Originally posted by Bobo "Mesterolone is an orally active, 1-methylated DHT. Like Masteron, but then actually delivered in an oral fashion. DHT is the conversion product of testosterone at the 5-alpha-reductase enzyme, the result being a hormone that is 3 to 4 times as androgenic and is structurally incapable of forming estrogen. One would imagine then that mesterolone would be a perfect drug to enhance strength and add small but completely lean gains to the frame. Unfortunately there is a control mechanism for DHT in the human body. When levels get too high, the 3alpha hydroxysteroid dehydrogenase enzyme converts it to a mostly inactive compound known as 3-alpha (5-alpha-androstan-3alpha,17beta-diol), a prohormone if you will. It can equally convert back to DHT by way of the same enzyme when low levels of DHT are detected."
Where is this quote from? I'm aware of self regulation and the interconversion between 3alpha and DHT. 3aHSD is also present at finite levels in the body. Once those levels are exceeded, this self-regulation will be overridden.
Another thing to consider is that the rules change when 3alpha is used transdermally. Skin contains considerable levels of 3aHSD, so a good portion of the the 3a will hit the bloodstream as DHT. 1. PA is not the only one. Many discussion over at CEM speculate the same thing so I don't personall think its a wash. Thats your opinion.
Not the only one talking about it converting instantaneously? Do you have a link to these other discussions?
I think it's possible, but not all of it would convert at once. It may convert immediately once it hits the enzyme, but may not reach it right away. 2. I don't think its a shot in the dark. I think its a wise assumption since the majority of the side effects are similar and its a precursor to test anyway. Its theorizing based on available data.
Fair enough, but almost all androgen sides are similar to a lesser or greater degree. 3. I think the conversion is instantaneous or happens in a very short amount of time. If we were to follow your theory once that number is reached, no more 4AD will ever convert. I think once the convreion is made, the enzyme is free to convert more. The limiting factor is the amount being absorbed and with a trans its more of a controlled slower delivery so I don't believe saturation is a big factor unless your taking insane amounts.
No, once the number is reached no more 4AD could convert until the enzymes are freed up. Then whatever is still in the bloodstream could convert. This explains the "ceiling" that many have noticed where adding extra 4AD will not produce greater results.
To your point, you do have to use a significant amount to achieve saturation. Also, as stated above, I think you are correct in assuming that the actual conversion takes little time. 4. I explained my reasons about natural levels of test above and I'm not really concerned about suppression. I more concerned to what substance or what metabolites are produced when test levels hit their maximum (converison of 4AD). If 4AD ability to convert test is limited, then what substance does it convert too when those levels are reached. I think its more active or inactive metabolites which could explain the increased estrogenic side effects that most see.
It's interesting way to look at it, but I still don't see why natural levels would constitute the cutoff point. If this theory is valid (and it might be) then the reactions you're speculating on would happen at the point of enzyme saturation, since that circumstance would leave a lot of 4AD floating around. Quote by PA
&quot;Enzymes do not have to recover any more than a toll booth has to recover after the car ahead of you goes through. I would imagine also that the conversion of a steroid molecule by this enzyme happens in like a nanosecond or something like that. Boom! Its done&quot;
&quot;I think we have to remember that there are competing enzymes that can do other things to the hormones, so its a matter of what percentage gets to interact first with the 3beta HSD, what percentage first gets hydroxylated, what percentage first gets converted to the 17ketone by 17b-HSD, what percentage gets dumped by the kidneys before any metabolism can occur, etc etc
But if 3beta HSD were the only enzyme in the body then perhaps you would be correct.
As it stands, i think its my guess that the majority of 4diols do get converted by 3beta-HSD before they undergo any other fates.&quot;
&quot;If it converts to testosteorne then surely you will also see formation of all metabolites of testosterone.
HOwever, there is apparently no DIRECT 5alpha reduction of 4-AD&quot;
These quotes certainly support the theory that there are other actives being produced. Other statements I've seen implied that the other coversions resulted in inactive metabolites. The above also explains why coversion rates are inherently limited.
However, it does not mean that enzyme saturation is impossible. Consider that blood levels of 4AD can reach ~4600 ng/dl -- that's a ****load of 4AD in the bloodstream at a constant level. If that's not enough to cause saturation, it's probably enough to ensure that any excess 4AD gets metabolised by another enzyme first. That is speculation on my part. These are the statements I base my opinion on. Its seems conversion is rather quick, and metabolites are produced (although we don't kow which ones) . From this I also assume saturation is rather tough to do unless your taking ridiculous amounts. If your doing that, you mine ass well take the real thing.
There's still the legality issue to deal with.