology. 42 (3): 220–9. PMID 18432528. doi:10.1080/00365590801943274.
- Canonico M, Plu-Bureau G, Lowe GD, Scarabin PY (May 2008). "Hormone replacement therapy and risk of venous thromboembolism in postmenopausal women: systematic review and meta-analysis". BMJ. 336 (7655): 1227–31. PMC . PMID 18495631. doi:10.1136/bmj.39555.441944.BE.
- Levy, Andy; Crown, Anna; Reid, Russell (2003-11-01). "Endocrine intervention for transsexuals". Clinical Endocrinology. 59 (4): 409–418. ISSN 0300-0664. doi:10.1046/j.1365-2265.2003.01821.x.
- Kirk, MD, Sheila (1999). Feminizing Hormonal Therapy For The Transgendered (1999 Edition). Pittsburgh, PA: Together Lifeworks. p. 52.
- Hembree WC, Cohen-Kettenis P, Delemarre-van de Waal HA, Gooren LJ, Meyer WJ, Spack NP, Tangpricha V, Montori VM (2009). "Endocrine treatment of transsexual persons: an Endocrine Society clinical practice guideline". J. Clin. Endocrinol. Metab. 94 (9): 3132–54. PMID 19509099. doi:10.1210/jc.2009-0345.
- Gooren LJ, van Trotsenburg MA, Giltay EJ, van Diest PJ (2013). "Breast cancer development in transsexual subjects receiving cross-sex hormone treatment". J Sex Med. 10 (12): 3129–34. PMID 24010586. doi:10.1111/jsm.12319.
- Brown GR, Jones KT (2015). "Incidence of breast cancer in a cohort of 5,135 transgender veterans" (PDF). Breast Cancer Res. Treat. 149 (1): 191–8. PMID 25428790. doi:10.1007/s10549-014-3213-2.
- Cuhaci N, Polat SB, Evranos B, Ersoy R, Cakir B (2014). "Gynecomastia: Clinical evaluation and management". Indian J Endocrinol Metab. 18 (2): 150–8. PMC . PMID 24741509. doi:10.4103/2230-8210.129104.
- Niewoehner CB, Schorer AE (2008). "Gynaecomastia and breast cancer in men". BMJ. 336 (7646): 709–13. PMC . PMID 18369226. doi:10.1136/bmj.39511.493391.BE.
- Christopher Li (11 November 2009). Breast Cancer Epidemiology. Springer Science & Business Media. pp. 266–. ISBN 978-1-4419-0685-4.
- Stella Pelengaris; Michael Khan (13 March 2013). The Molecular Biology of Cancer: A Bridge from Bench to Bedside. John Wiley & Sons. pp. 586–. ISBN 978-1-118-43085-9.
- Gilda Cardenosa (2004). Breast Imaging. Lippincott Williams & Wilkins. pp. 1–. ISBN 978-0-7817-4685-4.
- Gao YR, Walters KA, Desai R, Zhou H, Handelsman DJ, Simanainen U (2014). "Androgen receptor inactivation resulted in acceleration in pubertal mammary gland growth, upregulation of ERα expression, and Wnt/β-catenin signaling in female mice". Endocrinology. 155 (12): 4951–63. PMID 25076121. doi:10.1210/en.2014-1226.
- Jerome F. Strauss, III; Robert L. Barbieri (13 September 2013). Yen and Jaffe's Reproductive Endocrinology. Elsevier Health Sciences. pp. 236–. ISBN 978-1-4557-2758-2.
- Shlomo Melmed; Kenneth S. Polonsky; P. Reed Larsen; Henry M. Kronenberg (30 November 2015). Williams Textbook of Endocrinology. Elsevier Health Sciences. pp. 934–. ISBN 978-0-323-29738-7.
- Hughes IA, Werner R, Bunch T, Hiort O (2012). "Androgen insensitivity syndrome". Semin. Reprod. Med. 30 (5): 432–42. PMID 23044881. doi:10.1055/s-0032-1324728.
- Schoemaker MJ, Swerdlow AJ, Higgins CD, Wright AF, Jacobs PA (2008). "Cancer incidence in women with Turner syndrome in Great Britain: a national cohort study". Lancet Oncol. 9 (3): 239–46. PMID 18282803. doi:10.1016/S1470-2045(08)70033-0.
- Gooren L, Morgentaler A (2014). "Prostate cancer incidence in orchidectomised male-to-female transsexual persons treated with oestrogens". Andrologia. 46 (10): 1156–60. PMID 24329588. doi:10.1111/and.12208.
