ATD instead of HCG?

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  1. 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?
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  2. UH sounds really promising for heavy runs. Can't wait to see what the bloodwork reveals.
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  3. 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?

  4. Yeah He did use nolva




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

  5. 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!!!
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  6. 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.

  7. 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]

  8. 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.

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

  10. 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....

  11. 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?

  12. 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.


  13. 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.


  14. 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.

  15. 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
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    hair loss from steroids dot com

  16. 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

  17. 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...
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  18. 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.

  19. 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.

  20. 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.

  21. Quote Originally Posted by CEDeoudes59
    Neat Smilies
    this is a burger
    It just seemed right to add this one.
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  22. c'mon down, Author! When you get a chance, we'd all like some help on this one. And if anyone on the ALRI team cando so, help us out! Thanks!

  23. Doubt it.
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  24. Quick notes:

    - On testicular size and HPTA function - I have repeatedly said that nut size is not THE indicator of HPTA function. The best way to describe this is looking at HCG. It increases testicular size, but actually is SUPPRESSIVE of HPTA function while it and its metabolites are active.

    - On suppression/shutdown - Is anyone else sick and tired of people using hormones but whining about HPTA suppression?

  25. HCG isn't really that suppressive. The initial thought was based on animal studies but that effect wasn't seen in humans.


    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.



    Endogenous luteinizing hormone surges following administration of human chorionic gonadotropin: further evidence for lack of loop feedback in humans.

    Nader S, Berkowitz AS.

    Department of Obstetrics, Gynecology and Reproductive Sciences, University of Texas Medical School, Houston 77030.

    The existence of inhibitory short- and ultrashort-loop feedback mechanisms for luteinizing hormone (LH), while documented in animals, has been questioned in humans. Since human chorionic gonadotropin (hCG) binds to LH receptors but can be distinguished from LH in immunoassays, it is possible to identify LH surges in the face of exogenously administered hCG. The present study demonstrates LH surges at midcycle in normal volunteers and in women undergoing controlled ovarian hyperstimulation, given hCG. This provides further evidence for lack of loop feedback control of LH secretion in humans.



    Testicular size is more dependent on Sertoli cells (as in production of sperm) as opposed to Leydig cells. You could have normal production of testosterone and still have "shrinkage". Only way to know is bloodtest.
    For answers to board issues, read the Suggestion and News forum at the bottom of the main page.

  26. Sweet. Thanks Bobo.
    I also would like to point out that the ol boys just drop in outta nowhere mid-cycle sometimes.
    I just hate to see people think that feeling their balls is a substitute for bloodwork.

  27. 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.


    I don't think I could have put that in beelzelanguage any better. Maybe a beer analogy

  28. I guess my bottom line is that I'm using some UH that I have during a long cycle, instead of some HCG that I have. I really want to know if this is a good or bad idea. I trust Author's suggestion, but of course at this point, there is still a lot of speculation, not a lot of concrete proof. Anyone think I should go conservative and switch to HCG? I'm not far along enough to have an issue either way, so I have some time to decide really. I do believe that the ATD is absolutely working well for estrogen control and the boys are fine to this point. I'm just thinking maybe I'll use HCG towards the end.Thoughts?

  29. the thing is, ATD may be as good as HCG for restoring your HPTA function following the cycle - but i doubt it would be as good as mimicking swale's protocol of 250ius of HCG x 2 times a week.
    just my opinion, obviously no evidence suggests either way.
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  30. Quote Originally Posted by CEDeoudes59
    but i doubt it would be as good as mimicking swale's protocol of 250ius of HCG x 2 times a week.

    Agreed. We just don't have enough supporting data to make a call either way with much conviction. My hope is that people will continue to use ATD during their cycles and post bloodwork immediately following so that we gather the necessary data. Until that point, the safest protocol would be to stick to HCG during a cycle (if you literally don’t feel like putting your nuts on the line and being one of the gunieapigs). If you want to be extremely conservative, I see no reason to not run both during a cycle. At the least, ATD will keep estrogen in check.
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