Transfeminine HRT (Advanced)

Overview

Transfeminine hormone therapy (transfem HT) has two main goals: suppressing endogenous androgens (primarily testosterone) to levels within the cisgender female range, and raising estradiol to physiological female levels. Depending on the chosen protocol, these two goals can be achieved separately or simultaneously.

This guide covers the underlying hormonal mechanisms, all types of available estrogens and their esters, all types of antiandrogens with their efficacy profiles, risks and mechanisms of action, the use of progesterone, estradiol monotherapy, and how to interpret hormone panels.

If you haven't started HRT yet, I recommend starting with the beginner guide. If you need personalized help, you can reach out on our Discord.

Relevant hormonal physiology

Understanding HRT requires understanding the hypothalamic-pituitary-gonadal axis (HPG axis) and how androgens and estrogens interact with it.

The HPG axis and negative feedback

The hypothalamus secretes GnRH (gonadotropin-releasing hormone) in a pulsatile manner, which stimulates the pituitary gland to release LH (luteinizing hormone) and FSH (follicle-stimulating hormone). LH acts on the testicular Leydig cells to produce testosterone. Both estradiol and testosterone act negatively on the hypothalamus and pituitary gland, suppressing GnRH, LH, and FSH.

In transfeminine HRT, estradiol at sufficient doses can suppress LH production and, therefore, testicular testosterone production. This is the basis of estradiol monotherapy.

Peripheral conversion and aromatization

Testosterone is converted to estradiol by the enzyme aromatase (present in adipose tissue, muscle, brain, and liver). DHT (dihydrotestosterone) is formed from testosterone by 5α-reductase and is the most potent androgen at the androgen receptor; it cannot be aromatized into estrogens. DHT is primarily responsible for androgenic alopecia, prostate development, and part of body hair growth. In transfeminine people, DHT can be generated from progesterone in a subset of individuals, through a mechanism known as the "backdoor pathway" (androgen backdoor pathway). This mechanism completely bypasses testosterone as an intermediate step. In this group of people, the biochemical mechanism is as follows: Progesterone → 17α-hydroxyprogesterone (17-OHP) via the enzyme CYP17A1 → 5α-pregnan-17α-ol-3,20-dione, involving the enzyme 5-alpha reductase type 1 (SRD5A1) → 17-OH-allopregnanolone, involving the enzyme 3α-HSD (AKR1C2/4) → Androsterone, involving the previously mentioned enzyme CYP17A1 → Androstanediol → DHT via the enzymes 17β-HSD type 3 or 17β-HSD followed by a final oxidation (by RoDH/17β-HSD6). There is no conclusive information on why only a subset of people exhibit this mechanism so prominently, but it is believed to be due to the body having high expression of the previously mentioned enzymes.

Receptors and tissue sensitivity

Hormone effects depend on the density and sensitivity of their receptors in each tissue. The estrogen receptor (ER-α and ER-β) and the androgen receptor (AR) mediate the effects. Individual sensitivity to estrogens and androgens varies genetically, which explains why people with similar hormone levels have different physical responses.

SHBG (sex hormone-binding globulin)

SHBG binds sex hormones, deactivating them. Estradiol raises SHBG, which can reduce free (bioavailable) testosterone. Free testosterone (not bound to SHBG) is the biologically active fraction. On lab panels, total T is usually measured; free T is more relevant but less accessible. The rise in SHBG caused by estradiol contributes to androgen suppression even without antiandrogens.

Estrogens in transfeminine HRT

Types of estrogen

The estrogen used in transfeminine HRT is almost universally 17β-estradiol (the bioidentical human form). Synthetic estrogens such as ethinylestradiol (EE, found in contraceptives) were historically used, but have fallen out of favor in HRT due to their much higher thrombotic risk profile and because they aren't detected on standard E2 lab panels. Ethinylestradiol is 100 to 200 times more potent than 17β-estradiol, and it isn't broken down by the liver when taken orally. For this reason, it has almost 1000 times more hepatic impact than E2, which includes a drastic increase in the production of clotting factors.

Estradiol esters: mechanism and properties

Esters are prodrugs: estradiol molecules esterified at the C17 position with a fatty acid. When injected (usually in MCT or castor oil), they form a depot in muscle or subcutaneous tissue from which they're released slowly. Plasma esterases hydrolyze the ester, releasing active free estradiol. The length of the fatty acid's lipophilic chain determines the release rate and half-life.

