Transgender Mtf Hormones

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REFERENCES AND RECOMMENDED READING (from Gardner & Safer, 2013)
1.Gates GJ. How many people are lesbian, gay, bisexual, and transgender? The Williams Institute; 2011.
2. Sanchez NF, Sanchez JP, Danoff A. Healthcare utilization, barriers to care, and hormone usage among male-to-female transgender persons in New York City. Am J Public Health 2009; 99:713 – 719.
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Adapted from: Gardner, Ivy and Safer, Joshua D . 2013 Progress on the road to better medical care for transgender patients. Current Opinion in Endocrinology, Diabetes and Obesity 20(6): 553-558.
Hormone regimes for transgender men (female to men, FTM)
  2. Parenterally (i.m. or subcutaneous)
i.m., intramuscular.
*Not available in the USA.
Monitoring for transgender men (FTM) on hormone therapy:
Hormone regimes for transgender women (male to women, MTF) 
i.m., Intramuscular; MTF, male to female. aNot available in the USA.
Monitoring for transgender women (MTF) on hormone therapy:
3. Leinung MC, Urizar MF, Patel N, Sood SC. Endocrine treatment of transsexual * persons: extensive personal experience. Endocr Pract 2013; 19:644 – 650.
4. Gorin-Lazard A, Baumstarck K, Boyer L, et al. Is hormonal therapy associated *with better quality of life in transsexuals? A cross-sectional study. J Sex Med 2012; 9:531–541.
5. Obedin-Maliver J, Goldsmith ES, Stewart L, et al. Lesbian, gay, bisexual, and transgender-related content in undergraduate medical education. J Am Med Assoc 2011; 306:971 – 977.
6. Safer JD, Tangpricha V. Out of the shadows: it is time to mainstream treatment for transgender patients. Endocrine Pract 2008; 14:248 – 250.
7. Reiner WG, Gearhart JP. Discordant sexual identity in some genetic males with cloacal exstrophy assigned to female sex at birth. N Engl J Med 2004; 350:333 – 341.
8. Meyer-Bahlburg HFL. Gender identity outcome in female-raised 46,XY per- sons with penile agenesis, cloacal exstrophy of the bladder, or penile ablation. Arch Sex Behav 2005; 34:423 – 438.
9. Zhou J-N, Hofman MA, Gooren LJG, Swaab DF. A sex difference in the human brain and its relation to transsexuality. Nature 1995; 378:68 – 70.
10. Kruijver FP, Zhou JN, Pool CW, et al. Male-to-female transsexuals have female neuron numbers in a limbic nucleus. J Clin Endocrinol Metab 2000; 85:2034 – 204z
11. Berglund H, Lindstro ̈ m P, Dhejne-Helmy C, Savic I. Male-to-female transsex- uals show sex-atypical hypothalamus activation when smelling odorous steroids. Cerebr Cortex 2008; 18:1900 – 1908.
12. Rametti G, Carrillo B, Go ́mez-Gil E, et al. White matter microstructure in female to male transsexuals before cross-sex hormonal treatment. A diffusion tensor imaging study. J Psychiatr Res 2011; 45:199 – 204.
13. RamettiG,CarrilloB,Go ́mez-GilE,etal.Themicrostructureofwhitematterin male to female transsexuals before cross-sex hormonal treatment. A DTI study. J Psychiatr Res 2011; 45:949–954.
14. GreenR,NewmanL,StollerR.Treatmentofboyhood‘transsexualism’.Arch Gen Psychiatry 1972; 26:213–217.
15. Liao L-M, Audi L, Magritte E, et al. Determinant factors of gender identity: a commentary. J Pediatr Urol 2012; 8:597–601.
16. World Professional Association for Transgender Health. Standards of care for the health of transsexual, transgender, and gender nonconforming people. 7th ed.; 2011. http://www.wpath.org/documents/Standards%20of%20Care% 20V7%20-%202011%20WPATH.pdf (Accessed on 24 December 2012)
17. Hembree WC, Cohen-Kettenis P, Delemarre-van de Waal HA, et al. Endo- crine treatment of transsexual persons: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 2009; 94:3132 – 3154.
