Hormone replacement therapy ( HRT ) of the male-to-female ( MTF ) type is hormone replacement therapy and therapy sex change is used to alter the sexual characteristics of transgender secondary persons from masculine (or sex) to feminine. This is one of two types of HRT for transgender people (the other is female-to-male) and is mostly used for treating transgender women. Some intersex people also receive this form of HRT, either from childhood to confirm the sex assigned or later if the assignment is proven wrong.
The purpose of this HRT form is to lead to the development of secondary sex characteristics of desired sex, such as breast and feminine patterns of hair, fat, and muscle distribution. Can not undo many of the changes produced by natural puberty, which may require surgery and other treatments (see below). Drugs used in MTF-type HRT include estrogen, antiandrogen, and progestogen.
While HRT can not undo the effects of one's first puberty, developing secondary sex characteristics associated with different genders can alleviate some or all of the distress and discomfort associated with sex dysphoria, and may help people to "pass" or be seen as a gender which they identify. Introducing exogenous hormones into the body affects every level and many patients report changes in energy levels, moods, appetite, etc. The goal of HRT, and indeed all somatic treatment, is to provide patients with a more satisfying body that is more congruent. with their gender identity.
Video Hormone replacement therapy (male-to-female)
Medical use
- To produce feminization and/or demasculinization in transgender and transfeminine non-binary individuals.
- To produce feminization and/or demasculinization on intersex people.
Maps Hormone replacement therapy (male-to-female)
Requirements and accessibility
Contraindications
Some medical conditions may be the reason to withstand hormone replacement therapy because of the danger that can be caused to the patient. The mixed factors as described in medicine as contraindications.
Absolute contraindications - those that can cause life-threatening complications, and where hormone replacement therapy should not be used - include a history of estrogen sensitive cancers (eg, breast cancer), thrombosis or embolism (unless the patient receives concurrent anticoagulation), or macroprolactinoma. In such cases, the patient should be monitored by an oncologist, hematologist or cardiologist, or neurologist, respectively.
Relative contraindications - where the benefits of HRT may outweigh the risks, but caution should be used - including:
- 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 Circulating or freezing 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, lack of protein C, S protein deficiency, or lack of antithrombin III.
As the dose increases, the risk also increases. Therefore, patients with relative contraindications can start with low doses and gradually increase.
Security
Hormone therapy for transgender individuals has been shown in the medical literature to be safe when supervised by qualified medical professionals.
Interactions
The CYP3A4 induser and other P450 cytochrome enzymes can reduce the effect of MTF HRT.
Type of therapy
Estrogen
Estrogen is one of the two main sex hormones in women (the other is progesterone), and is responsible for the development and maintenance of feminine secondary sexual characteristics, such as breast, wide hip, and feminine fat distribution patterns. Estrogen acts by binding and activating estrogen receptors (ER), their biological targets in the body. Different forms of estrogen are available and used medically. The most common estrogens used in transgender women include estradiol (which is the dominant natural estrogen in women) and estradiol esters such as estradiol valerate and estradiol cypionate (which are estradiol prodrugs). Conjugated estrogens (CEEs), marketed as Premarin among other brand names, and ethinylestradiol are also occasionally used, but these are becoming less common. Estrogens can be administered orally, sublingually, transdermal (via patches), topically (via gel), by intramuscular or subcutaneous injection, or by implant.
Before genital replacement surgery, the dose of estrogen for transgender people is often higher than the replacement dose used for cisgender women. Hembree et al. (2009) recommends "keep the sex hormone levels within the normal range for the sex of the desired person". Doses usually decrease after orchiectomy (removal of the testis) or genital replacement surgery. However, the practice has been carried away from an era where very high doses of estrogen are needed to lower testosterone, since antiandrogen is not used at the same time. Today, the higher doses of the less potent estrogen estradiol, which is endogenous to the human body, rather than the risky etinilestradiol and conjugated estrogens used in the past - are recommended for the first ten years or more of HRT, with or without orchiectomy or genital assignment. After that period, the dose can be reduced.