Routes of administration

Intramuscular injection (IM)

Injection into muscle (glute, vastus lateralis of the thigh). Allows for high, stable levels. Absorption is somewhat faster than SubQ, which can produce a more pronounced initial peak depending on the ester. The depot disperses well in well-vascularized muscle tissue.

Subcutaneous injection (SubQ)

Injection into adipose tissue (abdomen, thigh, glute area). Slower and more sustained absorption than IM, giving more stable levels over time with some esters. Recent studies suggest that SubQ EEn can produce significantly higher E2 levels than IM at the same dose, due to lower vascularization. This means that switching from IM to SubQ may require a dose reduction. Less painful for many people, thinner needles (25–31G).

Oral (tablet/capsule)

Oral estradiol undergoes extensive first-pass hepatic metabolism: a large portion is converted to estrone (E1) before reaching systemic circulation. The E1:E2 ratio is reversed compared to normal physiology (E1 dominates). E2 levels are less predictable and more variable. It raises SHBG and clotting factors more than parenteral routes, increasing thrombotic risk. Generally not recommended as the primary route when another option is available.

Sublingual (tablet dissolved under the tongue)

Partially bypasses first-pass hepatic metabolism through direct absorption into the bloodstream via the mucous membranes. Produces higher but shorter-lived peaks (half-life ~2–4 h). Taken 2–4 times a day to maintain more stable levels. Better profile than oral, but with more variability than injectable. Useful when injectable isn't accessible.

Transdermal (gel, patch, cream)

Direct absorption through the skin, bypassing first-pass hepatic metabolism. Patches have controlled release (daily or weekly). Gel is applied daily. Absorption varies depending on application site, skin hydration, and temperature. For patches, fattier areas have higher absorption. Can reach high levels if enough is applied. Low impact on SHBG and clotting factors. Downside: inconsistent absorption between individuals, hard to predict levels. Scrotal/penoscrotal areas (for cream, gel, or sprays like Lenzetto) have much higher absorption than skin on the arm (up to 5–8x).

Rectal (suppository/tablet)

Allows for direct absorption, bypassing first-pass hepatic metabolism. Levels similar to sublingual but with a more sustained profile in some studies. Mainly used for progesterone (which has an oral bioavailability of 5-8%)

Estradiol monotherapy (suppression without an AA)

With sufficiently high, sustained E2 levels (>200 pg/mL, ideally >200–300 pg/mL), estradiol suppresses the HPG axis through negative feedback, reducing LH and FSH and, consequently, testicular testosterone production down to levels in the female range (<50 ng/dL, ideally <30 ng/dL).

Monotherapy with injectable EEn or EV is currently the most common protocol in DIY communities, due to its effectiveness and simplicity. It requires sufficient doses to keep E2 levels consistently elevated (not cycling through high peaks and low troughs).

Advantages over using an AA: fewer medications, fewer side effects, lower risk (without the specific adverse effects of AAs). The main goal is to achieve and maintain complete suppression, which may require some time for dose adjustment.

Not everyone achieves complete suppression with monotherapy. In people with very high testicular production or a limited individual response, combining with an AA may be necessary.

Antiandrogens (AAs)

General mechanisms of AAs

Antiandrogens act through different mechanisms to reduce androgenic activity:

• Androgen receptor (AR) antagonists: directly block the receptor, preventing testosterone and DHT from exerting their effects (bicalutamide, flutamide, enzalutamide, spironolactone in part).
• Androgen synthesis suppressors: reduce testosterone production by acting on the HPG axis (GnRH analogs, cyproterone acetate via gonadotropic suppression).
• 5α-reductase inhibitors: block the conversion of testosterone into DHT (finasteride, dutasteride). These aren't true AAs, but rather inhibitors of the peripheral conversion.
• Mixed mechanism: spironolactone combines weak AR antagonism with a mild reduction in testosterone synthesis.

Spironolactone

An aldosterone antagonist with secondary antiandrogenic activity . AA mechanism: weak AR antagonism and mild reduction in T synthesis. Widely used in the US due to availability and physician familiarity.

Cyproterone Acetate (CPA)

A synthetic progestogen with potent antiandrogenic activity. Mechanism: AR antagonism and gonadotropic suppression (acts on the HPG axis, reducing LH/FSH and therefore T synthesis). Very potent and effective. Widely used in Europe. Not commonly available in the US.

