bananafeet
Member
Interesting study on masteron (from ChatGPT):
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Key Takeaways from the 1977 Trams Study:
Study Title:
“Effect of Drostanolone Propionate on the Binding of Oestradiol and Dihydrotestosterone by Normal and Malignant Target Tissues”
(Eur J Cancer, 1977, DOI: 10.1016/0014-2964(77)90193-1)
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What They Found:
Drostanolone competes at androgen receptors.
It binds to androgen receptor (AR) sites, displacing DHT.
This is how it likely exerts anti-proliferative effects in androgen-sensitive tissues.
Drostanolone does not bind to estrogen receptors.
In both human breast cancer tissue and calf uterus:
No displacement of estradiol from estrogen receptor (ER).
Even with a 1000-fold excess of drostanolone, ER binding of estradiol remained unchanged.
Anti-cancer effect ≠ estrogen suppression.
This rules out the idea that its action is due to “lowering estrogen” or directly blocking E2 binding.
It likely works via androgen receptor signaling and potentially inhibition of prolactin (as mentioned in some rat data).
The study I attached also says that drostanalone works via the drug itself not it's metabolites.
Vigorous Steve's latest video talks about how in studies at high doses it didn't raise HCT in patients with anemia.
Anecdotally (again) I got my PSA checked after running 400mg of drostanalone for 6 weeks. Unfortunately I have no baseline reading.
Total PSA (Alinity) 0.26ug/L (0.25-2.10) Free PSA 0.1 ug/L
Free/Total ratio 39% (> 24)
I mean given all this drostalone should be relatively safe if it's anabolic due to not interfering with ER and displacing DHT.
---
Key Takeaways from the 1977 Trams Study:
Study Title:
“Effect of Drostanolone Propionate on the Binding of Oestradiol and Dihydrotestosterone by Normal and Malignant Target Tissues”
(Eur J Cancer, 1977, DOI: 10.1016/0014-2964(77)90193-1)
---
What They Found:
It binds to androgen receptor (AR) sites, displacing DHT.
This is how it likely exerts anti-proliferative effects in androgen-sensitive tissues.
In both human breast cancer tissue and calf uterus:
No displacement of estradiol from estrogen receptor (ER).
Even with a 1000-fold excess of drostanolone, ER binding of estradiol remained unchanged.
Anti-cancer effect ≠ estrogen suppression.
This rules out the idea that its action is due to “lowering estrogen” or directly blocking E2 binding.
It likely works via androgen receptor signaling and potentially inhibition of prolactin (as mentioned in some rat data).
The study I attached also says that drostanalone works via the drug itself not it's metabolites.
Vigorous Steve's latest video talks about how in studies at high doses it didn't raise HCT in patients with anemia.
Anecdotally (again) I got my PSA checked after running 400mg of drostanalone for 6 weeks. Unfortunately I have no baseline reading.
Total PSA (Alinity) 0.26ug/L (0.25-2.10) Free PSA 0.1 ug/L
Free/Total ratio 39% (> 24)
I mean given all this drostalone should be relatively safe if it's anabolic due to not interfering with ER and displacing DHT.