Antiandrogen
Androgens, such as testosterone and dihydrotestosterone (DHT), are the main sex hormones on individual XY chromosomes, and are responsible for the development and maintenance of secondary sexual characteristics of masculine, such as deep voice, broad shoulders, and masculine patterns in the hair. , muscle, and fat distribution. In addition, they stimulate sex drive and spontaneous erection frequency and are responsible for acne, body odor, and masculine hair loss patterns. Androgens act by binding and activating androgen receptors (AR), their biological targets in the body. Unlike androgens, antiandrogens are drugs that prevent androgen effects in the body. They do this by preventing androgens from binding to AR or by preventing androgen production. The most common antiandrogens used in transgender women are cyproterone acetate, spironolactone, and GnRH analogues.
Anti-steroidal antiandrogens
Anti-steroidal antiandrogens, namely spironolactone and cyproterone acetate, are the most commonly used antiandrogens for transgender women. Spironolactone, which is relatively safe and inexpensive, is the most commonly used antiandrogen in the United States. Cyproterone acetate, which is not available in the United States, is more commonly used in Europe and elsewhere in the world.
Spironolactone is a potassium-sparing diuretic mainly used for treating 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 with renal failure or elevated potassium levels. Spironolactone prevents androgen formation in the testes (though not in the adrenal gland) by inhibiting the enzymes involved in androgen production. It is also an androgen receptor antagonist (ie, prevents androgens from binding and activating androgen receptors).
Cyproterone acetate is a powerful antiandrogen and progestin that suppresses levels of gonadotropin (which in turn reduces androgen levels), inhibits androgens to bind and activate androgen receptors, and inhibits enzymes in androgen biosynthesis pathways. It has been used as a means of androgen deprivation therapy to treat prostate cancer. If used long-term in a dose of 150 mg or higher, it can cause damage or liver failure.
Nonsteroidal antandrogen
Non-steroidal antandrogens (NSAAs) used in HRT for transgender women include flutamide, nilutamide, and bicalutamide, all 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 decrease androgen levels; instead, they act only by preventing androgen binding to androgen receptors. However, they do it very strongly, and antiandrogens are very effective. Bicalutamide has improved tolerability and safety profiles relative to cyproterone acetate, as well as flutamide and nilutamide, and has replaced many of the latter two in clinical practice for this reason. Enzalutamide is a newer NSAA introduced with greater potency and efficacy as an antiandrogen than bicalutamide, but still under patent protection and in relation to this current (and for the foreseeable future) is very expensive. In addition, enzalutamide has been found to act as a negative allosteric modulator of GABA receptors and has been associated with central side effects such as anxiety, insomnia, and, most notably, seizures (in 1% of patients), the nature of which does not share with bicalutamide.
The NSAA may be an attractive option for transgender women who want to maintain sexual drive, sexual function, and/or fertility, as well as for those who want more selective action with fewer side effects than spironolactone and cyproterone acetate (which increases the risk of symptomatic depression, at among other side effects). Bicalutamide in particular may also be a safer drug than cyproterone acetate or spironolactone, because it has a much lower risk of hepatotoxicity compared with cyproterone acetate and, unlike spironolactone, has no risk of hyperkalemia or other antimineralocorticoid-related side effects. However, bicalutamide has a very small risk of hepatotoxicity, as well as interstitial pneumonitis.
Analog GnRH
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 causes the gonads to produce sex steroids such as androgens and estrogens. In adolescents of the sex with relevant indicators, GnRH analogues such as goserelin acetate may be used to stop undesirable puberty changes over a period of time without causing any change to the sex currently identified by the patient. GnRH agonists work initially to stimulate the pituitary gland, then rapidly decrease the sensitivity to the GnRH effect. After the initial spike, for several weeks, the production of gonadal androgens is greatly reduced. In contrast, GnRH antagonists act by blocking GnRH action in the pituitary gland.
There is considerable controversy about the earliest ages in which clinically, morally, and law are safe to use GnRH analogues, and for how long. The sixth edition of the World Professional Association for Transgender Health Care Standards allows it from Tanner stage 2 but does not allow the addition of hormones until the age of 16, which could be five years or more later. Sex steroids have important functions in addition to their role in puberty, and some skeletal changes (such as elevated elevations) that may be considered masculine are not impeded by GnRH analogues.
GnRH analog is often prescribed to prevent reactivation of testicular function when surgeon requires estrogen discontinuation before surgery.
The high cost of GnRH analogues is a significant factor in their lack of use in transgender people. However, they are prescribed as standard practice in the UK.
