ATD instead of HCG?

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  1. SS are you listening? We need you bro.

    I would test this theory myself, but I am unable at to do so at the moment.



  2. I will try to get bloodwork done 3 to 4 weeks into this cycle and post the results on here for you guys I have a bloodwork from about 6 months ago also that I`ll post as well
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  3. Quote Originally Posted by Neu
    I will try to get bloodwork done 3 to 4 weeks into this cycle and post the results on here for you guys I have a bloodwork from about 6 months ago also that I`ll post as well
    That would be nice bro. I know ALR said he would put UH against HCG anyday so I have been pretty curious myself.
  4. Transdermal HCG


    Quote Originally Posted by jminis
    That would be nice bro. I know ALR said he would put UH against HCG anyday so I have been pretty curious myself.
    Anyone heard of this or tried it. It's from Bodybuilding.com

  5. ...Author???...
    •   
       


  6. Quote Originally Posted by ryansm
    SS are you listening? We need you bro.

    I would test this theory myself, but I am unable at to do so at the moment.

    Ryan, question, your lipids and cardio profile actually improved while using Rxt (ATD product) for PCT... am i right?

    how did this happen if ATD destroys estrogen?
    My Little Site about Hair Loss & Anabolics-
    hair loss from steroids dot com

  7. UH sounds really promising for heavy runs. Can't wait to see what the bloodwork reveals.

  8. Quote Originally Posted by CEDeoudes59
    Ryan, question, your lipids and cardio profile actually improved while using Rxt (ATD product) for PCT... am i right?

    how did this happen if ATD destroys estrogen?
    didn't he use nolva too?

  9. Yeah He did use nolva




    Quote Originally Posted by Beelzebub
    didn't he use nolva too?

  10. im using ATD while on cycle....gaspri kilo sport one cap per day only..........i dont think it can replace HCG, my boys are shrinking, and im thinking to use real HCG to get them back.

    HCG raises testular size by influncing LH levels, ATD is just an anti-estrogen i dont how you guys got the Idea that ATD can replace HCG!!!

  11. Quote Originally Posted by mass_builder
    im using ATD while on cycle....gaspri kilo sport one cap per day only..........i dont think it can replace HCG, my boys are shrinking, and im thinking to use real HCG to get them back.

    HCG raises testular size by influncing LH levels, ATD is just an anti-estrogen i dont how you guys got the Idea that ATD can replace HCG!!!
    this is why we're all hanging around waiting for ALR (or anyone else) to explain (further) the possibility. "The Core" has some info, but clearly there are the unanswered questions.

  12. Quote Originally Posted by mass_builder
    im using ATD while on cycle....gaspri kilo sport one cap per day only..........i dont think it can replace HCG, my boys are shrinking, and im thinking to use real HCG to get them back.

    HCG raises testular size by influncing LH levels, ATD is just an anti-estrogen i dont how you guys got the Idea that ATD can replace HCG!!!

    Why do you need HCG? Simply, because the ar at a hypothalamic level is being overstimulated (and most likely the er a the pituitary) when and androgen levels are high. The hypothalamous produces less GnRH. The pituitary reacts to a reduced level of GnRH pulses and produces less LH and FSH (this negative feedback loop is even more pronounced at the pituitary when estrogen levels are high). So, we administer HCG to stimulate the testicles in the absence of LH.

    What if you could blunt the negative feedback loop where it begins? Specifically, that would be at the hypothalamous. Then would you need HCG? Nope. If the rate of LH production does not decline at the pituitary, you don't need HCG. In this case, we are going to block the androgen receptor centrally by specifically binding to that receptor at a higher rate.

    Is it possible? It has been shown to be true in mice.



    Effects of ATD on male sexual behavior and androgen receptor binding: a reexamination of the aromatization hypothesis.

    Kaplan ME, McGinnis MY.

    Department of Anatomy, Mount Sinai School of Medicine, CUNY, New York 10029.

