Gyno: Two Causes, Two Different Answers

📅 August 1, 2026 ⏱️ 2 min read ✍️ Team TPS

Gynecomastia has two completely different causes and one of them does not respond to the drug most people reach for.

Oestrogen-driven

The common route. Aromatising compounds raise oestrogen, oestrogen acts on receptors in breast tissue, tissue develops.

Aromatising compounds are the ones to watch: testosterone, dianabol, boldenone, anadrol. The dry DHT derivatives do not aromatise and do not cause it this way.

Prolactin-driven

The one people miss. Progestogenic compounds, nandrolone and trenbolone: can raise prolactin, and prolactin-driven tissue changes look similar but do not respond to an aromatase inhibitor at all.

This is why people conclude their AI is underdosed when the AI was never the right tool. A prolactin blood test settles it. See cabergoline and prolactin.

The early signs

Itching or sensitivity around the nipple, then a small firm lump directly beneath it. Tender rather than painful at first.

Catching it here matters enormously, because early tissue is reversible and established tissue is not.

Prevention versus treatment

An aromatase inhibitor lowers circulating oestrogen and is the preventative tool. See aromatase inhibitors compared.

A SERM like tamoxifen blocks the receptor in breast tissue specifically, which makes it the treatment tool once symptoms have started. Blocking the receptor where the problem is happening is more direct than lowering the hormone everywhere. See clomid vs nolvadex.

Do not run an AI blind

Taking an aromatase inhibitor pre-emptively without knowing your oestradiol is how people crash it, and crashed oestrogen brings joint pain, flat mood, no libido and worse lipids. See cholesterol and lipids.

When it is established

Once fibrous tissue has formed, no drug removes it, surgery is the only option. That is the argument for acting at the itching stage rather than waiting to be sure.

Supplied for research purposes only. Not medical advice.