5? -Reductase inhibitor
Certain antiandrogens do not reduce testosterone or prevent their action on the tissues, but prevent their metabolites, dihydrotestosterone (DHT), from formation. These medications can be used when the patient has male pattern hair loss and/or prostate enlargement (benign prostatic hyperplasia), both of which aggravate DHT. Two drugs are currently available to prevent the formation of DHT: finasteride and dutasteride. DHT levels can be reduced to 60-75% with the first, and up to 93-94% with the last. These medications are also found to be effective in the treatment of hirsutism in women.
Progestogen
Progesterone, progestogen, is another of the two major sex hormones in women. Unlike estrogen, progesterone is not openly involved in the development of secondary sexual characteristics of women, and is involved primarily in the menstrual cycle and pregnancy. For this reason, progestogen is not commonly prescribed for transgender women. However, there may be a progestogenous role in breast development (although controversial and debatable) and in the skin and hair regulation, and progesterone in particular may have a positive effect on sex drive, sleep, and anxiety levels. In addition, because of their antigonadotropic and/or antiandrogen effects, progestogens can be useful in helping to suppress androgen effects in the body. The most common progestogens used in transgender women include progesterone and progestin (synthetic progestogen) such as CPA and medroxyprogesterone acetate (MPA). These drugs are usually taken orally, but can also be given by intramuscular injection.
Antiandrogenic and androgenic Effects
High-dose progestogens provide negative feedback on the hypothalamus-pituitary-gonadal axis by activating the progesterone receptor. As a result, they have an antigonadotropic effect - that is, they suppress the production of sex hormones such as androgens. Thus, sufficient progestogen dose, such as cyproterone acetate, gestonorone caproate, hydroxyprogesterone caproate, megestrol acetate, and MPA, may decrease androgen levels. In addition, certain other progestogens, such as cyproterone acetate, megestrol acetate, drospirenone, and nomegestrol acetate, bind and block the activation of androgen receptors. On the other hand, certain other progestogens, including 19-nortestosterone derivatives such as levonorgestrel, norgestrel, norethisterone, and norethisterone acetate, and, to a lesser extent, 17? -hydroxyprogesterone MPA derivatives, have weak androgenic activity because they bind and activate androgen receptors similar to testosterone, and can produce androgenic effects such as acne, hirsutism, and increased sex drive.
Role in breast development
Progestogens, along with the hormone prolactin, are involved in the maturation of lobules, acini, and areola during pregnancy: the mammary structure that has little estrogen to have no immediate effect. However, there is no clinical evidence that progestogens increase breast size, shape, or appearance in either transgender women or cisgender women, and one study found no benefit for hemicircumference of breast over estrogen alone in a small sample of transgender women given both estrogen and oral progestogens (usually 10 mg/day medroxyprogesterone acetate). However, the authors state that the sample size is too small to make definite conclusions, and that further research should be done to ascertain whether the progestogen significantly affects breast size and/or shape in transgender women. In 2014, no additional studies will see this problem. Anecdotal evidence from transgender women suggests that those taking progesterone supplements may experience fuller breast development, including stage IV on the Tanner scale (many transgender women do not develop Tanner's stage V breast). However, there has been no formal research with a large enough sample size to confirm this.
Other effects
Progestogens reportedly alter the distribution of fat (for example, by increasing the fat in the buttocks and thighs), increasing sex drive (especially progesterone, through active allopregnanolone metabolites), this does not occur through activation of progesterone receptors), leading to increased appetite and weight (only in combination with estrogen), produces a sense of calm (ie, anxiolysis), and promotes sleep (ie, sedative and hypnotic effects).
Progesterone is particularly important for bone health and appears to have a role in skin elasticity and nervous system function. Other effects seen with progesterone include reduced seizures and smooth muscle relaxation; reduce gallbladder activity; widening bronchus, which helps breathing; reduce inflammation and immune response; and normalization of blood clots and vascular tone, zinc and copper levels, cell oxygen levels, and fat storage for energy use. Progesterone also helps thyroid function and bone formation by osteoblasts.
