I understand that several scientific articles show that tamoxifen and other SERMS such as clomifene and raloxifen are effective in reducing gynecomastia for humans in different age groups and different modes (developing painful gynecomastia and/or lipomastia) respectively:
Two articles about tamoxifen, for example:
Note: I don't have full access to these articles.
Gynecomastic tissue composition
Gynecomastic tissue can be made of at least one tissue:
- Adipose tissue ("watery")
- Mammary Gland Tissue ("viscous")
- Excessive skin tissue ("saggy")
- Connective Tissue fibrosis ("harsh")
- Possibly, in rare cases, also large chest lobe tissue and also tumor tissue
It was unclear to me when trying to read any article a non chemist (let alone biochemist), what is the mechanism of action of tamoxifen and other SERMs on gynecomastia.
What is the mechanism of action of tamoxifen and other SERMs on gynecomastia?
- In the first article I linked to, what is the difference between "lump" type gynecomastia and "fatty" type gynecomastia (aren't both subtypes of lipomastia?)
- Does it destroy "estrogen-dependent" fat cells up to necrosis? (if such cells at all exist)
- Does it destroy "estrogen-dependent" mammary-gland cells up to necrosis? (if such cells at all exist)?