Tamoxifen
Tamoxifen is a selective oestrogen receptor modulator (SERM) with decades of oncology trial data. It antagonises oestrogen at breast tissue (used to prevent and treat gynaecomastia) while acting as an oestrogen agonist at the hypothalamus/pituitary, raising LH, FSH and endogenous testosterone — which makes it a mainstay of post-cycle therapy (PCT).
01 Overview
Tamoxifen blocks the oestrogen receptor in breast tissue, which both prevents oestrogen-driven glandular growth and can partially reverse recent gynaecomastia. Crucially it does not lower systemic oestrogen — unlike an aromatase inhibitor it leaves oestradiol intact, avoiding the joint, libido and bone downsides of oestrogen crashing while still protecting the chest.
At the pituitary it behaves as an oestrogen antagonist, removing negative feedback so that LH and FSH rise and stimulate the testes; this is the basis of its use in PCT to restart the HPTA after suppressive cycles. It is well tolerated but can raise the risk of venous thromboembolism and, rarely, affect vision.
02 Mechanism
Selective oestrogen receptor modulator: antagonist at breast tissue and at the hypothalamic-pituitary axis (raising LH/FSH and testosterone), with tissue-selective agonist activity elsewhere (e.g. bone, endometrium).
03 Dosing
| Tier | Dose | Route | Notes |
|---|---|---|---|
| Gynaecomastia prevention | 10–20 mg/day | Oral | On-cycle to prevent or treat early oestrogen-driven breast tissue. |
| Breast cancer (label) | 20–40 mg/day | Oral | Oncology dosing. |
04 Effects
| Effect | Magnitude | Evidence | |
|---|---|---|---|
| Restored LH/FSH and testosteroneRemoves oestrogen feedback at the pituitary, raising gonadotropins and endogenous testosterone during PCT. | significant rise | Clinical | |
| Gynaecomastia prevention/reversalBlocks oestrogen at breast tissue; most effective against early, recent-onset gynaecomastia. | high efficacy early | Clinical |
05 Side effects
| Effect | Severity | Frequency | Evidence | Countermeasures |
|---|---|---|---|---|
| Venous thromboembolism riskIncreased risk of deep vein thrombosis and pulmonary embolism, well documented in oncology use. | Severe | Uncommon | Clinical | |
| Visual disturbanceRare retinal/corneal changes and visual disturbance with prolonged or high-dose use. | Moderate | Rare | Clinical | |
| Hot flushes / mood changesHot flushes, mood lability and reduced libido during use. | Mild | Common | Clinical |
06 Commonly used with
What tamoxifen is combined with, and why. This is about intent rather than safety — the interactions table below covers what is dangerous. Nothing here is listed without what it costs.
| Compound | Frequency | Purpose & trade-off |
|---|---|---|
| Support & ancillaries | ||
| Testosteronegyno prevention | Run on-cycle with aromatising testosterone to block estrogen at breast tissue and prevent gynecomastia.Trade-off: It masks rather than lowers systemic estrogen, so water retention and high-estrogen sides persist unaddressed. | |
| Post-cycle | ||
| ClomifenePCT | Paired as the classic SERM PCT duo to stimulate LH and FSH and restart natural testosterone after suppression.Trade-off: Combining two SERMs stacks their mood and visual side effects and offers limited benefit over one dosed well. | |
| hCGpre-PCT | Follows an hCG blast to restore testicular size before the SERM takes over pituitary stimulation in PCT.Trade-off: hCG raises estrogen, which can aggravate tamoxifen-era gyno flares and complicate recovery timing. | |
| NandrolonePCT | Used after long-acting nandrolone cycles as part of an extended SERM recovery once the ester clears.Trade-off: SERMs poorly counter progestogenic suppression, so recovery from nandrolone can still be slow and incomplete. | |