- Turo R, Jallad S, Prescott S, Cross WR (2013). "Metastatic prostate cancer in transsexual diagnosed after three decades of estrogen therapy". Can Urol Assoc J. 7 (7–8): E544–6. PMC . PMID 24032068. doi:10.5489/cuaj.175.
- Prostate Cancer. Demos Medical Publishing. 20 December 2011. pp. 460–. ISBN 978-1-935281-91-7.
- Hembree, Wylie, C; Cohen-Kettenis, Peggy; Delemarre-van de Waal, Henriette; Gooren, Louis; Meyer III, Walter; Spack, Norman; Tangpricha, Vin; Montori, Victor (September 2009). "Endocrine Treatment of Transsexual Persons: An Endocrine Society Clinical Practice Guideline" (PDF). Clinical Endocrinology & Metabolism. 94 (9): 11. PMID 19509099. doi:10.1210/jc.2009-0345. Retrieved 2014-06-07.
- Hembree, Wylie, C; Cohen-Kettenis, Peggy; Delemarre-van de Waal, Henriette; Gooren, Louis; Meyer III, Walter; Spack, Norman; Tangpricha, Vin; Montori, Victor (September 2009). "Endocrine Treatment of Transsexual Persons: An Endocrine Society Clinical Practice Guideline" (PDF). Clinical Endocrinology & Metabolism. 94 (9): 18. PMID 19509099. doi:10.1210/jc.2009-0345. Retrieved 2014-06-07.
- Wylie, Kevan; Barrett, James; Besser, Mike; Bouman, Walter; Brain, Caroline; Bridgman, Michelle; Clayton, Angela; Green, Richard; Hamilton, Mark; Hines, Melissa; Ivbijaro, Gabriel; Khoosal, Deenesh; Lawrence, Alex; Lenihan, Penny; Ivbijaro, Del; Ralph, David; Reed, Terry; Stevens, John; Terry, Tim; Thom, Ben; Thornton, Jane; Walsh, Dominic; Ward, David (2014). "Good Practice Guidelines for the Assessment and Treatment of Adults with Gender Dysphoria" (PDF). Sexual and Relationship Therapy. Taylor & Francis. 29: 35.
- Hembree, Wylie, C; Cohen-Kettenis, Peggy; Delemarre-van de Waal, Henriette; Gooren, Louis; Meyer III, Walter; Spack, Norman; Tangpricha, Vin; Montori, Victor (September 2009). "Endocrine Treatment of Transsexual Persons: An Endocrine Society Clinical Practice Guideline" (PDF). Clinical Endocrinology & Metabolism. 94 (9): 22. PMID 19509099. doi:10.1210/jc.2009-0345. Retrieved 2014-06-07.
- Hembree, Wylie, C; Cohen-Kettenis, Peggy; Delemarre-van de Waal, Henriette; Gooren, Louis; Meyer III, Walter; Spack, Norman; Tangpricha, Vin; Montori, Victor (September 2009). "Endocrine Treatment of Transsexual Persons: An Endocrine Society Clinical Practice Guideline" (PDF). Clinical Endocrinology & Metabolism. 94 (9): 22–23. PMID 19509099. doi:10.1210/jc.2009-0345. Retrieved 2014-06-07.
- Hembree W, Cohen-Kettenis P, Delemarre-van de Waal H, Gooren L, Meyer III W, Spack N, Tangpricha V, Montori V (September 2009). "Endocrine Treatment of Transsexual Persons: An Endocrine Society Clinical Practice Guideline" (PDF). The Endocrine Society/Journal of Clinical Endocrinology & Metabolism. Retrieved 20 July 2011.
- Dahl M, Feldman J, Goldberg J, Jaberi A, Bockting W, Knudson G, Goldberg J (January 2006). "Endocrine Therapy for Transgender Adults in British Columbia: Suggested Guidelines" (PDF). Vancouver Coastal Health Authority. Retrieved 20 July 2011.
- Tom Waddell Clinic Transgender Protocol - MTF and FTM clinical protocols aimed at providers
- Moore E, Wisniewski A, Dobs A (August 2003). "Endocrine treatment of transsexual people: a review of treatment regimens, outcomes, and adverse effects". J. Clin. Endocrinol. Metab. 88 (8): 3467–73. PMID 12915619. doi:10.1210/jc.2002-021967. Retrieved 31 October 2013.