Why ATD should never be used for post cycle therapy: new study

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    Why ATD should never be used for post cycle therapy: new study


    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]

    Effects of ATD on male sexual behavior and androge...[Horm Behav. 1989] - PubMed Result

    just abstract plus


    I have been saying for over a year now that there seems to be a peculiar amount of "failed PCT help" threads popping up with ATD used generously in PCT. I think this study backs up my claims.

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    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.
    This might explain why some people, myself included, experience a complete libido shutdown on average doses of ATD.

    However, in the study it does say they used 15mg/day on a rat. A male rat weighs about .6kg, and that's a dose of ~25mg/kg. At an average dose of 50mg for 200lb, or 90kg human male, that's 1.5mg/kg.

    Big difference in the dose/weight ratio there.

    Even still, Im not a fan of ATD at doses over 15mg - for PCT I vastly prefer 6-OXO.

    BV
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    It's not an obscure sexual move, but it'll suffice.
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    Quote Originally Posted by BigVrunga View Post
    This might explain why some people, myself included, experience a complete libido shutdown on average doses of ATD.

    However, in the study it does say they used 15mg/day on a rat. A male rat weighs about .6kg, and that's a dose of ~25mg/kg. At an average dose of 50mg for 200lb, or 90kg human male, that's 1.5mg/kg.

    Big difference in the dose/weight ratio there.

    Even still, Im not a fan of ATD at doses over 15mg - for post cycle therapy I vastly prefer 6-OXO.

    BV
    well yes of course the doses used were ridiculous, but in this case i dont think the dose used is relevant.

    they were testing for the basic function of ATD on receptor level, the results of which would be transferable to humans regardless of amount used.

    jomi notes-
    dosage irrelevant, ATD will act the same way with receptors in mice or humans
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    Are you saying ATD shouldnt be used in PCT b/c of the sex drive inhibition? That seems to be the only problem with using ATD in pct though...right? It looks like ATD will help recover testosterone levels more rapidly though because of the antagonistic binding of the androgen receptors in 4 brain areas. So it does what clomid does to the estrogen feedback loop, but on the androgen side of testicular shutdown. I can live without sex drive for a little while if it means i will recover(test levels) more rapidly...and retain more muscle.

    "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" (in brain tissue predominantly)
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    Its surprising because every time i've used atd I've had good strength gains.
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    I figured it did this the first time I tried it. After a very brief libido boost..probably from E dropping...You don't even think about sex or anything sexual on higher doses of ATD. That goes beyond mere estrogen repression.

    Does the trick on gyno though.
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    im just throwing it out there soma....i havent seen any studies on "testosterone rebound" or what happens when you block androgen receptors and then free them up. its a bit like playing with gasoline. id also like to point out that there are a LOT of "failed pct" threads with ATD compounds thrown in there.

    i may be completely wrong..hell. id just like to see an intelligent discussion. how many people even KNEW this compound reacted with androgen receptors?
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    Quote Originally Posted by Jstrong20 View Post
    Its surprising because every time i've used atd I've had good strength gains.
    same here as a matter of fact....
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    Well, I also have a sneaking suspicion it has anabolic properties of it's own..but I could be wrong. It's kind of a Jack of all Trades. lol
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    Quote Originally Posted by jomi822 View Post
    well yes of course the doses used were ridiculous, but in this case i dont think the dose used is relevant.

    they were testing for the basic function of ATD on receptor level, the results of which would be transferable to humans regardless of amount used.

    jomi notes-
    dosage irrelevant, ATD will act the same way with receptors in mice or humans

    Not necessarily. You have to factor in binding affinity. ATD might preferentially bind to estrogen receptors but if they're all taken, it would bind (imperfectly) to T receptors. So, under that hypothesis, dosage really would matter. Just the right amount and you'd get the desired effect...but too much ATD sloshing around in the system and it would bind to everything it had even mild binding affinity with.
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    Quote Originally Posted by yeahright View Post
    Not necessarily. You have to factor in binding affinity. ATD might preferentially bind to estrogen receptors but if they're all taken, it would bind (imperfectly) to T receptors. So, under that hypothesis, dosage really would matter. Just the right amount and you'd get the desired effect...but too much ATD sloshing around in the system and it would bind to everything it had even mild binding affinity with.
    i was thinking the same thing......good point
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    So ATD potentially blocks both T from binding to androgen receptors AND essentially inhibits aromatization/blocking estrogen receptors (am I saying this right?).

    I always try to put **** in plain english, so my first question is do we naturally produce ATD at all? I know there are way more hormones floating around then receptors, so does that still mean increasing a certain hormone level betters the chance of that hormone reaching a receptor? Sorry, Im rambling a bit, but curious.
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    destroyed my libido too...i wasnt gonna ever use it again anyway but now this helps to confirm that
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    my head hurts... ...is there EVER a time to use ATD..if you want a libido?
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    LG Sciences Formadrol is ATD and Diadzein. This is the unbeatable combination of exactly the things you don'twant during PCT

    Diadzein was added, and expressed in their writeup due to the fact that it will take up estrogen receptors. Unfortunately, it's a strong enough phytoestrogen to cause estrogenic sides. To top it all of, it's ability to increase in LH has been shown to lead to zero increase in testosterone due to the fact that it also blocks receptors in the testes from producing Testosterone.
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    Not necessarily. You have to factor in binding affinity. ATD might preferentially bind to estrogen receptors but if they're all taken, it would bind (imperfectly) to T receptors. So, under that hypothesis, dosage really would matter. Just the right amount and you'd get the desired effect...but too much ATD sloshing around in the system and it would bind to everything it had even mild binding affinity with.
    This does seem to make sense - at a low dose I'm fine with ATD. Anything over 30mg/day and sexual desire is seriously suppressed.

