conversion rates

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  1. Originally posted by Dio


    I don't really see the point. Frontloading is used with gear when injecting long acting esters. The point is to maximize levels initially, so you don't have to wait a for levels to rise. With transdermal use max levels would be reached within 24 hours, so there's no need to frontload.

    Also, I'm not sure how you'd front load with an oral, unless you just mean using a higher dose for the first few days. If that's the case it could get your gains kickstarted, but you'd suppress test levels faster too.
    hehe yea, excuse the newbie. thats what i meant. just using a much higher dose for a few days.(orally)

    thx


  2. [QUOTE]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

    "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"

    "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."

    "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"


    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.
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  3. [QUOTE]Originally posted by Dio
    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

    "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"

    "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."

    "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"


    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.
    1. Its a quote from the Proviron profile on BC's page. Do you have any references on when this self regulation is discontinued? Also will will transdermal 3a overide this self regulation?

    2. I will try to find the links but I think they had nothing to do with the title of thread. They were just included in the debates (nandi, fonz, macro if I remember correctly)

    3. This ties into the whole point. Once that celing is hit, it seems less 4AD is converted (if any at all) and other metabolites are produced. To me the ceiling is more important than the amount of enzymes available because it seems that conversion happend quickly and it would take an enermous amount to achieve saturation. This is the reason why more estrogenic effects could occur because the active metabolites of test cause this. I am assuming test and 4AD could have similar metabolites. I think we agree nobody knows exctaly what is produced.

    4. Actually I think the celing could be more important than the saturation point. Once that celing it hit, more 4AD has a better chance of converting into something else which could cause more side effects. Like I've said, its all speculation since nobody really understand whats happening but it seems like a logical step.

    5. I believe saturation is possible but it would take an enormous amount and like we see, more is not always better. As you've stated you can have a huge amount of circulating 4AD that will not get converted. Now could this be caused by saturation or the cuttoff point of natural levels? THe saturation point we don't know and is mere specualtion but we know the cutoff point exists to a degree because then everyone using 4AD would test positive for Test use due to supraphysiologocal levels. So it seems to point to the "cutoff" point being more important and it could also explain more metabolites being produced and causing more side effects. But its all specualtion....Seems logical to me though.
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  4. 1. Big Cat is inconsistant with this kind of thing, although I'm sure he's basing that statement on something. I think I know which study that came from, but unless I'm mistaken (and there's one dealing specifically with proviron) that study details the mechanism, but does not actually spell out what would happen.

    On my end I'm speculating too, I could provide you with a reference on finite levels of enzymes and 3aHSD levels in the skin, but I don't have anything defining limits.

    I'm basing that on: Par's experience with transdermal 3alpha, the difference between those results and the feedback I've seen orally, Derek Cornelius's comments on the potency of injecting straight DHT, and the aforementioned feedback on the 4AD ceiling.

    2. I'll probably find it sooner or later. I've just started checking that board out.

    3-4. If you don't think it's the enyzmes, then what do you think causes the ceiling? There has to be something limiting further conversions. Interesting idea on the estrogen, that would help explain it. My personal theory was that only 1 of the 3 isozymes of 3bHSD was able to convert 4AD to test and that it was present in muscle. So the higher estrogen levels in the blood were a result of test that had already converted.

    I spent a fair amount of time looking for some research to support this, but didn't find anything. I learned a ****load about enzymes though

    5. Again, if it's not the enzymes then what are you speculating the cause of the ceiling to be?

  5. Originally posted by Dio
    1. Big Cat is inconsistant with this kind of thing, although I'm sure he's basing that statement on something. I think I know which study that came from, but unless I'm mistaken (and there's one dealing specifically with proviron) that study details the mechanism, but does not actually spell out what would happen.

    On my end I'm speculating too, I could provide you with a reference on finite levels of enzymes and 3aHSD levels in the skin, but I don't have anything defining limits.

    I'm basing that on: Par's experience with transdermal 3alpha, the difference between those results and the feedback I've seen orally, Derek Cornelius's comments on the potency of injecting straight DHT, and the aforementioned feedback on the 4AD ceiling.

