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  1. #1
    Andros's Avatar
    Andros is offline Associate Member
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    Is there such a thing as a 3a-HSD suicide inhibitor

    As a bodybuilder and a Biomedicine graduate I am quite interested in the idea of turning off this enzyme much like aromasin /letro do for aromatase.

    This would allow DHT (endogenous and exogenous) to exert anabolic effects in muscle tissue.

    Has anyone ever researched this, are there any studies in regards?

  2. #2
    skipp is offline Senior Member
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    Wow I never even thought of that, DHT would be MUCH more anabolic than testosterone .. sweet idea.

  3. #3
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    AnabolicAndre is offline Anabolic Member
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    I dont even get what your asking. I have about a year and a half of bio med studies.

    Maybe its the wine getting to me

  4. #4
    AnabolicAndre's Avatar
    AnabolicAndre is offline Anabolic Member
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    Hmmm well if you think about it, it makes sense 3a-HSD enzyme inactivates the adrogenic properties of the steroid , leaving you with soley the anabolic properties.

    How do suggest inhibiting this enzyme??

  5. #5
    Schmidty's Avatar
    Schmidty is offline Test Is Best!
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    bump

  6. #6
    Andros's Avatar
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    Quote Originally Posted by AnabolicAndre
    Hmmm well if you think about it, it makes sense 3a-HSD enzyme inactivates the adrogenic properties of the steroid , leaving you with soley the anabolic properties.

    How do suggest inhibiting this enzyme??

    Well I've just started looking into it and I was hoping to find some preliminary studies, but so far not much luck.

  7. #7
    AnabolicAndre's Avatar
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    I have a pdf but it was done on rats ill send you the link gimme a min

  8. #8
    Andros's Avatar
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    http://www.pubmedcentral.gov/article...?artid=1133240

    Is this the study Anabolic Andre? They seem to report success at selectively inhibiting the enzyme.

    They even give instructions on how to make the inhibitors from raw substances.

    Not sure I'd be willing to test it on myself though.

    If it worked it would reduce 3a-HSD in muscle cells and allow DHT to bind to the AR receptors in them as much as it does in other tissues.

    This would make taking Test a much more potent AAS for our uses and would even allow taking DHT straight and build serious quality muscle.

  9. #9
    rock75's Avatar
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    DO IT DO IT!!!!!

    send it to a lab to test????

  10. #10
    SVTMuscle* is offline Banned
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    Subscribed. By the end of this thread I hope I can figure out wtf is going on! haha

  11. #11
    littleguy289 is offline New Member
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    As much as I hate to necromance old threads, I actually just joined this site bc I came across this doing some googling on the very same topic. Has anyone ever made any progress on this? To the OP (if you are still on here and/or interested in this), I've just recently learned that Indomethacin functions as a fairly powerful 3a-HSD blocker (link to article removed due to "minimum 25 posts" rule- pm me for link). This especially caught my eye because I have been on and off Indomethacin for years as part of my treatment regimen for a back injury I sustained years ago. I may end up being the guinea pig for this.

  12. #12
    Splifton's Avatar
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    In the strive for increased pharmacodynamics associated with dihydrotestosterone's affinity for androgen receptors (a intracellular receptor/nuclear receptor) by utilizing 3-Alpha-HSD inhibitors wouldn't outweigh the plausibility of detrimental alterations to endegenous neuroactive steroids associated with LGIC (Ligand-gated ion channel) modulators. Remember that all muscular activity occurs at the neurological/cellular level regarding ion channel transportation according to it's relative electrochemical gradients (Na+,K+,Ca...). It could lead to unwanted disruptions in pre-synaptic, post-synaptic pulses, or even unforeseen alterations to threshold potential. Yes you may be able to "upregulate" per say the androgenicity of testosterone 's 5au-reductase derivatives i.e DHT, but at what cost?

    In case of an unpredictable reaction, what would you use to counteract the ligand cleavage that occurred to the alpha-keto reductase family receptors?

    Where does one draw the line at playing "God" with our endocrine system? Chemical enhancement through AAS use has very well established and successful methods of success, and this system isn't necessarily broken. So why would one try to fix it? You gotta draw the line at some point regarding the complexity of the game you are playing.

    Eventually it's just Russian Roulette, but you opted to completely load every chamber....

    To any veterans or moderators I didn't mean to also add to revival of this old thread, but to me this just sounds a little too obnoxious..
    Last edited by Splifton; 12-19-2015 at 12:55 AM.

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