Some interesting studies....

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    Some interesting studies....


    I came across these studies and I thought they were pretty interesting. Feel free to comment.

    The effects of fluoxymesterone administration on testicular function
    TM Jones, VS Fang, RL Landau and RL Rosenfield


    Long term daily administration of fluoxymesterone (9alpha-fluoro- 17alpha-methyl-11beta, 17beta-dihydroxyandrost-4-en-3-one) was associated with a modest suppression of sperm production and a profound suppression of testosterone levels in the absence of significant effects on plasma gonadotropin levels. Nine normal male volunteers took either 10, 20, or 30 mg of fluoxymesterone daily for twelve weeks. Plasma samples were obtained for testosterone, estrogen, LH and FSH levels at biweekly intervals before, during and for up to 12 weeks after fluoxymesterone treatment. Samples were obtained for dehydroepiandrosterone sulfate, testosterone binding globulin and free testosterone assays at representative times before, during and after treatment. Although lower sperm counts were observed at several points during both the treatment and follow up periods, Reduced plasma testosterone levels were seen within 24 h after beginning fluoxymesterone, and further reductions were noted throughout the treatment period. Changes in plasma estrogen levels did not correlate with fluoxymesterone administration. Neither plasma LH nor plasma FSH levels were significantly altered by fluoxymesterone. A significant consistent suppression of spermatogenesis could not be demonstrated.short term study utilizing a single dose of fluoxymesterone yielded similar findings. It is proposed that fluoxymesterone has a local effect on the Leydig cell which is not mediated by gonadotropins


    Aromatization mediates testosterone's short-term feedback restraint of 24-hour endogenously driven and acute exogenous gonadotropin-releasing hormone-stimulated luteinizing hormone and follicle-stimulating hormone secretion in young men.

    Schnorr JA, Bray MJ, Veldhuis JD.

    Division of Endocrinology, Department of Internal Medicine, General Clinical Research Center, Center for Biomathematical Technology, University of Virginia School of Medicine, Charlottesville, Virginia 22908, USA.

    The present clinical study examines the neuroregulatory hypothesis that feedback restraint of LH and FSH secretion by testosterone requires in vivo aromatization. To test this postulate, we prospectively and randomly assigned 47 healthy young men to 1 of 5 parallel short-term (5-day) double-blind interventions with: 1) placebo; 2) high-dose ketoconazole (KTCZ, 400 mg orally 4 times daily) to block both Leydig-cell and adrenal steroidogenesis; 3) KTCZ and transdermal testosterone delivery (7.5 mg daily); 4) KTCZ and transdermal estradiol (0.05 mg daily); or 5) KTCZ, testosterone, and the selective and potent aromatase inhibitor, anastrazole (5 mg orally twice daily). Blood was sampled every 10 min for 27 h on the last day of intervention to quantitate 24-h mean spontaneous and 3-h post-GnRH-stimulated (100 ng/kg iv bolus) LH and FSH release. KTCZ administration lowered the serum total testosterone concentration markedly from (mean +/- SEM) 423 +/- 57 ng/dL (15 +/- 2.0 nmo/L) during placebo ingestion to 58 +/- 8.6 ng/dL (2.0 +/- 0.3 nmol/L) (P < 10(-3)). Transdermal androgen addback along with KTCZ blockade increased testosterone levels to 607 +/- 57 ng/dL (21 +/- 2.0 nmol/L). KTCZ exposure alone drove a 3-fold increase in serum LH concentrations (P < 10(-3)) and a 2.5-fold rise in FSH secretion (P = 0.015), as assessed by high-specificity immunoradiometric assays. Concomitant transdermal testosterone (or estradiol) delivery repressed the elevated secretion of both LH and FSH to mid-normal baseline values. A 3-fold administration of anastrazole, KTCZ, and testosterone completely opposed exogenous testosterone's suppression of 24-h LH and FSH secretion. Anastrazole coadministration likewise abolished testosterone-dependent inhibition of 3-h GnRH-stimulated LH and FSH release. In summary, assuming the specificity of anastrazole's inhibition of aromatase activity, we conclude that circulating testosterone in healthy men curtails endogenously driven as well as exogenous GnRH-stimulated LH and FSH secretion conditional on its in vivo aromatization.

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    I should of pointed out that fluoxymesterone is halo. I believe Dr. D once stated that he ran halo inbetween cycles and recovered fine. Interesting......
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    The effects of fluoxymesterone administration on testicular function.

    Jones TM, Fang VS, Landau RL, Rosenfield RL.