    2. I'll probably find it sooner or later. I've just started checking that board out.

    3-4. If you don't think it's the enyzmes, then what do you think causes the ceiling? There has to be something limiting further conversions. Interesting idea on the estrogen, that would help explain it. My personal theory was that only 1 of the 3 isozymes of 3bHSD was able to convert 4AD to test and that it was present in muscle. So the higher estrogen levels in the blood were a result of test that had already converted.

    I spent a fair amount of time looking for some research to support this, but didn't find anything. I learned a ****load about enzymes though

    5. Again, if it's not the enzymes then what are you speculating the cause of the ceiling to be?
    1. BC can be inconsistent when you look back on what he wrote in the past but he always corrects himself if he finds new information. At least thats the impression I get everytime I've interacted with him. I know you guys hashed it out over hair loss in the past so you might have a different perspective. I think overall he's proven to be reliable on most of the information he presents (there is a lot of it) so I always give him the benefit of the doubt. I've learned too much from him over the years so I get I'm biased. When you post the amount of information he has in the past couple of years, your bound to be wrong occasionally.

    2. Its a very good board especially the Anabolic Pharmacology section. You can really learn a lot over there. I know I have on several issues.

    3. Truthfully I have absolutely no idea. Your theory sounds good. The only thing I would question is that if the natural limit is reached, the amount of test aromatized wouldn't be that much (compared to supraphysiological levels). Then again if it metabolizes into E2 or any version, that could easily cause side effects. They are extremely potent.

    I'll see what I can dig up on what could cause the celing. As you know the amount of studies on these types of things is enormous.
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  6. 1. BC later admitted he was wrong about that. I have much more respect for him now. I think he gets many things right, but when you try to cover all the bases on several broad topics, you're bound to miss some things. That's why i used the word inconsistant as opposed to bashing him

    3. Yeah, but as you indirectly note my theory doesn't take the ceiling into account. I'm not sure that the natural limit would play into this theory though, since if it's true you could actually have supraphysiological levels and no way of measuring them. Definitely agree on E2's potency.

    I'd be very interested in seeing what you turn up. I'll keep an eye out for it too.

    Either way this has been fun

  7. Originally posted by Dio
    Another interesting item is that despite a supposedly being more androgenic than test, hair loss is not as commonly reported as you'd think it would be.
    Not that interesting if we just take into account that 4-diol doesn't go through 5-alfa-reduction and is just SLIGHTLY more androgenic than testosterone, it's not 120% more androgenic but 120% as androgenic, so it's just a 20% more androgenic.

  8. Originally posted by Bobo
    Its good for libido, I can attest to that. It will raise DHT levels to the highest they naturally can be so that could account for hairloss problems. Thats an area I'm not too familiar wiht. I think the idea is that the conversion is instantanious is which my opinion rests. I agree there is a saturation point but how long does that last? From different readings is seems in real world time its instantantious and is freed up fairly quickly. Usually test derivatives (methytest) aromatize heavily to E2 or 17 methyl E2 so my assumption that 4AD or target hormone or metabolites could even do this in small amounts IMO. If test levels are raised slightly over natural levels even for a very short time then this could occur also. I think we agree there are mechanism that are just unknown at this time.
    4-AD will not raise DHT, it's testosterone conversion from 4-AD which will raise DHT, not 4-AD by itself.

  9. That was referring to Proviron. I already mentioned the possibility of other metabolites converting from 4AD's target hormone (test). DHT is one of them.
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  10. Originally posted by neurotic


    Not that interesting if we just take into account that 4-diol doesn't go through 5-alfa-reduction and is just SLIGHTLY more androgenic than testosterone, it's not 120% more androgenic but 120% as androgenic, so it's just a 20% more androgenic.
    Good point, but test does not need to convert to DHT to cause hair loss. It's potent enough to do it on it's own. Something 20% more androgenic would be more potent. Not to mention that DHT created from the test conversion.
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