    The aromatization hypothesis asserts that testosterone (T) must be aromatized to estradiol (E2) to activate copulatory behavior in the male rat. In support of this hypothesis, the aromatization inhibitor, ATD, has been found to suppress male sexual behavior in T-treated rats. In our experiment, we first replicated this finding by peripherally injecting ATD (15 mg/day) or propylene glycol into T-treated (two 10-mm Silastic capsules) or control castrated male rats. In a second experiment, we bilaterally implanted either ATD-filled or blank cannulae into the medial preoptic area (MPOA) of either T-treated or control castrated male rats. With this more local distribution of ATD, a lesser decline in sexual behavior was found, suggesting that other brain areas are involved in the neurohormonal activation of copulatory behavior in the male rat. To determine whether in vivo ATD interacts with androgen or estrogen receptors, we conducted cell nuclear androgen and estrogen receptor binding assays of hypothalamus, preoptic area, amygdala, and septum following treatment with the combinations of systemic T alone. ATD plus T, ATD alone, and blank control. In all four brain areas binding of T to androgen receptors was significantly decreased in the presence of ATD, suggesting that ATD may act both as an androgen receptor blocker and as an aromatization inhibitor. Competitive binding studies indicated that ATD competes in vitro for cytosol androgen receptors, thus substantiating the in vivo antiandrogenic effects of ATD. Cell nuclear estrogen receptor binding was not significantly increased by exposure to T in the physiological range. No agonistic properties of ATD were observed either behaviorally or biochemically. Thus, an alternative explanation for the inhibitory effects of ATD on male sexual behavior is that ATD prevents T from binding to androgen receptors.

    PMID: 2925181 [PubMed - indexed for MEDLINE]

  13. Quote Originally Posted by bow
    Why do you need HCG? Simply, because the ar at a hypothalamic level is being overstimulated (and most likely the er a the pituitary) when and androgen levels are high. The hypothalamous produces less GnRH. The pituitary reacts to a reduced level of GnRH pulses and produces less LH and FSH (this negative feedback loop is even more pronounced at the pituitary when estrogen levels are high). So, we administer HCG to stimulate the testicles in the absence of LH.

    What if you could blunt the negative feedback loop where it begins? Specifically, that would be at the hypothalamous. Then would you need HCG? Nope. If the rate of LH production does not decline at the pituitary, you don't need HCG. In this case, we are going to block the androgen receptor centrally by specifically binding to that receptor at a higher rate.

    Is it possible? It has been shown to be true in mice.



    Effects of ATD on male sexual behavior and androgen receptor binding: a reexamination of the aromatization hypothesis.

    Kaplan ME, McGinnis MY.

    Department of Anatomy, Mount Sinai School of Medicine, CUNY, New York 10029.

    The aromatization hypothesis asserts that testosterone (T) must be aromatized to estradiol (E2) to activate copulatory behavior in the male rat. In support of this hypothesis, the aromatization inhibitor, ATD, has been found to suppress male sexual behavior in T-treated rats. In our experiment, we first replicated this finding by peripherally injecting ATD (15 mg/day) or propylene glycol into T-treated (two 10-mm Silastic capsules) or control castrated male rats. In a second experiment, we bilaterally implanted either ATD-filled or blank cannulae into the medial preoptic area (MPOA) of either T-treated or control castrated male rats. With this more local distribution of ATD, a lesser decline in sexual behavior was found, suggesting that other brain areas are involved in the neurohormonal activation of copulatory behavior in the male rat. To determine whether in vivo ATD interacts with androgen or estrogen receptors, we conducted cell nuclear androgen and estrogen receptor binding assays of hypothalamus, preoptic area, amygdala, and septum following treatment with the combinations of systemic T alone. ATD plus T, ATD alone, and blank control. In all four brain areas binding of T to androgen receptors was significantly decreased in the presence of ATD, suggesting that ATD may act both as an androgen receptor blocker and as an aromatization inhibitor. Competitive binding studies indicated that ATD competes in vitro for cytosol androgen receptors, thus substantiating the in vivo antiandrogenic effects of ATD. Cell nuclear estrogen receptor binding was not significantly increased by exposure to T in the physiological range. No agonistic properties of ATD were observed either behaviorally or biochemically. Thus, an alternative explanation for the inhibitory effects of ATD on male sexual behavior is that ATD prevents T from binding to androgen receptors.

