ATD instead of HCG?

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    Exclamation ATD instead of HCG?


    I just posted this in ALRI's section, which apparently is not possible:

    1. How much ATD is suggested to replace HCG in a long AAS cycle?
    2. How much ATD is in a cap of ULTRA HOT/ULTRA HOTTER (or a 3 cap serving)?
    3. Should one use ATD for the entire cycle, or only part(s) thereof?
    4. Can ATD cause too much estrogen suppression, thereby inhibiting gains?
    5. Is therer anything HCG can do that ATD can't?

    others with questions, please chime in. Hope to hear from the ALRI team, DS, and anyone else in the know!

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    bump for info. Someone knows this stuff....
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    curious on this as well.
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    bumped up, bear in mind that the only person who compared HCG to ATD (vice-versa) was ALRI...

    hopefully we can get all opinions though
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    I can only speculate based off of my expericnce with ATD used in this manner. I recently ran a cycle of SD/ATD that went something along the lines of this:

    week 1 30mgs SD 100mgs ATD
    week 2 30mgs SD 75mgs ATD
    week 3 30mgs SD 50mgs ATD
    week 4 30mgs SD 25mgs ATD

    week 5 40mgs Nolva 25mgs ATD
    week 6 30mgs Nolva 50mgs ATD
    week 7 20mgs Nolva 75mgs ATD
    week 8 10mgs Nolva 100mgs ATD

    I understand that this is not a long ester AAS cycle, but I did have the BEST pct I have ever had, and retained all of my gains along with gaining strength during pct. Next up I will add ActivaTe to the mix.

    To add I did use fenugreek, but I always do.

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    ALR hinted at this in "The Core"....I'm definitely interested in what he has to say as well.

    The theory make sense. Use a good HPTA stimulator to keep things going as opposed to just forcing testicular stimulation with the hCG.
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    Quote Originally Posted by ryansm
    I can only speculate based off of my expericnce with ATD used in this manner. I recently ran a cycle of SD/ATD that went something along the lines of this:

    week 1 30mgs SD 100mgs ATD
    week 2 30mgs SD 75mgs ATD
    week 3 30mgs SD 50mgs ATD
    week 4 30mgs SD 25mgs ATD

    week 5 40mgs Nolva 25mgs ATD
    week 6 30mgs Nolva 50mgs ATD
    week 7 20mgs Nolva 75mgs ATD
    week 8 10mgs Nolva 100mgs ATD

    I understand that this is not a long ester AAS cycle, but I did have the BEST pct I have ever had, and retained all of my gains along with gaining strength during pct. Next up I will add ActivaTe to the mix.

    To add I did use fenugreek, but I always do.
    if this is the case, HCG is definately more cost effective.
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    I wouldn't combine ATD with dry AAS for long periods... Your estrogen will be completely nill
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    Quote Originally Posted by Beelzebub
    if this is the case, HCG is definately more cost effective.
    My thoughts....exactly

    I bet we see bulk ATD some time in the near future, though....I'm sure its coming.
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    Quote Originally Posted by milwood
    I just posted this in ALRI's section, which apparently is not possible:

    1. How much ATD is suggested to replace HCG in a long AAS cycle?
    Currently running a six week cycle of tren/test prop/(prostan first three weeks) - (sd second three weeks). Have been supplementing with 50 mg’s ATD throughout cycle. Did this simply out of curiosity….I wanted to test Author’s idea of ATD being a site specific AR agonist. My observations so far (nearly five weeks into cycle are) are that I have experienced virtually no shutdown, loss of libido or noticeable loss of testicular size. Yes, these are not quantitative results as I have not had bloodwork.


    Quote Originally Posted by milwood
    2. How much ATD is in a cap of ULTRA HOT/ULTRA HOTTER (or a 3 cap serving)?
    No idea. I would guess that three caps of the original formula have somewhere in the neighborhood of 50 mg’s ATD.


    Quote Originally Posted by milwood
    3. Should one use ATD for the entire cycle, or only part(s) thereof?
    If ATD is truly a site specific AR agonist, you need to run throughout. Otherwise, if some degree of shutdown has occurred, you are not going to create a strong enough negative feedback loop within the HPTA to restart endogenous testosterone production in the presence of exogenous hormones.