Effects
The main effects of HRT MTF types are as follows:
- Breast enlargement and enlargement
- Skin softening and thinning
- Reduced growth and body hair density
- Redistribution of body fat in the feminine pattern
- The decrease in muscle mass and strength
- Hip widening (if epiphyseal closure has not occurred; see below)
- Reduced acne, oily skin, hair loss on scalp, and body odor
- Reduced penis size, scrotum, testicle, and prostate
- spermatogenesis and suppressed or deleted fertility
- Production of semen decreases/ejaculation volume
- Mood swings, emotions, and behaviors
- Reduced sex drive and spontaneous erectile incidence
The psychological effects of hormone replacement therapy are more difficult to define than physical changes. Because HRT is usually the first physical step taken for transition, the initial action has a significant psychological effect, which is difficult to distinguish from hormonal changes.
Physical changes
Breast development
Breast, nipple, and isolar development vary widely depending on genetics, body composition, HRT initiation age, and many other factors. Development can take several years to nearly a decade for some people. However, many transgender women report there are often "kiosks" in breast growth during transition, or significant breast asymmetry. Transgender women in HRT often experience less breast development than cisgender women (especially if started after young adulthood). For this reason, many look for breast enlargement. Transgender patients opt for rare breast reduction. The shoulder width and size of the ribs also play a role in breast size that can be understood; both are usually larger in transgender women, causing the breast to appear proportionately smaller. Thus, when a transgender woman chooses to do breast augmentation, the implant used tends to be larger than that used by cisgender women.
In clinical trials, cisgender women have used stem cells from fat to regrow their breasts after mastectomy. This could someday eliminate the need for implants for transgender women.
In transgender women in HRT, as in cisgender women during puberty, breast ducts and Cooper ligaments develop under the influence of estrogen. Progesterone causes the milk bag (mammae alveoli) to develop, and with appropriate stimulation, a transgender woman can breastfeed. In addition, HRT often makes the nipple more sensitive to stimulation.
Skin Changes
The top layer of skin, stratum corneum, becomes thinner and more translucent. Spider veins may appear or more visible as a result. Collagen decreases, and tactile sensation increases. The skin becomes softer, more susceptible to rips and irritation from scratches or shearing, and the color is slightly lighter due to a slight decrease in melanin.
Activation of sebaceous glands (which are triggered by androgens) decreases, reducing oil production in the skin and scalp. As a result, the skin becomes less prone to acne. It also becomes drier, and lotion or oil may be needed. The pores become smaller because the amount of oil produced is lower. Many apocrine glands - a type of sweat gland - become inactive, and body odor decreases. The remaining body odor becomes less metallic, sharp, or sharp, and sweeter and musky.
When subcutaneous fat accumulates, dimpled, or cellulite, it becomes clearer on the thighs and buttocks. Stretch marks (striae distensae) can appear on the skin of this area. Vulnerability to sunburn increases, perhaps because the skin is thinner and less pigmented.
Hair change
Antiandrogens affect only few facial hairs; patients may see slower growth and decreased density and coverage. Those who are less than a decade past puberty and/or lack of large amounts of facial hair may have better results. Patients taking antiandrogen tend to have better results with electrolysis and laser hair removal than those who do not. In patients in their teens or early twenties, antiandrogens prevent new facial hair from developing if testosterone levels are within the range of normal women.
Body hair (on the chest, shoulders, back, abdomen, buttocks, thighs, tops of the hands, and upper legs) changes, over time, from the terminal hair ("normal") into small, blond vellus hairs. The arms, perianal, and perineal hairs are reduced but may not change into vellus hair in the last two areas (some cisgender women also have hair in this area). The armpits of hair change slightly in texture and length, and pubic hair becomes more typical of women in the pattern. The lower leg hair becomes less dense. All of these changes depend on a certain degree of genetics.
Head hair can change slightly in texture, curls, and color. This is very possible with hair growth from previously bald areas. Eyebrows do not change because they are not androgenic.
Eye change
The lens of the eye changes the curvature. Because androgen levels decrease, the meibom glands (sebaceous glands in the upper and lower eyelids exposed at the edges) produce less oil. Because oil prevents tear films from evaporating, these changes can cause dry eyes.
Fat changes
The distribution of adipose tissue (fat) changes slowly for months and years. HRT causes the body to accumulate new fat in a distinctive feminine pattern, including in the hips, thighs, buttocks, pubes, upper arms, and breasts. (Fats on hips, thighs and buttocks have a higher concentration of omega-3 fatty acids and are intended to be used for lactation.) The body starts to burn old adipose tissue around the waist, shoulders, and back, making the area smaller.
Subcutaneous fats increase in the cheeks and lips, making the face appear more rounded, with less emphasis on the jaw when the bottom of the cheek is filled.