    PMID: 2925181 [PubMed - indexed for MEDLINE]
    wow bro...........ATD could be an androgen recptor bloacker!, that would reduce the efficincy of my AAS, since less androgen can bind to the receptors.

    it looks like ATD downregulate androgen receptors. hum i think i should switch to nolva to reduce estrogen during cycle.

    that make me think that more research need to be done before people start using this stuff for PCT.

    so i gusse ATD+AAS is not a good combo.

  14. So if i'm understanding this correctly, you need to use UH from the start of a cycle. Right?

  15. Quote Originally Posted by mass_builder
    wow bro...........ATD could be an androgen recptor bloacker, that would reduce the efficincy of my AAS.

    hum i think i should switch to nolva to reduce estrogen during cycle.

    so i gusse ATD+AAS is not a good combo.

    Not if ALR's contention is correct, which is that it binds at a much lower rate peripherally. Which begs the question, can an AI show a higher binding rate for certain tissues? Let me give you a hint, you mentioned Tamoxifen....

  16. Quote Originally Posted by bow
    Why do you need HCG? Simply, because the ar at a hypothalamic level is being overstimulated (and most likely the er a the pituitary) when and androgen levels are high. The hypothalamous produces less GnRH. The pituitary reacts to a reduced level of GnRH pulses and produces less LH and FSH (this negative feedback loop is even more pronounced at the pituitary when estrogen levels are high). So, we administer HCG to stimulate the testicles in the absence of LH.

    What if you could blunt the negative feedback loop where it begins? Specifically, that would be at the hypothalamous. Then would you need HCG? Nope. If the rate of LH production does not decline at the pituitary, you don't need HCG. In this case, we are going to block the androgen receptor centrally by specifically binding to that receptor at a higher rate.

    Is it possible? It has been shown to be true in mice.



    Effects of ATD on male sexual behavior and androgen receptor binding: a reexamination of the aromatization hypothesis.

    Kaplan ME, McGinnis MY.

    Department of Anatomy, Mount Sinai School of Medicine, CUNY, New York 10029.

    The aromatization hypothesis asserts that testosterone (T) must be aromatized to estradiol (E2) to activate copulatory behavior in the male rat. In support of this hypothesis, the aromatization inhibitor, ATD, has been found to suppress male sexual behavior in T-treated rats. In our experiment, we first replicated this finding by peripherally injecting ATD (15 mg/day) or propylene glycol into T-treated (two 10-mm Silastic capsules) or control castrated male rats. In a second experiment, we bilaterally implanted either ATD-filled or blank cannulae into the medial preoptic area (MPOA) of either T-treated or control castrated male rats. With this more local distribution of ATD, a lesser decline in sexual behavior was found, suggesting that other brain areas are involved in the neurohormonal activation of copulatory behavior in the male rat. To determine whether in vivo ATD interacts with androgen or estrogen receptors, we conducted cell nuclear androgen and estrogen receptor binding assays of hypothalamus, preoptic area, amygdala, and septum following treatment with the combinations of systemic T alone. ATD plus T, ATD alone, and blank control. In all four brain areas binding of T to androgen receptors was significantly decreased in the presence of ATD, suggesting that ATD may act both as an androgen receptor blocker and as an aromatization inhibitor. Competitive binding studies indicated that ATD competes in vitro for cytosol androgen receptors, thus substantiating the in vivo antiandrogenic effects of ATD. Cell nuclear estrogen receptor binding was not significantly increased by exposure to T in the physiological range. No agonistic properties of ATD were observed either behaviorally or biochemically. Thus, an alternative explanation for the inhibitory effects of ATD on male sexual behavior is that ATD prevents T from binding to androgen receptors.