    Long term daily administration of fluoxymesterone (9alpha-fluoro-17alpha-methyl-11beta, 17beta-dihydroxyandrost-4-en-3-one) was associated with a modest suppression of sperm production and a profound suppression of testosterone levels in the absence of significant effects on plasma gonadotropin levels. Nine normal male volunteers took either 10, 20, or 30 mg of fluoxymesterone daily for twelve weeks. Plasma samples were obtained for testosterone, estrogen, LH and FSH levels at biweekly intervals before, during and for up to 12 weeks after fluoxymesterone treatment. Samples were obtained for dehydroepiandrosterone sulfate, testosterone binding globulin and free testosterone assays at representative times before, during and after treatment. Although lower sperm counts were observed at several points during both the treatment and follow up periods, significant consistent suppression of spermatogenesis could not be demonstrated. Reduced plasma testosterone levels were seen within 24 h after beginning fluoxymesterone, and further reductions were noted throughout the treatment period. Changes in plasma estrogen levels did not correlate with fluoxymesterone administration. Neither plasma LH nor plasma FSH levels were significantly altered by fluoxymesterone. A short term study utilizing a single dose of fluoxymesterone yielded similar findings. It is proposed that fluoxymesterone has a local effect on the Leydig cell which is not mediated by gonadotropins.

    IOW, even though LH wasn't reduced that much testosterone was and LH did not initiate ledig cell production.
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    Bobo, do you have access to the study in its entirety? I'd like to see the extent of the testosterone supression and liver values, lipids,etc.
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    Nope as it was done in 1977. Its widely known that Halo suppresses testosterone a good deal. THe LH levels are virtually meaningless as many streoids exibit this effect (dbol does as well) but they suppress simply because leydig cell response is non-existant.

    If test levels reacted 24 hours after administration, its pretty potent.
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    Alrighty, thanx Bobo. You make a good point about the comparison to Dbol---never thought of that.
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    Bobo, what other steroids strongly exhibit this effect of suppressing leydig response? The suppression of Halo seems to be almost mostly non-gonodatropin.
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    Correct me if i'm wrong but since LH levels are not surpressed then wouldn't your test production come back relatively quickly in comparison to using an aas that does surpress LH levels.

    If this is true than couldn't one use halo, or dbol after running lets say a test/fina cyle and before pct to make pct easier. Or am i completely off here.
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    Not really because its the response of leydig cells TO LH that increases recovery. LH returns VERY quick after a cycle (within 1 week). When you use something like HCG you directly stimulate leydig cell production so when LH returns the responsiveness is hardly effected.
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    Quote Originally Posted by MarcusG
    Bobo, what other steroids strongly exhibit this effect of suppressing leydig response? The suppression of Halo seems to be almost mostly non-gonodatropin.
    All of them.
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    Quote Originally Posted by Bobo
    All of them.

    So testosterone strongly suppresses the leydig response as well?

    And so, are all steroids basically more or less equally suppressive in that manner?
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    If you take it in supraphysiological doses, yes.

    They all suppress but some more than other due to potency of the parent hormone and/or metabolites. Usually the more potent, the more suppressive.
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    Quote Originally Posted by Bobo
    If you take it in supraphysiological doses, yes.

    They all suppress but some more than other due to potency of the parent hormone and/or metabolites. Usually the more potent, the more suppressive.

    Basically what I was trying to get at was whether steroids are somewhat equally suppressive at non-LH mechanisms.

    If so, can halo can be considered to be less suppressive than since LH is relatively unchanged.
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    Nope. As I said before, LH levels are basically meaningless at this point in time. It actually could be worse since it has a localized effect on Leydig cell production.
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    Quote Originally Posted by Bobo
    Nope. As I said before, LH levels are basically meaningless at this point in time. It actually could be worse since it has a localized effect on Leydig cell production.
    Ok then which steroids are oddballs (especially hard or mild at non-LH suppression?
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    Quote Originally Posted by MarcusG
    Ok then which steroids are oddballs (especially hard or mild at non-LH suppression?
    How would winstrol be in this regard?
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    Quote Originally Posted by MarcusG
    Ok then which steroids are oddballs (especially hard or mild at non-LH suppression?
    Tren, Deca are very suppressive. Most 17-AA are also pretty suppressive simply because their metabolites are very potent.
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    Seeing SuperSoldier's lab work, M1T is suppressive w/in 3 days.
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    But it aslso says that aromatase inhibitors are benificial in avoiding suppression,which is contrary to what I´ve heard,or did I misunderstand it?
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    That's what I was curious about too. Perhaps because it was such a low amount (7.5mg of transdermal) of testosterone. They also ran a disgusting amount Anastrazole, 5mg. Maybe that had something to do with it. We need some knowledgeable bros to comment (Bobo?).
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    Quote Originally Posted by Fastflight
    But it aslso says that aromatase inhibitors are benificial in avoiding suppression,which is contrary to what I´ve heard,or did I misunderstand it?
    Where did it state that?