    If however ATD is somehow directly stimulating the leydig cells (like HCG), then supplementing at the tail end of a cycle would be beneficial. I have heard several members argue of late that this is the more likely mechanism of action for ATD.

    Either way, the conservative route would be to run throughout the cycle. Worst case (if either of the above theories prove to be bunk) you keep estrogen in check during the cycle. Simply, we need to see more bloodwork to know.


    Quote Originally Posted by milwood
    4. Can ATD cause too much estrogen suppression, thereby inhibiting gains?
    Absolutely. ATD has a relatively high binding affinity (ki) and will severely depress estrogen at high enough dosages. Until we have seen the results of more bloodwork, I would not exceed 100 mg’s day during a cycle.

    Quote Originally Posted by milwood
    5. Is therer anything HCG can do that ATD can't?
    Again, until we are sure as to what the exact mechanism of action is with regards to ATD and minimizing suppression, it’s impossible to speculate.
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    Quote Originally Posted by kwyckemynd00
    My thoughts....exactly

    I bet we see bulk ATD some time in the near future, though....I'm sure its coming.
    custom has some caps pretty cheap. I forget the brand name.
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    Quote Originally Posted by wastedwhiteboy2
    custom has some caps pretty cheap. I forget the brand name.
    Juggernaut Nutrition...here's the link:
    First offering form Juggernaut Nutrition

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    Quote Originally Posted by bow
    Currently running a six week cycle of tren/test prop/(prostan first three weeks) - (sd second three weeks). Have been supplementing with 50 mg’s ATD throughout cycle. Did this simply out of curiosity….I wanted to test Author’s idea of ATD being a site specific AR agonist. My observations so far (nearly five weeks into cycle are) are that I have experienced virtually no shutdown, loss of libido or noticeable loss of testicular size. Yes, these are not quantitative results as I have not had bloodwork.
    .
    I wondered about ATD instead of HCG myself.

    To compare results, I am on the same supper supplement cycle with no ATD and no HCG, clomid etc. I am 8 weeks in and no loss of libido, infact I am REALLY nailing anything that doesn't move too fast lol. No appreciable loss in testicular size either.

    More input by other people would be good.


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    I am on cycle right now and I was on Ultra Hot for the first half of the cycle and I then switched to Arimidex because I ran out of the UH. At the time I didn't think it was doing anything but I have noticed an extreme amount of shrinkage of the boys since switching to Arimidex.



    Quote Originally Posted by CROWLER
    I wondered about ATD instead of HCG myself.

    To compare results, I am on the same supper supplement cycle with no ATD and no HCG, clomid etc. I am 8 weeks in and no loss of libido, infact I am REALLY nailing anything that doesn't move too fast lol. No appreciable loss in testicular size either.

    More input by other people would be good.


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    Quote Originally Posted by CROWLER
    To compare results, I am on the same supper supplement cycle with no ATD and no HCG, clomid etc.
    Am I reading this correctly. No HCG and NO ATD, yet still no shutdown? Intersting. Maybe you have an endocrine system made of steel I just know from past experience that ordinarily, at the dosages I am taking, I would be shut down after about the third week.
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    I will NOT say I don't have shut down as I have heard testical size is not an indicator of shut down or not.

    I do know the libido is through the roof of course because the test and testicals are still basically the same size. When you say shut down in the past how do you mean shut down.


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    thanks for that info, bow. That's more than I've been able to find almost anywhere. I've PM'd tge ALRI team, but either they don't know or they aren't telling. Actually, aflex told me that 6 caps (daily) of UH, and 3 caps of UHotter would be a sufficient dose to compare to standard HCG dosing. I guess that suggests that hotter either has more ATD, or more likely I guess that the methylation increases efficacy to that degree. I still don't know how much ATD is in the stuff, and I really would like to. Someone get a hold of the A man and tell him that Enquiring AnabolicMinds wanna know!

