T-bol increases free test levels!!!

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    T-bol increases free test levels!!!


    [The pharmacokinetics of Oral-Turinabol in humans]

    [Article in German]

    Schumann W.

    Institut fur Mikrobiologie und experimentelle Therapie (ZIMET), Jena.

    Disposition and excretion of the anabolic steroid Oral-Turinabol (1;4-chloro-17 alpha-methyl-androsta-1,4-diene-17 beta-hydroxy-3-one) were investigated in male volunteers. Following single p.o. and i.v. administration of the tritium-labelled compound the plasma concentration courses of total radioactivity (1 and 1-metabolites) and of the unchanged parent drug as well as the urinary excretion were estimated. From these data model independent pharmacokinetic parameters based on statistical moments were calculated. 1 is almost completely absorbed after p.o. administration of 10 mg per volunteer. Peak concentrations of total radioactivity and of 1 in plasma were reached about 3 h p.a. Irregularities observed in the plasma level profile following both p.o. and i.v. administration of 1 are due to a marked enterohepatic circulation. Orally given 1 is subject to a first-pass effect, resulting in a diminished systematic availability. The AUC-ratio of the unchanged drug and the total radioactivity of 1 : 13 shows the predominance of metabolites in plasma. After i.v. administration the disposition of unchanged 1 was found biphasically with a terminal half-life of 16 h. 1 and its metabolites are preferentially excreted via the kidneys. The urinary total radioactivity represented about 60% of the dose following both administrations. Due to its affinity to SHBG 1 is able to compete for the protein binding of testosterone, resulting in an increased plasma level of non protein-bound testosterone.


    ---------------------------------------------

    It seems like T-bol binds to SHBG and thus increase levels of free test, similar to proviron(sp)

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    Very interesting study!
    It seems that we dont need ActivaTe with T-bol
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    Most 17-aa androgens have a higher SHBG affinity than endogenous steroids. Oral-Turinabol is not alone in this ability.
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    Quote Originally Posted by DR.D
    Most 17-aa androgens have a higher SHBG affinity than endogenous steroids. Oral-Turinabol is not alone in this ability.
    So what others might fall in this category of effectiveness?
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    Quote Originally Posted by Work
    So what others might fall in this category of effectiveness?
    What other steroids displace test from SHBG? Halo, anadrol, dbol, winni, anavar, nilavar, even methylated pro-hormones. The alkylation sub creates a molecule that favors SHBG but often fits poorly at the AR as the trade-off.
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    So in essence almost any methylated hormone increases free test? Not trying to be an ass, just trying to learn. I've never heard this before. Quite possibly this is why stacking orals with test works so well.
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    Quote Originally Posted by Work
    So in essence almost any methylated hormone increases free test? Not trying to be an ass, just trying to learn. I've never heard this before. Quite possibly this is why stacking orals with test works so well.
    It's one of the reasons why stacks are synergistic with an oral and an injectable, and some work better than others in this reguard. Also, there are exceptions I'm sure. For example, I know some 17-aa hormones do fit well at the AR (like Mibolerone), but off hand I don't remember which have highest affinity for SHBG. As a rule of thumb, they all do more so than test.
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    Proviron does the same thing but free test is metabolized too quickly to have any effect.


    The effect of mesterolone administration to normal men on the pituitary-testicular function.

    Aakvaag A, Stromme SB.

    Publication Types:

    * Clinical Trial
    * Controlled Clinical Trial


    So even though mesterolone competes with test for SHBG binding, the diplaced test is cleared from the system faster as the author states:

    "the MCR [metabolic clearance rate] is inversely related to the degree of protein binding."
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    Quote Originally Posted by Work
    So in essence almost any methylated hormone increases free test? Not trying to be an ass, just trying to learn. I've never heard this before. Quite possibly this is why stacking orals with test works so well.
    No, orals work well with test because you are increasing testosterone to supraphysiological levels along with the addition of supraphysiological levels of a 17-AA steroid.

    Free test (as in the effect of orals) has nothing to do with it.
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    Quote Originally Posted by Bobo
    No, orals work well with test because you are increasing testosterone to supraphysiological levels along with the addition of supraphysiological levels of a 17-AA steroid.

    Free test (as in the effect of orals) has nothing to do with it.
    It does contribute, but I agree that it's not to a great extent, especially after suppression kicks in. Orals stack with test mainly by boosting creatine synthesis as test and other non-alkylateds promote nitrogen retention by the path of protein synthesis. The clearance of free test is 10-100 minutes, so the cotribution that displacement causes is real, but not the primary explaination of benefit.
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    I doubt it. I haven't seen any evidence to show that at all. Actually, quite the opposite whenit comes to 17-AA orals. The increase in free test initially shows no benefit (especially when you combine that with supraphysiological doses of test)

    There isn't one reason why orals stack best with test. There are too many factors in why androgens in general cause increased gains. Some say it the increase in AR expression by an increase in mRNA. This increase causes increased gene expression which will have more an effect on hpyertrophy than any ribosome dependent protein synthesis.

