sbstrum_MD
Member
See my comments in the context of your message above:
Gman86: Primobolan decreases E2. Forget the exact mechanism by which it does this, but most DHT derivatives will lower E2 in ur serum and on a blood test, or inhibit E2‘s effects, but won’t visibly show a lowering of E2 on a blood test.
ss: If most DHT derivatives will lower E2 but not show it on a blood test then I cannot conclude the first part of your contradictory statement above. It just makes no sense.
And, the peer-reviewed literature on primobolan is so scant and so old that no article I can find discusses primobolan vs. E2. Moreover, despite this being an interesting hormone (Methenolone Acetate), it appears that a reliable source of it in the US and most of Europe is not the case.
Gman86: Masteron is an example of inhibiting E2’s effects, but not lowering E2 in the serum/ on a blood test. It was initially created to treat breast cancer. Hence the prefix “mast”.
ss: this is another very old drug that has scant literature on it. The chemical name is drostanolone proprionate. The articles I found dated 1970 to 1987 with most from the 70s. I was treating breast cancer in the '70s and never came across this drug in the US. One paper from 2020 is Borodi, G.; Turza, A.; Bende, A. Exploring the Polymorphism of Drostanolone Propionate. Molecules 2020, 25, doi:10.3390/molecules25061436. Here is the abstract:
2alpha-Methyl-4,5alpha-dihydrotestosterone 17beta-propionate, known as drostanolone propionate or masteron, is a synthetic anabolic-androgenic steroid derived from dihydrotestosterone. The crystal structures of two polymorphs of drostanolone propionate have been determined by single crystal X-ray diffraction and both crystallizes in the monoclinic crystal system. One is belonging to the P2(1) space group, Z = 2, and has one molecule in the asymmetric unit while the second belongs to the I2 space group, Z = 4, and contains two molecules in the asymmetric unit. Another polymorph has been investigated by an X-ray powder diffraction method and solved by Parallel tempering/Monte Carlo technique and refined with the Rietveld method. This polymorph crystallizes in the orthorhombic P2(1)2(1)2(1) space group, Z = 4 having one molecule in the asymmetric unit. The structural configuration analysis shows that the A, B, and C steroid rings exist as chair geometry, while ring D adopts a C13 distorted envelope configuration in all structures. For all polymorphs, the lattice energy has been computed by CLP (Coulomb-London-Pauli), and tight-binding density functional theory methods. Local electron correlation methods were used to estimate the role of electron correlation in the magnitude of the dimer energies. The nature of the intermolecular interactions has been analyzed by the SAPT0 energy decomposition methods as well as by Hirshfeld surfaces.
As you can see, this publication has little human clinical relevance; at least not to me as a medical oncologist. I do not know how you have information on Masteron (aka Masteril).
One of the papers I obtained from 1970 (Treatment of Advanced Breast Carcinoma Treatment of Advanced Breast Carcinoma with with Drostanolone Propionate) had only this to say regarding mechanism of action:
Deshpanda (1967) demonstrated that drostanolone propionate reduced the uptake of oestradiol-17B by tumour cells, reduced the uptake of oestradiol-17B by tumour cells, whereas Altman and Chayen (1967) suggested that whereas Altman and Chayen (1967) suggested that the drug acted by diverting the reduced co-enzyme the drug acted by diverting the reduced co-enzyme NADPH into the metabolically wasteful diaphorase NADPH thus limiting the amount of biosynthesis in the carcinoma.}. None of the other paper's titles appear to address aromatization.
Gman86: They studied it in this regard due to its inhibition of E2.
ss: assuming you are referring to drostanolone. I purchased one paper that might shed clues on the mechanism of action of drostanolone (Masteron, Masteril, Masterid).
Trams, G. Effect of drostanolone propionate on the binding of oestradiol and dihydrotestosterone by normal and malignant target tissues. Eur J Cancer (1965) 1977, 13, 149-153, doi:10.1016/0014-2964(77)90193-1
Drostanolone was.found to compete with androgen binding sites but not with oestrogen receptors. Therefore it is unlikely that the growth inhibitory effect of drostanolone propionate in human breast cancer is mediated through interaction with oestradiol binding proteins as suggested earlier by other authors.
Sorry, but unless you come up with some validation of your statements, it appears that you are presenting your own opinions, and not facts as we think we known them.
Gman86: Primobolan actually lowers E2 in the serum, and since E2 is the main stimulator of prolactin release in the male body, prolactin will subsequently tend to go down as E2 goes down.
ss: Primobolan (aka methenolone acetate) is an anaobolic steroid. Like DHT and T it stimulates the AR (androgen receptor). By raising T and DHT, it might reflexly ↓ E2. But I cannot find any articles to that effect. Please share such articles with us. I have not found in my use of androgen deprivation therapy (ADT) in thousands of men, a decrease in prolactin and have had to use a prolactin inhibitor like cabergoline (Dostinex®) to achieve lowering. There is a reflex inter-relationship between prolactin and dopamine but I have not seen this to be the case between raising T ⇢ lowering E2 ⇢ lowering prolactin . You sound convincing so maybe you have the articles to support this. I share two articles I referred to above.
Stephen B. Strum, MD, FACP