18. Gooren LJ. Care of transsexual persons. N Engl J Med 2011; 364:2559– 2560.
19. BhasinS,SaferJ,TangprichaV.Thehormonefoundation’spatientguideto the endocrine treatment of transsexual persons. J Clin Endocrinol Metab 2009; 94:.
20. Bockting WO, Miner MH, Swinburne Romine RE, et al. Stigma, mental health, * and resilience in an online sample of the US transgender population. Am J Public Health 2013; 103:943 – 951.
21. Olshan JS, Spack NP, Eimicke T, et al. Evaluation of the efficacy of sub-cutaneous administration of testosterone in female to male transexuals and hypogonadal males. Endocr Rev 2013; 34:(03_MeetingAbstracts): MON- 594.
22. Nagarajan V, Chamsi-Pasha M, Tang WHW. The role of aldosterone receptor antagonists in the management of heart failure: an update. Cleve Clin J Med 2012; 79:631 – 639.
23. Asscheman H, Giltay EJ, Megens JAJ, et al. A long-term follow-up study of mortality in transsexuals receiving treatment with cross-sex hormones. Eur J Endocrinol 2011; 164:635 – 642.
24. Wierckx K, Mueller S, Weyers S, et al. Long-term evaluation of cross-sex * hormone treatment in transsexual persons. J Sex Med 2012; 9:2641–2651.
25. Wallien MSC, Cohen-Kettenis PT. Psychosexual outcome of gender-dysphoric children. J Am Acad Child Adolesc Psychiatry 2008; 47:1413 – 1423. 26. Cohen-Kettenis PT, Delemarre-van de Waal HA, Gooren LJG. The treatment of adolescent transsexuals: changing insights. J Sex Med 2008; 5:1892–1897.
27. De Vries ALC, Steensma TD, Doreleijers TAH, Cohen-Kettenis PT. Puberty suppression in adolescents with gender identity disorder: a prospective follow-up study. J Sex Med 2011; 8:2276 – 2283.
28. Safer JD, Pearce EN. A simple curriculum content change increased medical & student comfort with transgender medicine. Endocrine Pract 2013; 33:39–44.

Male to Female Transition and Self Medicating Guide.
It’s a fact that some transsexuals choose—usually because it’s the only option available to them—to self-prescribe hormones and/or androgen-blocking drugs. This article compares recommendations from medical and non-medical sources, and explains conditions that could result from HRT, whether therapy is medically monitored or not. This information is not provided or intended as a substitute for professional medical advice or care.
I am not a medical professional. Please also note that the glossary at the end of this article is just that: a glossary, and not a dictionary. The descriptions of the terms in the glossary are meant to help you interpret their use in this article only, and are not comprehensive definitions.
There are no generally agreed upon recommended dosages, or recommended drugs within categories. The following recommendations are based upon three sources, but the categorization of drugs into “recommended” and “less recommended” come from “Hormone Treatment in Transsexual People” (Asscheman and Gooren 1992). Dosage recommendations and notes, unless otherwise noted, are also from Asscheman and Gooren.
It is recommended that MTFs take both an anti-androgen and a source of estrogen before having an orchiectomy, and discontinue using anti-androgens after an orchiectomy (Asscheman & Gooren). Taking only an anti-androgen incurs risk of serious bone density loss, and taking only estrogen does not significantly lower testosterone levels. You should only be using one drug at the recommended dosage from each category.
Note that mg is an abbreviation for milligrams, not to be confused with µg, the abbreviation for micrograms. A microgram is 1/1,000 of a milligram. To avoid some confusion, the abbreviation for micrograms is not used in these tables. Other abbreviations that have been replaced for clarity are t.i.d., which is the Latin abbreviation for “three times a day,” p.o., which indicates an oral dose, and i.m., for intramuscular injections.
For common names and descriptions of commercially available preparations of the drugs, click the generic name.