    Other say it works posttranscriptionally, by stabilizing AR mRNA.

    Others say androgens regulate the production of ribosomal RNA.


    So its not one factor.


    Now I have to go eat my cottage cheese
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    Actually, I was wrong about much of this! (Don't tell Bobo, he's got a big enough head already ) I had it just backwards. Looking through the books, I see that these factors decrease SHBG binding:

    1) 17-a subs (like methyl and ethynyl)
    2) unsaturation at the C-1 or C-6
    3) 19-nor derivatives

    So orals don't displace test actively as I stated earlier, but still may cause passive disassociation to increase free test. Wether or not this is of signifigance is still debatable, but I have to think it makes a difference. For example, positive evidence of this can be suggested by the success of Activate (a designer lignand, not a steroid however). Also, concerning only steroid molecules, a 17b-OH function appears essential to SHBG binding.

    As for the mechanism of androgenic action, it is certain that cellular growth and differentiation are regulated through protein synthesis mostly, though 17-aa steroids often enhance creatine biosynthesis too, while test does not as evident by reduced creatinine excretion. Numerous androgen induced proteins have been identified to validate this. And while steroid-receptor-bound RNP formed in the nucleus does return to the cytoplasm and aid protein synthesis, enhanced mRNA transcription and/or translocation is doing most of the work I think.
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    Quote Originally Posted by DR.D
    Looking through the books,

    Mind I ask what book? Or any other references?

    This is good stuff. I'd like to know more, please.
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    Quote Originally Posted by rhinochaser48
    Mind I ask what book? Or any other references?

    This is good stuff. I'd like to know more, please.
    I understand, I'm a total nerd too! It's fascinating stuff, I've studied it since I started using as a teen skipping lunch and going to the library and stuff like that(when I wasn't trying to chase the ladies)

    My main ref on this one is: The Male Sex Hormone Analogs, R.E. Counsell & Robert Brueggemeire, Dept of Pharmacology, U of Michigan Medical School, Chap.28
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    Quote Originally Posted by DR.D
    n that cellular growth and differentiation are regulated through protein synthesis mostly, though 17-aa steroids often enhance creatine biosynthesis too, while test does not as evident by reduced creatinine excretion. Numerous androgen induced proteins have been identified to validate this. And while steroid-receptor-bound RNP formed in the nucleus does return to the cytoplasm and aid protein synthesis, enhanced mRNA transcription and/or translocation is doing most of the work I think.
    But the point is that protein synthesis is regulated by many factors, not just one, even in 17-AA steroids.
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    Also


    Also, methylated androgens also tend to reduce metabolism of all steroids by the liver extending the half-life and increasing the plasma concentration of steroids in the body.
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    Quote Originally Posted by Bobo
    But the point is that protein synthesis is regulated by many factors, not just one, even in 17-AA steroids.
    Yes, I agree with you completely. I didn't mean it to sound like I was trying to bottleneck the point with orals or androgens in general or by an single mechanisms. Just trying to break it down and understand what's involved with this.
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    Quote Originally Posted by DRknow
    Also, methylated androgens also tend to reduce metabolism of all steroids by the liver extending the half-life and increasing the plasma concentration of steroids in the body.
    You are right, this is a very valid point that I failed to address. All androgens, especially orals, by virtue of their structure are enzyme inhibitors to some extent, thus prolonging the life of related steroids in the body.
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    Quote Originally Posted by DR.D
    I've studied it since I started using as a teen skipping lunch and going to the library and stuff like that...
    You rebel
    great info Mr. D, or should I say, Dr. D.
    Very interesting.
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    its said oral steroid works in many ways:

    Bining to AR, and perhapes increasing AR density
    Increasing prostaglandins maily PGF-2a, and PGE-1
    Increasing nitorogen in muscle
    Cell volumizing, which increase cell size and work force


    there are also many factors i dont know.
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    Echo?
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    Quote Originally Posted by DR.D
    I understand, I'm a total nerd too! It's fascinating stuff, I've studied it since I started using as a teen skipping lunch and going to the library and stuff like that(when I wasn't trying to chase the ladies)

    My main ref on this one is: The Male Sex Hormone Analogs, R.E. Counsell & Robert Brueggemeire, Dept of Pharmacology, U of Michigan Medical School, Chap.28

    I'm having trouble finding this. I've tried every possible search I can think of including medical school library searches. I can't find any trace of it. Any ideas?

    Thanks in advance.
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    Quote Originally Posted by rhinochaser48
    I'm having trouble finding this. I've tried every possible search I can think of including medical school library searches. I can't find any trace of it. Any ideas?

    Thanks in advance.
    Well, I was hoping you were better than me at searches. I haven't found it online either. All I have is a few hundred pages that I photocopied from a kick-ass library at a government research facility I used to work at. I left years ago and haven't risked trying to get back in without a current window sticker. I wish I would have just "acquisitioned" them all, lost them, and payed for them when I had them available.
  

  
 

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