Bicalutamide

A pure androgen receptor antagonist (it doesn't lower T levels, but instead blocks its action in tissues). It doesn't suppress androgen synthesis, so T and DHT levels may remain the same or even rise while their effects are blocked at the receptor level.

GnRH analogs (agonists and antagonists)

GnRH agonists (leuprorelin, triptorelin, goserelin, histrelin) act paradoxically: by delivering GnRH continuously (rather than pulsatile), they desensitize the pituitary receptors, inhibiting LH and FSH release and, therefore, suppressing testicular T production to castrate levels. They initially produce a transient "flare" (T elevation for 1–2 weeks) before suppression sets in.

GnRH antagonists (degarelix, relugolix) directly block the GnRH receptor without the initial flare. Newer and generally more expensive.

Rectal progesterone as a mild AA

Progesterone at high doses has antigonadotropic activity (suppresses LH/FSH), which contributes to lowering T. Rectal use allows for higher bioavailability than oral (from 5-8% to nearly 100%). At a dose of 200 mg rectally at night, it can contribute to androgen suppression as a complementary component. Discussed further in the Progesterone section.

Other antiandrogens and strategies

5α-reductase inhibitors (5-ARIs): finasteride and dutasteride

These aren't true AAs: they don't block the AR or reduce total T. They inhibit the conversion of T into DHT, which is the most potent androgen at peripheral androgen receptors (skin, scalp, prostate).

Finasteride: mainly inhibits 5α-reductase type 2. Reduces DHT by ~70%. Useful for androgenic alopecia and stubborn body hair when T is only partially suppressed. Dose: 1–5 mg/day.

Dutasteride: inhibits both type 1 and type 2 5α-reductase. Reduces DHT by ~90–95%. Greater efficacy for alopecia. Dose: 0.5 mg/day.

In transfeminine HRT with good T suppression, DHT will already be very low, so 5-ARIs offer little added benefit. They're more relevant when T is only partially suppressed and DHT-dependent symptoms persist.

Flutamide

A first-generation nonsteroidal AR antagonist, a precursor to bicalutamide. Notably worse hepatotoxicity profile than bicalutamide. Practically abandoned in transfeminine HRT in favor of bicalutamide. Not recommended.

Enzalutamide, apalutamide, darolutamide

Last-generation AR antagonists used in castration-resistant prostate cancer. More potent than bicalutamide, but very expensive and with a more pronounced side effect profile (seizure risk with enzalutamide). Insufficient evidence for routine transfeminine HRT use. Mentioned for completeness; not commonly used.

Drospirenone

A synthetic progestogen with antimineralocorticoid activity and moderate antiandrogenic activity. Found in contraceptives. Can be used as a mild adjunct AA, but its antiandrogenic efficacy is lower than CPA or bicalutamide. Safer profile than CPA regarding meningioma risk.

Combinations and mixed strategies

Some protocols combine mechanisms: for example, bicalutamide (AR blockade) + moderate doses of E2 (partial T suppression). Or low-dose CPA + E2 monotherapy. The combination of mechanisms can allow for lower doses of each component and, with it, fewer side effects from each.

Bicalutamide post-Tanner 3: advanced use

One of the most debated and relevant uses in advanced transfeminine HRT is that of bicalutamide after reaching Tanner stage 3 of breast development (where the areola and nipple form a clearly distinct secondary projection).

Stages of breast development (Tanner Scale)

Why use bicalutamide post-Tanner 3?

The hypothesis, derived from observations in the context of transfeminine HRT in adolescents and studies on breast tissue sensitivity, is as follows: during early breast development (Tanner 2–3), the breast tissue is highly sensitive to androgens, which can inhibit glandular growth. Androgen exposure during this critical phase may limit the final developmental potential.

Once Tanner 3 is reached, glandular tissue is already established and the risk of androgenic inhibition of development is lower. At this point, some people on E2 monotherapy (which may not fully suppress T) or on an AA that doesn't directly block the AR, could benefit from adding bicalutamide to block any residual androgenic effect on breast tissue and other sensitive tissues.

Mechanism and theoretical rationale

Since bicalutamide is a pure AR antagonist, it blocks the action of any residual T or DHT directly at the receptors in target tissues (breast, skin, scalp, etc.). This can be particularly useful for people who:

• Have partially suppressed T that isn't fully within the female range (>50 ng/dL)
• Experience residual androgenic effects (body hair, hair loss, acne) despite adequate E2
• Want to optimize breast development without increasing their E2 dose or adding a suppressive AA (CPA) with more side effects

Evidence and limitations

Direct evidence in adult transfem populations post-Tanner 3 is limited; the hypothesis is extrapolated from studies in different contexts (oncology, pediatric endocrinology, pharmacology). No randomized clinical trial has demonstrated that adding bicalutamide post-Tanner 3 improves final breast development compared to not doing so.