    And I'll get that other info to you as soon as I can dig it up, bow. (I didn't forget! )
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    I am pretty sure that it is the methylation that reduces the dosage requirement with the same effectiveness as the 6 caps. I also know the boys were hanging really well when I was on UH before my cycle.



    Quote Originally Posted by milwood
    thanks for that info, bow. That's more than I've been able to find almost anywhere. I've PM'd tge ALRI team, but either they don't know or they aren't telling. Actually, aflex told me that 6 caps (daily) of UH, and 3 caps of UHotter would be a sufficient dose to compare to standard HCG dosing. I guess that suggests that hotter either has more ATD, or more likely I guess that the methylation increases efficacy to that degree. I still don't know how much ATD is in the stuff, and I really would like to. Someone get a hold of the A man and tell him that Enquiring AnabolicMinds wanna know!

    And I'll get that other info to you as soon as I can dig it up, bow. (I didn't forget! )
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    I read ALR said 3 caps of UH allowed some of his test subjects to take 250 mg of testosterone enanthate a week and retain healthy testicular function. This probably doesn't sound that impressive since 250 mg of test is a drop in the bucket compared to what some people are taking.

    PA on bodybuilding.com forums also said UH had approx 17 mg of ATD per a cap but others have speculated it could be as low as 13 mg.
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    Thats low....

    But,t hat does mean ~50mg/day would probalby be okay. may be worth a shot!
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    I am 1 week in a e-max(20mg ed) Prostan(100mg ed) ATD(100mg ed) cycle and so far so good I know its early on but My boys are full and I feel really good I know that dosn`t mean a thing without bloodwork so I`ll have to wait and see how things go just for reference I ran Max-lmg (solo) a few months ago and max shut me down hard in the first week
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    Speaking of the boys being full I have seen guys say after just a couple weeks of Superdrol or M1T that their testies have gotten smaller. Is that normal?

    It just seems as if they REALLY shut a person down.

    Another question is there ANY way to tell if your HPTA is shut down except with a blood test?

    And I am guessing that you would really need a before and during/after test to really see correct?


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    Quote Originally Posted by CROWLER
    I will NOT say I don't have shut down as I have heard testical size is not an indicator of shut down or not.

    I do know the libido is through the roof of course because the test and testicals are still basically the same size. When you say shut down in the past how do you mean shut down.


    CROWLER

    Testicular size nor libido can be directly correlated (correlcation coefficient = 1) to hpta shutdown. However, they are the two best subjective measures we have excluding bloodwork. Tren is famous for shutting down users within about four weeks, even when administered with the proper amount of test (at dosages >= 75 mg's/eod). While I agree libido and testicular size is far from a perfect indicator, it is still unusual to experience virtually zero testicular attrophy or loss of libido after four weeks.

    What confuses me even more with regards to ATD and tren is that ATD, if it is actually a site specific ar agonist, should still eventually shut you down. While ATD may prevent overstimulation of the er receptors at the pitutary and the ar receptors at the hypothalamous, tren is still going to overstimulate the progesterone receptors. What this leads me to believe is the ARL may have missed his interpretation of the results (the study when ATD was administered to four methyl-test users for eight weeks). Perhaps ATD is not at all a site specific ar agonsit, but as suggested above, perhaps it is somehow directly stimulating the leydig cells.

    Moral is, we need more bloodwork.
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    I never heard of guys on 75mg EOD with say 600mg test a week got shut down. NOT saying it doesn't happen as I never really researched for it.

    I actually started a thread about how the libido is OUT OF CONTROL. I like the cattle pellet route myself that is the reason no HCG>


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    S...

    Some input from the big dogs would be nice...
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    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.

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    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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    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.
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    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
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    ...Author???...
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    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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    UH sounds really promising for heavy runs. Can't wait to see what the bloodwork reveals.
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    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?
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    Yeah He did use nolva




    Quote Originally Posted by Beelzebub
    didn't he use nolva too?
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    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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    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.
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    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]
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    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.
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    So if i'm understanding this correctly, you need to use UH from the start of a cycle. Right?
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    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....
  

  
 

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