Recommended anti-androgens and their dosage:
Less recommended anti-androgens and their dosage:
Recommended estrogens and their dosages:
[1] Asscheman and Gooren 1992 [2] Lawrence [3] Futterweit 1998
How reliable are websites and mailing lists created by other trans women for providing safe, accurate information about hormone therapy? One way to gauge their reliability is to compare the concrete dosage recommendations against those provided by medical sources.
I subscribed to an electronic mailing list on which transsexuals who are self-medicating (primarily MTFs) exchange advice on hormone therapy, and selected twenty-one individual posters who identified their own regimens, including drug names and dosage, and did not report dissatisfaction or ask for help in modifying their hormone regimens. Of those, four (19%) reported hormone regimens that were within the guidelines given by Asscheman and Gooren or Lawrence.
Of those who were not within the guidelines, the differences ranged from the possibly ineffective to the potentially dangerous. Five (25%) used an anti-androgen considered less effective by Asscheman and Gooren. Two (10%) reported cycling doses, which has no known therapeutic value. Five (25%) used a higher dose of anti-androgen than recommended, and four (19%) used a lower dose of anti-androgen than recommended. A high number (7, one third) reported using a lower dose of estrogen than recommended by Asscheman and Gooren, while one used a higher than recommended dose. Included in the numbers already reported, four (19%) used lower than recommended doses of both the anti-androgen and estrogen. Three (14%) who did not report having had orchiectomies said they used no anti-androgen. Of those reported above, one trans woman was taking three times the normal dose of anti-androgen, and another twice the normal dose of estrogen.
Phytoestrogens work by weakly binding with estrogen receptors, giving in some cases very mild feminizing effects. However, the doses required to achieve any effects at all are prohibitively large and toxic. (FAQ: Hormone Therapy for M2F Transsexuals) Most sources do not recommend that trans women use black cohosh, dong quai, milk thistle, or any other phytoestrogenic herb as a replacement for hormone therapy, even as a low-dose measure, because of their inefficacy. Because of the way that phytoestrogens compete with estrogen for receptors, using them in addition to hormone therapy may also be counterproductive.
Combined treatment with estrogen and cyproterone acetate is associated with increases in thromboembolic events (Asscheman, Gooren, & Eklund). The more serious risk of thromboembolism, according to a later study by two of the same researchers, is greatly reduced by the use of transdermal estrogen therapy in patients over the age of 40, in whom “a high incidence of venous thromboembolism was observed with oral oestrogens.” (van Kesteren et al 1997) A 1998 study in which estrogen was administered by injection or orally reported incidence of thromboembolic events as “negligible” (Schlatterer et al).
In a 1989 retrospective study, combined treatment with estrogen and cyproterone acetate was associated with increases in hyperprolactinemia (Asscheman, Gooren, & Eklund). An article dealing specifically with the risks of self-treatment by transsexual women also noted increased rates of hyperprolactinemia (Becerra Fernandez et al 1999). The complications of hyperprolactinemia are limited, but can include blindness and hemorraging (Schenenberger & Knee 2001). In one case study, prolactin-producing pituitary adenoma was linked with long-term estrogen use (Kovacs et al 1994). In study of elevated prolactin levels in transsexual women, of fifteen patients with persistently high prolactin levels, the patients were also reported to have developed enlarged pituitary glands. The study linked elevated prolactin levels with higher estrogen dosage as well as with increased age, and suggested using the lowest effective dosages of estrogen (Asscheman et al 1988). Another study of transsexual women with elevated prolactin levels “suggest that the risk of inducing prolactinomas through cross-gender hormone treatment is likely to be small.” (Gooren et al 1985)
Combined treatment with estrogen and cyproterone acetate [an androgen-blocker] is associated with transient elevation of liver enzymes (Asscheman, Gooren, & Eklund). An article dealing specifically with the risks of self-treatment by transsexual women also noted elevation of liver enzymes (Becerra Fernandez et al 1999). The liver function issues in the 1989 study were attributed to other causes, such as alcohol abuse and hepatitis B, and were mainly successfully treated, either with other medications or temporarily halting hormone treatment.