    PMID: 2925181 [PubMed - indexed for MEDLINE]
    can you translate this into beelzelanguage?

  17. Quote Originally Posted by CEDeoudes59
    Ryan, question, your lipids and cardio profile actually improved while using Rxt (ATD product) for PCT... am i right?

    how did this happen if ATD destroys estrogen?
    ATD is a steroidal AI, similar to the effects 6-oxo or Exemestane have on lipids, which is actually to improve them. I am not versed on this myself, actually skeptical truthfully until I saw the blood test results. I can dig up the studies, but there are some of Exemestane and others that show improvement in lipid profiles.

    No I did not use Nolva.


  18. Quote Originally Posted by Beelzebub
    can you translate this into beelzelanguage?
    Bow has a better hold on this than I, but in theory ATD would negate both negative feedback loops allowing recovery of the HPTA.

    Of course cortisol is still an issue.

    By the way check the new smilies.


  19. Quote Originally Posted by ryansm
    Bow has a better hold on this than I, but in theory ATD would negate both negative feedback loops allowing recovery of the HPTA.

    Of course cortisol is still an issue.

    By the way check the new smilies.
    Gee I wonder what brought this one on.

  20. Quote Originally Posted by ryansm
    ATD is a steroidal AI, similar to the effects 6-oxo or Exemestane have on lipids, which is actually to improve them. I am not versed on this myself, actually skeptical truthfully until I saw the blood test results. I can dig up the studies, but there are some of Exemestane and others that show improvement in lipid profiles.

    No I did not use Nolva.
    Thanks Ryan, I didn't think you used Nolva.
    Neat Smilies
    this is a burger
    My Little Site about Hair Loss & Anabolics-
    hair loss from steroids dot com

  21. Quote Originally Posted by ryansm
    No I did not use Nolva.
    Oops My bad thought you did but that`s what I get for thinking

  22. Quote Originally Posted by ryansm
    Bow has a better hold on this than I, but in theory ATD would negate both negative feedback loops allowing recovery of the HPTA.

    Of course cortisol is still an issue.

    By the way check the new smilies.
    (im exagerrating here)
    so why then, could I not run an ATD based product from now until the rest of my life? (or extended periods)
    I thought lack of estrogen is havoc on the cardio profile...
    My Little Site about Hair Loss & Anabolics-
    hair loss from steroids dot com


  23. Thse smilies are fun!

    Now the question...So would it be a bad idea to run an ATD with tren? I am giving tren a serious thought for january bulker to try and keep my boys swimming strong. I am just trying to figure out if using an ATD will make tren/test lest effective by binding to angrogen recepters. I'm guessing everyone else is in the dark as I am at the moment, at least by the looks of the thread it seems so.

  24. Quote Originally Posted by snakebyte05

    Now the question...So would it be a bad idea to run an ATD with tren? I am giving tren a serious thought for january bulker to try and keep my boys swimming strong. I am just trying to figure out if using an ATD will make tren/test lest effective by binding to angrogen recepters. I'm guessing everyone else is in the dark as I am at the moment, at least by the looks of the thread it seems so.
    As Bow hinted at earlier by referencing tamoxifen, ATD is thought to bind at much higher rate at the Hypothalmus than in the rest of the body. So no it wont make your cycle less effective (or if so very marginally) but 'should' help reduce suppression through reducing overstimulation of the AR at the hypothalmus.
    Trens stimulation of the progesterone receptor may still prove problematic, but thats not something i know enough about to comment on.

  25. Quote Originally Posted by 200wannabe
    As Bow hinted at earlier by referencing tamoxifen, ATD is thought to bind at much higher rate at the Hypothalmus than in the rest of the body. So no it wont make your cycle less effective (or if so very marginally) but 'should' help reduce suppression through reducing overstimulation of the AR at the hypothalmus.
    Trens stimulation of the progesterone receptor may still prove problematic, but thats not something i know enough about to comment on.
    The reason for the ATD was for me to not be supressed as much during my 6 week cycle of it. Progesterone I would deal with in another way.
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