    Suppression was induced in that study.
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    Quote Originally Posted by Bobo
    Not really because its the response of leydig cells TO LH that increases recovery. LH returns VERY quick after a cycle (within 1 week). When you use something like HCG you directly stimulate leydig cell production so when LH returns the responsiveness is hardly effected.
    Ok but that raise the question how does HCG subvert this. HCG is just an analog of LH (to the best of my knowlege). If LH can stay high on dbol but test levels are crashing how does HCG increase test output on cycle. I'm not trying to discredit just trying to learn something I've never took the time to examine.
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    An analog to LH? Explain. Do you meanr just in action?


    HCG is obtained from the placenta of pregnant women.

    HCG seems to act directly on Leydig Cell production and bypasses the feedback loop that signals a drop in GnRH. LH and HCG can both accomplish the same thing but they seem to exert these effect in different ways.


    Inability to demonstrate an ultrashort loop feedback mechanism for luteinizing hormone in humans.

    Kyle CV, Griffin J, Jarrett A, Odell WD.

    Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City 84132.


    hCG has biological properties similar to those of LH, but can be measured separately from LH by current radioimmunometric assays. To investigate the possible existence of an autoregulatory mechanism for LH in humans, we compared the basal LH concentrations and the LH response to a GnRH stimulus with and without prior administration of hCG. On two separate occasions, at least 1 week apart, six normal (eugonadal) males and six normal postmenopausal females were given, in random order, either 10,000 IU hCG or saline followed by iv injection of a 200-micrograms bolus of GnRH. Blood samples were then taken 30, 60, 90, 120, 180, 240, and 300 min after GnRH. Serum concentrations of LH and hCG were measured at each time by two monoclonal antibody sandwich assays developed in our laboratory. After exogenous hCG, serum hCG concentrations rose rapidly to 200-500 IU/L (15,000-35,000 pg/mL) in both the men and women, remaining at this high level throughout the study. In the men, sex steroid concentrations did not change in response to the hCG during the 9 study hours. Compared to saline-treated controls, hCG had no significant effect in either men or postmenopausal women on the basal LH concentration or the response to a GnRH bolus, as determined by peak response and area under the LH/time curve between 0-300 min after GnRH. We conclude that an ultrashort loop feedback mechanism for LH on its own secretion does not exist in humans, as assessed by the present protocol.

    If you weant to know exactly why its act so much differently, nobody knows. Its mostly theoretical but the effects of HCG are widely known in HRT circles.
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    If one compares gonadotropin inhibiting activity of steroids by measure of nitrogen retention of a dose needed to give a medium anabolic effect, they go like this:

    Strong:
    Test, DHT, Dec, Tren, Mib, MENT, EthylNorTest, MethylTest, Methandrodiol

    Weak, relatively:
    Halo, Winni, A50, Dbol, Primo

    Remember that Ledig cells have an estrogen receptor too, so aromatizing stuff is not innocent. Like Bobo said, at high enough doses, they all do it. But if you've ever used Halo, you know it's good like that, no matter what the reports say. As far as that goes, so is NMT 20mg A50.
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    And its those estrogen receptors within Leydig cells which cause desensitiaztion over time to HCG.
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    My head hurts....
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    Quote Originally Posted by XxCrisisxX
    My head hurts....
    Just remember that if you cheat, Halo is a pretty good one to use. Or low dose anadrol.
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    Uhh.....


    Don't agree at all.


    Both are very suppressive.
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    Quote Originally Posted by Bobo
    Uhh.....


    Don't agree at all.


    Both are very suppressive.
    Your such a goody-2-shuz Bobo !!

    XxCrisisxX,
    If your going to take advice, Bobo is a good source. He plays by the rules and knows how this stuff is suppose to work. I on the other hand have broken every rule in the book at some point, and have learned my lessons the hard way in may cases. My education is mixed with contradictory personal experience and my metabolism is somewhat atypical.
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    The majority of what I say about suppression and exogenous hormones is based on research and on what Swale has seen first hand with his clients in a clinical setting for many, many years.

    Oh, and I've been known to use "certain" things in the past.
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    Yea, by no means was I gonna bridge with halo. In fact, I tend to stay away from all orals (even though I have 10 grams of dbol powder always tempting me). I have a great deal of respect for both of you.

    I just thought the studies were interesting
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    I'm not setting myself up as any kind of "expert" but my research and experience matches closely with all that Bobo has said.
  

  
 

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