Suggested protocol (informational)

When bicalutamide is used in this context:

• Typical dose: 25 mg/day. Some people use 12.5 mg/day as the minimum effective dose.
• The E2 protocol is maintained without significant changes.
• Liver monitoring (ALT/AST) at 3 months after starting and then every 6–12 months thereafter.
• Duration: variable; many people continue it until reaching their desired breast development, or indefinitely if it's well tolerated and levels are adequate.
• Keep in mind that circulating T and DHT don't drop with bicalutamide (they may rise): T panels aren't indicators of blocking efficacy in this case.

Progesterone

Progesterone (P4) is the endogenous progestational hormone. In cis women, it's present primarily during the luteal phase of the menstrual cycle. Its role in transfeminine HRT is controversial but increasingly studied.

Bioidentical progesterone vs. synthetic progestogens

It's essential to distinguish between:

• Bioidentical (micronized) progesterone: identical to human P4. Examples: Seidigestan, Utrogestan, Prometrium. Acts on progesterone receptors (PR), not the AR.
• Synthetic progestogens: progesterone analogs (medroxyprogesterone acetate, norethisterone acetate, drospirenone, levonorgestrel, CPA...). They have different activity profiles, many with additional androgenic or antiandrogenic effects. They are NOT equivalent to bioidentical P4 in their effects on the PR nor in their safety profile.

Effects of progesterone in transfeminine HRT

The evidence is mixed and partly based on community observations. Reported potentially beneficial effects include:

• Improved breast development in some people (especially the shape of the breast and the areola-nipple complex), with a possible effect on Tanner staging
• Improved libido (P4 can act on neurosteroid receptors and has effects on sexual desire)
• Effects on sleep (allopregnanolone, a P4 metabolite, has GABAergic action, producing drowsiness)
• Contribution to androgen suppression (antigonadotropic effect at high doses)
• Possible cardioprotective and bone effects (less studied in transfem people)

Route of administration: why rectal?

Oral progesterone has very low bioavailability and undergoes extensive first-pass hepatic metabolism, which converts it into metabolites (5α- and 5β-reduced), reducing active circulating P4. The metabolite allopregnanolone (5α-reduced) has sedative/anxiolytic activity (GABA-A agonist), which explains the drowsiness caused by oral progesterone.

The rectal route (micronized tablet/capsule inserted rectally) largely bypasses the first-pass hepatic metabolism, producing significantly higher circulating P4 levels (comparable to the mid-luteal phase) with the same 200 mg that would produce much lower levels orally. This makes the rectal route pharmacologically superior for achieving systemic P4 levels.

When to consider adding progesterone

The most common recommendation in the community, and among some progressive endocrinologists, is to wait at least 1 year of HRT with E2 before adding progesterone, to give breast tissue time to develop in an estrogenic environment first. Adding P4 too soon could (theoretically) prematurely advance Tanner staging to 5 before there's enough glandular tissue, limiting the final result.

Standard dose: 200 mg rectally at night. The oral route isn't recommended if the goal is a systemic P4 effect; it can be reserved for cases where the sedative effect is what's wanted.

Target hormone levels

Target ranges are reference points, not absolute truths. Individual tissue response varies, and levels should be interpreted alongside observed symptoms and effects.

When to test and how to interpret

With injectables, testing should be done at the trough (the day before, or the same day as, the next injection, prior to injecting), to measure the sustained minimum level. The post-injection peaks are temporary and don't represent the sustained average level. With transdermal, gel, or patch, test midway through the application period or at the end (before the next application).

With sublingual, levels fluctuate a lot; test 2–4 h post-dose for peak, or right before the next dose for trough.

Advanced protocols

Protocol 1: Injectable EEn monotherapy (SubQ or IM)

The most popular protocol in DIY communities today.

• Medication: Estradiol enanthate (EEn) in oil (typically 40/50 mg/mL)
• Starting dose: 5–6 mg weekly
• Frequency: every 7 days
• Route: SubQ (preferred for more stable levels) or IM
• Goal: trough E2 >200 pg/mL, T <50 ng/dL
• Adjustment: if T isn't adequately suppressed after 3 months, increase the dose; if E2 is too high and side effects occur, reduce it
• Consideration: some people don't achieve full T suppression with monotherapy and require an AA

Protocol 2: E2 + low-dose CPA

A classic protocol in Europe. Effective and well studied. Low-dose CPA minimizes risks.

