I find it interesting that the community focuses solely on TT so intensely when clearly the active metabolites are the operational factors.
Agreed. While further parts of the problem include, as you point out, estrogen levels being ignored or not given sufficient attention, the focus on total testosterone is mistaken, as the free value gives the full information on biological effect.
(The total value is only the product, so to speak, of the free value and the amounts of SHBG and serum albumin.)
I have always understood E2 to be one of two, primary Estrogen derivatives of Free T. I have not seen anything regarding any further break down.
For a little further detail, the two highly estrogenic metabolites are estradiol and estrone; a third weakly-estrogenic metabolite is estriol.
Further downstream metabolites of the estrogens include catechol estrogens which unfortunately are carcinogenic, but aren't relevant to bodybuilding other than that this would be a reason, though of very low risk, to avoid allowing estrogen levels to become too abnormally elevated.
Regarding DHT. It appears to be documented as the other primary, and andogen type derivate from Free T. I also understand the DHT further metabolizes into 2 or 3 other active components.
The only significantly active metabolite I can think of is 5alpha-androstanediol.
I understood masteron (Drostanolone), to be one of them.
No, Masteron (dromostanolone) can only be produced synthetically.
I personally am not sure how any of them actually work, as they are rarely discussed due to the apparent lack of interest in the nuts and bolts, that the average AAS user exhibits. I would like to know more.
Dromostanolone presumably interacts with the androgen receptor in the same manner as testosterone. It presumably also has non-androgen-receptor mediated activities, or AR-mediated non-genomic activities, in the same manner as testosterone. The relative potency between these different means of activity may not be the same between the compounds. As a guess -- and it is only from practical observation, not scientific data -- dromostanolone may tend to be mostly effective directly via AR-mediated genomic activity (Class I) rather than predominantly by other activities (Class II.)
The lack of a double bond prevents aromatization or metabolism by the 5AR enzyme.
The 2alpha-methyl group that distinguishes it from DHT inhibits metabolism by the 3bHSD enzyme, thus preventing or minimizing conversion to an androstanediol derivative. Such metabolism is believed to partially deactivate DHT in muscle, causing it to be a poorer anabolic than otherwise might be expected.
I recently read that masteron actually competes with E2 receptor activity, thus limiting one's exposure to the ravaging devil it is...
I find this very interesting. If there is anything to E2 contributing to, or being the primary cause of prostate cancer, then not only would it not be as harmful as a DHT opponent would believe, but indeed mayber beneficial. So if there is anything to E2 causing prostate enlargement of any type, SOLO may find himself even further swollen up with his discontinuation..!!..??
The suggestions I was giving wouldn't have raised estradiol.
My off beat thoughts on this: If there is truth to this then it would add merit to my "swing/swap" and "single receptor type" hypothesis. That all of these type hormone receptors are capable of interacting with both sex hormones, at that a predominance by occupation defines this. In short, androgens reside in the muscle tissue receptors due to their preponderance, and relevance to these tissues. The same for fatty tissue. I believe the prostate can equally swing either way, and that this is the root of the prostate problem as related to hormones. That control of these receptors is based solely on who got their first, and that this control may slide in either direction based on temporary conditions of infux and recession of which.
Back to current publication. I also read this:
The 2 Alkylation Found in drostanolone(Masteron) considerably intensifies the anabolic effects of dihydrotestosterone which, without the 2 alkaylation would not be highly active in muscle tissues. Because of this drostanolone can be used with great effect as a bulking agent. Drostanolone provides the user with a consistent gain of high quality muscle mass. For advanced effect, drostanolone can also be used along side other steroids. Users that mix drostanolone with steroids such as Nandrolone Decanoate can see some encouraging result, providing high muscle gain while retaining very little water.
The source is questionable as I am unsure of it.. Could you please take this opportunity to give your thoughts on those two issues? And could you please expound on the various durivatives of DHT, and a brief synapsis of your understanding of them. I would also appreciate a quick comment of my statement of personal thought on the hormonal receptor issue. There is no need to blast with with demands for documentation. Just tell me I am crazy if you think so and a brief polite explanation would suffice. I only ran it by you out of respect.
The writeup on Masteron is a reasonable one, though if there is a suggestion that there is a need to stack with Deca, this is not the case.
You are on the right track in thinking that there is often "cross-talk" so to speak between steroid hormones and receptors other than their nominal target. For example it's not unusual for androgenic steroids to have some interaction at glucocorticoid receptors, and it's possible for some androgens to have some blocking activity at estrogen receptors.
But it's not out of the predominance of the number of that sort of receptors in the tissue, but of the relative affinities of the steroids for the receptors. As an example, while it may be true (I don't recall: it is the case for a very similar compound at least, and may well be for this one) that Masteron can occupy but does not activate the estrogen receptor, even a rather high concentration of dromostanolone may occupy only a fairly modest percentage of estrogen receptors, while rather tiny concentrations of estradiol are all that are needed to occupy a high percentage of the receptors, as estradiol has far higher affinity for the ER.
So the most that could be expected is some tempering of the effect of estradiol, rather than powerfully suppressing it.
? Hmm Then what could ya do with that?
