Talk:Pharmaceutical feminizing HRT
This is not a Guide
We strive to provide non-biased, well cited, and accurate information, but this wiki is written by people who may or may not be professionals.
This is a note!
It contains the early rough scribblings of an article, which you could grow to a more thorough page, or simply deranged science musings! ❤
- 1 Starting Off
- 2 Basic regimen overview
- 3 Effects and side effects
- 4 Resources
- 5 References
Your first order of business is to get bloodwork done. See Blood tests and staying safe for where to order bloodwork and how to interpret it. If you think you ever want biological kids of your own, you should bank sperm before or immediately after starting HRT. You'll become temporarily infertile a month or two into HRT, and permanently infertile around 9 months in on average, I've heard. Going off hormones to bank later is not fun, and dysphoria may be much worse than it was before you started HRT. See Fertility (AMAB) for more info.
Basic regimen overview
Generally speaking, most feminizing HRT regimens will include an anti-androgen, to suppress the effects of testosterone on the body, alongside some form of estrogen and potentially some form of progestogen. This is analogous to the treatment of AFAB people suffering from conditions such as PCOS. However if an orchiectomy has been preformed then treatment with an anti-androgen may no longer be necessary, and AFAB people who wish to still be on estrogen but have had a hysterectomy will also need this regimen. Though if ovaries are intact simply stopping testosterone intake can often allow AFAB people to feminize through the usual aromatase pathway.
- Bioidentical 17β-estradiol is preferable over common xenoestrogens like ethinyl estradiol
- Transdermal routes of administration like patches or gel
- Higher levels of hormones can increase risks, especially when exceeding cis levels of hormones
- People with conditions that can be affected by estrogen should start at lower doses
- Some of the conditions that could be exacerbated by estrogen:
- can cause hyperkalemia
- can lower blood pressure
- Cyproterone acetate
- is hepatoxic
- can cause depression
- can cause fatigue/drowsiness
- 5-alpha reductase inhibitors
Feminizing regimens in WPATH SOC
Use of oral estrogen, and specifically ethinyl estradiol, appears to increase the risk of VTE. Because of this safety concern, ethinyl estradiol is not recommended for feminizing hormone therapy. Transdermal estrogen is recommended for those patients with risks factors for VTE. The risk of adverse events increases with higher doses, particular those resulting in supraphysiologic levels (Hembree et al., 2009). Patients with co-morbid conditions that can be affected by estrogen should avoid oral estrogen if possible and be started at lower levels. Some patients may not be able to safely use the levels of estrogen needed to get the desired results. This possibility needs to be discussed with patients well in advance of starting hormone therapy.
Androgen reducing medications (“anti-androgens”)
A combination of estrogen and “anti-androgens” is the most commonly studied regimen for feminization. Androgen reducing medications, from a variety of classes of drugs, have the effect of reducing either endogenous testosterone levels or testosterone activity, and thus diminishing masculine characteristics such as body hair. They minimize the dosage of estrogen needed to suppress testosterone, thereby reducing the risks associated with high-dose exogenous estrogen (Prior, Vigna, Watson, Diewold, & Robinow, 1986; Prior, Vigna, & Watson, 1989). Common anti-androgens include the following:
- Spironolactone, an antihypertensive agent, directly inhibits testosterone secretion and androgen
binding to the androgen receptor. Blood pressure and electrolytes need to be monitored because of the potential for hyperkalemia.
- Cyproterone acetate is a progestational compound with anti-androgenic properties. This
medication is not approved in the United States because of concerns over potential hepatotoxicity, but it is widely used elsewhere (De Cuypere et al., 2005).
- GnRH agonists (e.g., goserelin, buserelin, triptorelin) are neurohormones that block the
gonadtropin releasing hormone receptor, thus blocking the release of follicle stimulating hormone and luteinizing hormone. This leads to highly effective gonadal blockade. However, these medications are expensive and only available as injectables or implants.
- 5-alpha reductase inhibitors (finasteride and dutasteride) block the conversion of testosterone
to the more active agent, 5-alpha-dihydrotestosterone. These medications have beneficial effects on scalp hair loss, body hair growth, sebaceous glands, and skin consistency.
Cyproterone and spironolactone are the most commonly used anti-androgens and are likely the most cost-effective.
With the exception of cyproterone, the inclusion of progestins in feminizing hormone therapy is controversial (Oriel, 2000). Because progestins play a role in mammary development on a cellular level, some clinicians believe that these agents are necessary for full breast development (Basson & Prior, 1998; Oriel, 2000). However, a clinical comparison of feminization regimens with and without progestins found that the addition of progestins neither enhanced breast growth nor lowered serum levels of free testosterone (Meyer III et al., 1986). There are concerns regarding potential adverse effects of progestins, including depression, weight gain, and lipid changes (Meyer III et al., 1986; Tangpricha et al., 2003). Progestins (especially medroxyprogesterone) are also suspected to increase breast cancer risk and cardiovascular risk in women (Rossouw et al., 2002). Micronized progesterone may be better tolerated and have a more favorable impact on the lipid profile than medroxyprogesterone does (de Lignières, 1999; Fitzpatrick, Pace, & Wiita, 2000).
Effects and side effects
Effects and side effects in WPATH SOC
|Likely increased risk||* Venous thromboembolic diseaseA |
* Elevated liver enzymes
* Weight gain
|Likely increased risk with
presence of additional risk factorsB
|* Cardiovascular disease|
|Possible increased risk||* Hypertension |
* Hyperprolactinemia or prolactinomaA
|Possible increased risk with
presence of additional risk factorsB
|* Type 2 diabetesA|
|No increased risk or inconclusive||* Breast cancer|
|Effect||Expected Onset||Expected Maximum Effect|
|Body fat redistribution||3-6 months||2-5 years|
|Decreased muscle mass/
|3-6 months||1-2 yearsA|
|Softening of skin/
|Decreased libido||1-3 months||1-2 years|
|1-3 months||3-6 months|
|Breast growth||3-6 months||2-3 years|
|Decreased testicular volume||3-6 months||2-3 years|
|Decreased sperm production||variable||variable|
|Thinning and slowed growth
of body and facial hair
|6-12 months||> 3 yearsB|
|[Androgenetic alopecia]||No regrowth, loss
stops 1-3 months
- WPATH Standards of Care contains "diagnostic criteria", medical treatment recommendations, timelines etc.
- Hormones: a guide for MTFs is a great, human-readable guide on what to expect from hormonal transition.
- https://s3.amazonaws.com/amo_hub_content/Association140/files/Standards%20of%20Care%20V7%20-%202011%20WPATH%20(2)(1).pdf | Standards of Care for the Health of Transsexual, Transgender, and Gender Nonconforming People (page 40)
- https://s3.amazonaws.com/amo_hub_content/Association140/files/Standards%20of%20Care%20V7%20-%202011%20WPATH%20(2)(1).pdf | Standards of Care for the Health of Transsexual, Transgender, and Gender Nonconforming People (page 38)