• Injectable or transdermal E2 at moderate doses (target trough E2 100–200 pg/mL)
• CPA: 6.25–12.5 mg/day (can be done by splitting 50 mg tablets into quarters/eighths)
• Monitoring: prolactin, liver enzymes, mood
• CPA duration: many people reduce or discontinue CPA once E2 alone is sufficient for suppression

Protocol 3: E2 + Bicalutamide

Useful when CPA isn't available or is contraindicated, or when a pure AR antagonist is preferred.

• Injectable or transdermal E2 at doses sufficient for feminization
• Bicalutamide: 25–50 mg/day
• Free T will remain elevated; this is expected.
• The goal of this protocol is to block T's tissue action, not to lower its serum level
• Monitoring: liver ALT/AST

Protocol 4: Injectable E2 + Bicalutamide post-Tanner 3

An advanced optimization protocol for people on E2 monotherapy who have reached Tanner 3 and want to enhance residual androgen blockade.

• Continue the existing E2 protocol unchanged
• Add bicalutamide 12.5–25 mg/day
• Evaluate at 3–6 months: effects on body hair, hair loss, skin, breasts

Protocol 5: E2 + Rectal progesterone (late phase)

For people with >1–2 years of HT who want to add progesterone.

• Maintain E2 at established levels
• Add 200 mg of rectal micronized P4 at night
• Evaluate: sleep, libido, breast changes, mood
• There aren't very useful lab markers for evaluating subjective efficacy; go by symptoms

Protocol for transitioning from SubQ to IM or vice versa

When switching between SubQ and IM with the same ester, E2 levels can vary significantly. SubQ tends to produce higher levels than IM at the same EEn dose. It's recommended to reduce the dose by 20–30% when switching from IM to SubQ, or increase it proportionally in the reverse direction, and retest after 6–8 weeks.

Blood tests: interpretation

Lab panels are the main tool for monitoring HRT. Here's a breakdown of what to order, when, and how to interpret it.

Basic hormone panel in transfem HT

• Estradiol (E2): the central marker of estrogen therapy
• Total testosterone: marker of androgen suppression
• LH and FSH: indicators of HPG axis status
• SHBG: to calculate free testosterone if needed and to assess E2's hepatic effect
• Prolactin: especially if using CPA or if there are symptoms suggestive of hyperprolactinemia

Extended panel by medication

Bicalutamide-specific lab interpretation

With bicalutamide, serum T should NOT be interpreted the same way as with other AAs. T may be in the male range or even elevated (a reflex rise from loss of AR negative feedback in the hypothalamus). This is normal and expected. Treatment success is judged by tissue effects (feminization, breast growth), NOT by blood T levels.

LH may also be elevated with bicalutamide (through the same feedback-blocking mechanism). This doesn't indicate anything of concern.

Free vs. total testosterone

Total T measures all T in the blood. Free T (not bound to SHBG) is the biologically active fraction. With high SHBG levels (induced by E2), free T can be much lower than total T, even when total T is in the low-male range. In people with very high SHBG (due to oral E2 or high doses of injectable E2), free T can be in the female range even when total T is borderline.

Risks, side effects, and monitoring

Thromboembolic risk

The risk of deep vein thrombosis (DVT) and pulmonary embolism (PE) is the most serious risk of transfeminine HRT. It varies significantly depending on the E2 administration route:

• Oral E2: higher risk (first-pass hepatic metabolism increases clotting factors)
• Injectable, transdermal, sublingual E2: considerably lower risk
• Ethinylestradiol (EE): the highest risk of all; don't use in transfem HRT

Factors that increase risk: smoking, obesity, prolonged immobility, hereditary thrombophilia, recent surgery, advanced age. Thrombophilia screening before starting HRT is advisable for people with a family history of thrombosis.

Bone health

Estrogens are essential for maintaining bone mineral density (BMD). In transfem HRT with adequate E2 levels, osteoporosis risk is low. Risk increases with prolonged periods of insufficient E2, or if puberty blockers are used without adequate simultaneous estrogen supplementation. With long-term GnRH analogs and inadequate E2, bone loss can be significant. Supplementing calcium (1000–1200 mg/day) and vitamin D (1000–2000 IU/day) is a reasonable preventive measure.