In a German case study, bone loss was reversed in an MTF woman by adding 2 mg of oral estradiol valerate daily to the 100 mg of cyproterone daily she was already taking. She was losing bone mass at the rate of 5% per year while taking androgen-blockers without also taking estrogen (Hierl et al 1999). A case study comparing trans women who had been on estrogen for less than two years with those who’d been on it for longer found increased bone density in the women who’d been on estrogen longer (Reutrakul et al 1998).
In a 1989 retrospective study, combined treatment with estrogen and cyproterone acetate [an androgen-blocker] was associated with increases in depressive mood changes (Asscheman, Gooren, & Eklund). Depression has been tied to both high and low testosterone levels in women (Rohr 2002) and to the isolation of transsexuals (Rauchfleisch 1998).
An article dealing specifically with the risks of self-treatment by transsexual women noted higher levels of total cholesterol, LDL cholesterol, and triglycerides. (Becerra Fernandez et al 1999) However, the higher levels of cholesterol and triglycerides were still within normal levels (Citkowitz 2001, Isley 2002) and the lower incidence of other factors associated with heart disease, such as elevated plasma tHcy levels (Giltay et al 1998), suggest this is an acceptable risk.
Spironolactone use can cause hyperkalemia, an excessive amount of potassium in the blood. Hyperkalemia, an often symptomless condition, can cause serious kidney problems, including renal failure, and heart problems, including difficult to cure cardiac rhythm disturbances. (RxList). People using spironolactone are advised to avoid excessive potassium in their diets, including salt substitutes containing potassium chloride.
This site is not intended to provide medical advice, diagnosis, treatment or prevention. All linked products are active and can be ordered without a prescription.
We are not medical professions and are not endorsing self-medicating. We are just proving you with the resources to do so if you choose the route of self-medicating at your own risk.
The products, information, services and other content provided on and through this Site, including information that may be provided on the Site (directly or via linking to third-party sites by a healthcare or nutrition professional, are provided for informational purposes only.
Please consult with your physician or other healthcare professionals (collectively, “Healthcare Professional”) regarding any medical or health-related diagnosis or treatment options.
This site is not intended to provide medical advice, diagnosis, treatment or prevention.
The products, information, services and other content provided on and through this Site, including information that may be provided on the Site (directly or via linking to third-party sites by a healthcare or nutrition professional, are provided for informational purposes only.
Please consult with your physician or other healthcare professional (collectively, “Healthcare Professional”) regarding any medical or health-related diagnosis or treatment options.
Works by interfering with testosterone or DHT production. Also has receptor-blocking properties. Originally developed as a diuretic, it has antihypertensive properties.
Antigonadotropic. Less effective than cyproterone and spironolactone
150 mg/month intramuscular injection
Androgen receptor blocker. Not as effective for MTF hormone therapy, because it can potentially stimulate androgen production.
Works by interfering with testosterone or DHT production. Not as effective for MTF hormone therapy, because it can potentially stimulate androgen production.
Most potent estrogenic drug. Slowly metabolized by the liver, but has a large effect on other metabolic pathways in the liver. Very cheap and easily available. Can be obtained as the oral contraceptive pill, which is always combined with progestogen.
5-10 mg/day orally 1.25-2.5 mg/day orally 
Active dose in postmenopausal women is 0.625-1.25 mg, but for cross-gender hormone therapy the active dose is 5-10 mg (Meyer et al ., 1986). Largely metabolized at first liver passage. Conjugated estrogens in a dose of 2.5 and 5 mg orally per day are clearly associated with an increased risk of thrombosis.
2-4 mg/day orally 6-8 mg/day orally 10 mg/2 weeks to 200 mg/month intramuscular injection
Most potent of the three forms of native estrogens in the human body. Produced synthetically. Largely metabolized at first liver passage.
50-100 micrograms/day transdermally two 0.1 mg patches, applied simultaneously
Patches are replaced twice weekly. Low number of estrogen-induced side effects. Can cause skin irritation. Most expensive form. Very strongly recommended for patients over the age of 40, because of the risk of thromboembolism.
In cross-gender hormone treatment, high doses are necessary.

https://www.bumc.bu.edu/endo/clinics/transgender-medicine/guidelines/
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