Hormones 101: Testosterone
What Are Hormones?
Hormones are chemical messengers in your body. They travel through your bloodstream and tell cells what to do — like "grow facial hair" or "deepen the voice".
For trans masculine HRT, we focus on three main players:
- Testosterone — the primary masculinising hormone
- Estrogen — the primary feminising hormone we want to suppress
- Progestins — used optionally for bleeding control
Testosterone
Testosterone is the primary male sex hormone. It belongs to a class of hormones called androgens.
What Testosterone Does
| Effect | Details |
|---|---|
| Voice deepening | Thickens vocal cords, enlarges larynx |
| Facial/body hair growth | Converts vellus hair to terminal hair |
| Muscle mass increase | Promotes protein synthesis |
| Fat redistribution | Shifts fat from hips/thighs to abdomen |
| Bottom growth | Enlarges clitoral tissue |
| Menstrual cessation | Suppresses ovarian cycle |
| Bone density | Maintains bone mass |
| Libido | Increases sexual desire |
| Red blood cells | Stimulates erythropoiesis |
The Testosterone Molecule
Testosterone's chemical formula is C₁₉H₂₈O₂ (molar mass: 288.42 g/mol). It is a steroid hormone built on a four-ring carbon backbone.
Key features:
- Ketone (=O) at C3 on ring A
- Hydroxyl (–OH) at C17β on ring D
- Methyl groups (–CH₃) at C18 and C19
How Testosterone Works
Testosterone enters cells and binds to androgen receptors (AR), activating genes that drive masculine development. It can also be converted to:
- DHT (dihydrotestosterone) — a much more potent androgen, responsible for facial hair, body hair, and male pattern baldness
- Estradiol — via the aromatase enzyme; a small amount of T is always converted to E2
DHT: The Potent Metabolite
DHT is approximately 2–3× more potent than testosterone (some sources cite up to 5× depending on tissue and assay). It is produced by the enzyme 5α-reductase converting T to DHT in specific tissues (skin, scalp, prostate).
| Effect | Mostly T | Mostly DHT |
|---|---|---|
| Voice deepening | ✅ | |
| Muscle mass | ✅ | |
| Bottom growth | ✅ | ✅ |
| Facial hair | ✅ | |
| Body hair | ✅ | |
| Scalp hair loss | ✅ | |
| Libido | ✅ | ✅ |
The HPG Axis in Trans Men
The hypothalamus–pituitary–gonadal (HPG) axis controls hormone production:
- Hypothalamus releases GnRH
- Pituitary responds with LH and FSH
- Ovaries produce estrogen in response to FSH
Exogenous testosterone suppresses this axis via negative feedback:
- High T → hypothalamus reduces GnRH → pituitary reduces LH/FSH → ovaries produce less estrogen
- This is why menstruation typically stops within 2–6 months of starting T
Estrogen
In trans men, high estrogen is undesirable because it opposes masculinisation. Testosterone therapy naturally suppresses E2 in most people.
| E2 Level | Interpretation |
|---|---|
| < 50 pg/mL | Well-suppressed (typical on T therapy) |
| 50–100 pg/mL | Borderline |
| > 100 pg/mL | Elevated; may need intervention |
If E2 remains high despite adequate T levels, an aromatase inhibitor (anastrozole, letrozole) may be considered.
Sex Hormone Binding Globulin (SHBG)
SHBG binds to sex hormones and regulates how much is "free" (active). Testosterone lowers SHBG, which means:
- More free T is available at the same total T level
- Trans men on T typically have lower SHBG than cis men at the same total T
Hormone Level Targets
| Hormone | Target Range | Purpose |
|---|---|---|
| Total T | 300–1,000 ng/dL | Masculinisation |
| Free T | 50–200 pg/mL | Activity marker |
| E2 | < 50 pg/mL | Suppress feminising effects |
| SHBG | 10–50 nmol/L | Binding protein |
| Hematocrit | < 54% | Prevent polycythemia |
Summary
| Hormone | Role in Trans Masculine HRT | How We Modify It |
|---|---|---|
| Testosterone | Primary masculinising hormone | Added via injections, gel, patches, pellets, buccal |
| Estrogen | Feminising hormone to suppress | Suppressed by T therapy |
| DHT | Potent androgen (hair, bottom growth) | Produced from T; finasteride blocks conversion |
| SHBG | Binds sex hormones; regulates free T | Decreases on T therapy |
| LH/FSH | Signals ovaries to produce E2 | Suppressed by exogenous T |
References
Hembree WC, et al. (2017). Endocrine Treatment of Gender-Dysphoric/Gender-Incongruent Persons. JCEM. https://academic.oup.com/jcem/article/102/11/3869/4157558
WPATH (2022). Standards of Care, Version 8. https://www.tandfonline.com/doi/full/10.1080/26895269.2022.2100644