Muscle changes
HRT causes a decrease in muscle mass and distribution of the proportion of women.
Bone/skeletal changes
Male-female hormone therapy causes the hip to rotate slightly due to tendon changes. Hip discomfort is not uncommon.
If estrogen therapy begins before the ossification pelvis, which occurs around the age of 25 years, the pelvic outlet and inlet are slightly open. Femora also widened, because they are connected to the pelvis. The pelvis retains some masculine characteristics, but HRT's end result is a wider hip than a cisgender man and closer to a cisgender woman.
Unaffected characteristics
HRT does not reverse the bone changes that puberty has established. Consequently, it does not affect height; length of arms, legs, arms, and legs; or shoulder width and ribs. However, details of bone shape change throughout life, with bones becoming heavier and deeper engraved under the influence of androgens, and HRT prevents these changes from progressing further.
The width of the hip is not affected in the individual for whom epiphyseal closure (fusion and bone end closure, which prevents further elongation) have occurred. This happens to most people between 18 and 25 years. The existing changes in hip shape can not be undone by HRT whether epiphyseal closure has occurred or not.
The well-established changes in facial bone structure are also unaffected by HRT. Most craniofacial changes occur during adolescence. Post-adolescent growth is much slower and minimal by comparison. Also unaffected is the superiority of thyroid cartilage (Adam's apple). These changes can be reversed by surgery (facial feminization and shaving tracheal surgery, respectively).
During puberty, the sound gets deeper and becomes more resonant. This change is permanent and is not affected by HRT. Sound therapy and/or surgery can be used instead to achieve a more female-sounding voice.
Facial hair develops during puberty and is only slightly affected by HRT. However, it can be removed almost permanently by laser hair removal, or permanently by electrolysis.
Psychological changes
Mood changes, including depression, can occur with hormone replacement therapy. However, many transgender women report significant mood lifting effects as well. The risk of side-effects of depression is more common in patients taking progestin. Medroxyprogesterone acetate, in particular, has been shown to cause depression in certain individuals, possibly by affecting dopamine levels.
Sex sponge
Some transgender women report significant decreases in libido, depending on the antiandrogen dose. A small number of post-operative transgender women take low-dose testosterone to increase their libido. Many pre-operative transgender women wait until after the reassignment surgery to start an active sex life. Increasing doses of estrogen or adding progestogens increases libido in some transgender women.
Spontaneous and morning erections are significantly reduced in frequency, although some patients who have undergone an orchiektomi still have an erection in the morning. Voluntary erection may or may not be possible, depending on the amount of hormone and/or antiandrogen taken.
Neurological changes
Recent studies have shown that hormone therapy in transgender women can reduce brain volume to the proportion of women.
All of the above mentioned physical changes can, and reportedly, alter the sensation experience compared to before HRT. Affected areas include, but are not limited to, basic senses, erogenous stimuli, emotional perceptions, perceptions of social interaction, and processing of feelings and experiences.
Cardiovascular effects
The most significant cardiovascular risk for transgender women is the pro-thrombotic effect (increased blood clotting) of estrogen. This manifests most significantly as an increased risk for thromboembolic disease: deep vein thrombosis (DVT) and pulmonary embolism, which occurs when blood clots from the DVT break out 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 palpitations of the heart, sometimes without leg pain or swelling.
Deep venous thrombosis is more common in the first year of treatment with estrogen. The risk is higher with oral estrogens (especially ethinylestradiol and conjugated estrogens) compared with injection, transdermal, implantable, and nasal formulations. The risk of DVT also increases with age and in patients who smoke, so many doctors recommend the use of safer estrogen formulations in smokers and patients older than 40.
Because the risk of warfarin - used to treat blood clots - in relatively young and otherwise healthy populations is low, while the risk of adverse physical and psychological outcomes for untreated transgender patients is a high pro-thrombotic mutation (such as factor V). Leiden, antithrombin III, and lack of protein C or S) are not absolute contraindications to hormonal therapy.
Gastrointestinal/metabolic changes
Estrogen can increase the risk of gallbladder disease, especially in older people and obesity. They can also increase transaminase levels, indicating liver toxicity, especially when taken in oral form.