Cardiovascular health

Transfem HRT can affect the lipid profile: E2 tends to raise HDL and reduce LDL (beneficial), but it can also raise triglycerides. Overall cardiovascular risk in trans women on well-monitored HRT is debated; some studies suggest it may be higher than in cis women but lower than in cis men, though the long-term data is limited. Annual monitoring of the lipid profile (total cholesterol, HDL, LDL, TG).

Liver health

Injectable or transdermal E2 have minimal hepatic impact. The main risk comes from AAs: CPA (hepatotoxicity at high doses, rare at low doses), bicalutamide (rare but real idiosyncratic hepatotoxicity, more documented at high oncology doses), flutamide (high hepatotoxicity; obsolete). Monitoring with ALT/AST is essential when using these medications.

Fertility

Prolonged suppression of spermatogenesis may be partially reversible upon discontinuing HRT, but full recovery isn't guaranteed, especially after several years. If preserving fertility is a goal, sperm cryopreservation before starting HRT is the recommended option. Once HRT has started, fertility recovery is possible but uncertain.

Mental health

HRT generally has positive effects on psychological well-being in trans people. However, hormonal fluctuations (poor dose adjustment, periods of low levels), the use of CPA (depression risk), or excessively high or low E2 levels can cause emotional instability. Monitor mood and adjust the protocol if needed.

Genital atrophy

Androgen suppression causes atrophy of penile and scrotal tissue: the skin becomes thinner, the tissue loses elasticity, and it can become painful over time. This is expected and partially reversible, but can be problematic, especially if a vaginoplasty is planned (which requires enough tissue for neovaginal construction).

Prevention

• Maintain regular erections (at least 2 times per week). Erections keep the tissue oxygenated and elastic. They don't need to end in orgasm.
• If there's severe erectile dysfunction, PDE5 inhibitors (sildenafil, tadalafil) can help maintain erections for this purpose.

Treatment of established atrophy

• Topical testosterone cream (low dose): using 0.5–2% T cream on the affected tissue (without significant systemic absorption if used locally and in small amounts) can reverse atrophy without affecting systemic feminization. Should be prescribed and monitored by a doctor.
• Topical estriol: estriol creams can improve lubrication and mucosal tissue health without a significant systemic effect.
• Tissue expanders: if vaginoplasty is planned, surgeons often recommend pre-procedure tissue expansion techniques if there's significant atrophy.

Atrophy and vaginoplasty

Severe atrophy can complicate vaginoplasty. The amount of available tissue determines the possible vaginal depth. If surgery is planned, communicate this to the surgeon in advance to plan atrophy management.

Expected changes with transfem HRT

For reference, the following table summarizes typical physical changes, onset times, and time to maximum effect.

Source: Transfemscience.

Glossary

E2

Estradiol (17β-estradiol), the main bioidentical estrogen.

EEn

Estradiol enanthate, an injectable ester with a ~5–7 day half-life.

EV

Estradiol valerate, an injectable ester similar to EEn.

EC

Estradiol cypionate, an injectable ester with a ~8–14 day half-life.

T

Testosterone.

DHT

Dihydrotestosterone, the most potent androgen at the androgen receptor; a product of 5α-reductase.

RA

Androgen receptor.

RE

Estrogen receptor (α and β).

AA

Antiandrogen.

CPA

Cyproterone acetate, a potent antiandrogenic progestogen.

Bica

Bicalutamide, a pure AR antagonist.

5-ARI

5α-reductase inhibitor (finasteride, dutasteride).

GnRH

Gonadotropin-releasing hormone.

LH

Luteinizing hormone.

FSH

Follicle-stimulating hormone.

SHBG

Sex hormone-binding globulin.

HPG

Hypothalamic-pituitary-gonadal axis.

P4

Progesterone.

SubQ

Subcutaneous injection.

IM

Intramuscular injection.

DIY

Do It Yourself; self-managed HRT without a medical prescription.

Reflex rise

A reactive rise in T (and LH) when using AR antagonists like bicalutamide, due to the loss of androgenic negative feedback on the HPG axis.

First-pass hepatic metabolism

Metabolism of a drug in the liver before it reaches systemic circulation when taken orally.

Tanner

The Marshall and Tanner scale of pubertal development stages (1–5).

DMO

Bone mineral density.

TVP / EP

Deep vein thrombosis / Pulmonary embolism.