The patient's metabolic rate may change, leading to an increase or decrease in body weight and energy levels, changes in sleep patterns, and temperature sensitivity. Androgen deprivation causes slower metabolism and loss of muscle tone. Building muscle requires more work. The addition of progestogen can increase energy, although it can increase appetite as well.
Bone changes
Both estrogen and androgens are needed in all humans for bone health. Healthy young women produce about 10 mg of testosterone every month, and higher bone mineral density in men is associated with higher serum estrogens. Both estrogen and testosterone help stimulate bone formation, especially during puberty. Estrogen is the main sex hormone that slows bone loss, even in men.
The risk of hormone-sensitive cancers
Regardless of induction of breast development, transgender women undergoing HRT have no increased risk of breast cancer. Only a few cases of breast cancer have ever been described in transgender women who have undergone male-female HRT. This is consistent with studies in cisgender men in whom gynecomastia was found to be unrelated to an increased risk of breast cancer, suggesting a protective role of chromosomes in the determination of male sex. On the other hand, men with Klinefelter syndrome (two X chromosomes and one Y chromosome), which causes hypoandrogenism, hyperestrogenism, and a very high incidence of gynecomastia (80%), have a dramatic increased risk (20- to 58-fold) of breast cancer compared with men with one X chromosome, closer to the level of homogametic women. The incidence of breast cancer in male karyotype (46, XY karyotype), men with Klinefelter syndrome (47, XXY karyotype), and karyotype women (46, XX karyotype) were about 0.1%, 3%, and 12.5%. Individuals with 46, XY karyotype affected by complete androgen insensitivity syndrome have never developed male sex characteristics and have normal and complete female morphology, and accelerated breast growth during puberty, but appear to have few (or perhaps none) breast cancer incidence. The risk of breast cancer in women with Turner syndrome (45, XO karyotype) also seems to decrease significantly, although this may be related to ovarian failure/hypogonadism rather than supposedly from genetics.
Prostate cancer is very rare in transgender orchidectomy women who have been treated with estrogen for long periods of time. While as many as 70% of men showed prostate cancer in their 80s, only a few cases of prostate cancer in transgender women have been reported in the literature. Thus, and in accordance with the fact that androgens are responsible for the development of prostate cancer, HRT appears to be very protective against prostate cancer in transgender women.
Other changes
Migraine may be aggravated or unconstrained by estrogen therapy.
Estrogen can also cause prolactinoma. The release of milk fluid from the nipple may be a sign of increased prolactin levels. If prolactinoma becomes large enough, it can cause visual changes (especially decreased peripheral vision), headache, depression or other mood swings, dizziness, nausea, vomiting, and symptoms of pituitary failure, such as hypothyroidism.
Hormone level
Especially in the early stages of hormone replacement therapy, blood work is often done to assess hormone levels and liver function. The Endocrine Society recommends that patients undergo a blood test every three months in the first year of HRT for estradiol and testosterone, and that spironolactone, if used, will be monitored every 2-3 months in the first year. The optimal range for estradiol and testosterone is unlimited but includes the following:
The optimal range for estrogens applies only to individuals using estradiol (or estradiol esters), and not to those who use other synthetic or non-bioidentic preparations (eg, CEEs or ethinylestradiol).
Doctors also recommend broader medical monitoring, including full blood counts; tests kidney function, liver function, and lipid and glucose metabolism; and monitoring prolactin levels, weight, and blood pressure.
See also
- Hormone replacement therapy (female-to-male)
- Hormone replacement therapy (menopause)
- Hormonal breast enhancement
- Pharmacologic body change
- High-dose estrogen
- Androgen replacement therapy
References
External links
- 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 in Transsexual Persons: Clinical Practice Guidelines for Endocrine Society" (PDF) . The Endocrine Society/Journal of Clinical Endocrinology & amp; Metabolism. Archived from the original (PDF) on September 27, 2011 . Retrieved July 20 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 Advice" (PDF) . Vancouver Coastal Health Authority . Retrieved July 20 2011 .
- The Tom Waddell Clinic Transgender Protocol - the MTF and FTM clinical protocols intended for providers
- Moore E, Wisniewski A, Dobs A (August 2003). "Endocrine treatment in transsexual people: review of treatment regimens, outcomes, and side effects". J. Clin. Endocrine. Metab . 88 (8): 3467-73. doi: 10.1210/jc.2002-021967. PMID 12915619 . Retrieved October 31 2013 .
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