    BV
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    I definitely have more and more decreased sex drive as i up the doseage of ATD to more than 25 mgs daily. I just assumed that it was caused by the brains adrogen receptors being occupied by ATD or its metabolites, not necessarily a decrease in Test or tests affinity for androgen receptors in muscle tissue. I thought Dr. D posted something along these lines a while back...long time ago. If your trying to recover from a reduced libido i dont think ATD is the way to go...unless you use a low doseage(maybe not even then either). Thanks for the study Jomi, definitely an interesting topic to me.

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    Sweet sweetness.
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    id also like to point out something i remembered today...

    androgen receptors UPregulate in the presence of testosterone.

    my question is...what happens when an antagonistic substance like ATD is introduced?
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    Great thread, jomi822 ... repped!
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    Quote Originally Posted by soma View Post
    ... It looks like ATD will help recover testosterone levels more rapidly though because of the antagonistic binding of the androgen receptors in 4 brain areas. ...
    Exactly. Blocking androgen boosts LH far better than blocking estrogen, which really only elevates FSH. So why don't people use anti-androgens more you say? The libido issue! Other than that, ATD is exceptionally well suited for PCT because of it's dual action.

    You know dual action, like now I hear that Jomi goes both ways with Chad all the time and stuff.
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    Quote Originally Posted by DR.D View Post
    Exactly. Blocking androgen boosts LH far better than blocking estrogen, which really only elevates FSH. So why don't people use anti-androgens more you say? The libido issue! Other than that, ATD is exceptionally well suited for post cycle therapy because of it's dual action.

    :
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    Quote Originally Posted by DR.D View Post
    .

    You know dual action, like now I hear that Jomi goes both ways with Chad all the time and stuff.
    AAAAAAAHHHHHHHHHHAHAHAHAHAHAHA H BURNED!!!!!!!!
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    That was a pretty lame one right, oh well, wrong thread
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    Quote Originally Posted by DR.D View Post
    Exactly. Blocking androgen boosts LH far better than blocking estrogen, which really only elevates FSH. So why don't people use anti-androgens more you say? The libido issue! Other than that, ATD is exceptionally well suited for post cycle therapy because of it's dual action.

    You know dual action, like now I hear that Jomi goes both ways with Chad all the time and stuff.
    yea actually used to throw out that same rhetoric but to be honest...ive never seen a study on the subject. between that fact that i havent seen a study on what happens when the AR is blocked by ATD and the fact that so many people seem to suffer reductions in libido and/or testosterone levels post ATD use (along with delayed onset gyno), im not inclined to just take it at face value.

    i didnt see anything about raising testosterone levels in that study i just posted.....furthermore if the AR down regulates with the addition of ATD...the supposed increase in testosterone isnt really going anywhere...is it?

    id prefer to see some concrete proof. there seems to be a lot of anecdotal evidence showing something is going on with ATD we dont quite know about.
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    Yeah, I admit I'm not fond of it at 50mg or more. That's when it starts killing my libido. 25mg is a lift actually, but 50-75 gets bad after a few weeks, especially stacked with Nolva. It's like it's a totally different compound at that dose. I can say it does elevate test levels quite well though from the blood I've seen and people I've talked with. Like you say though, it's biggest problem is also it's best advantage- it blocks central ARs and the sides seem very dose dependent. The test boosting effects are greater in direct proportion to dose on the other hard, so a happy medium is the key with ATD. I still think it's well suited for pct or very androgenic cycles because of this though.
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    Quote Originally Posted by TripDog View Post
    AAAAAAAHHHHHHHHHHAHAHAHAHAHAHA H BURNED!!!!!!!!
    Maybe if we put like 5000mg of ATD in Chad's cereal every morning, the sheep wouldn't have to run scared around there no more.
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    Interesting thread.

    Quote Originally Posted by DR.D View Post
    Yeah, I admit I'm not fond of it at 50mg or more. That's when it starts killing my libido. 25mg is a lift actually, but 50-75 gets bad after a few weeks, especially stacked with Nolva. It's like it's a totally different compound at that dose. I can say it does elevate test levels quite well though from the blood I've seen and people I've talked with. Like you say though, it's biggest problem is also it's best advantage- it blocks central ARs and the sides seem very dose dependent. The test boosting effects are greater in direct proportion to dose on the other hard, so a happy medium is the key with ATD. I still think it's well suited for post cycle therapy or very androgenic cycles because of this though.
    So would you say that 50 mg would be the max recommended dosage?
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    its funny right after reading this thread i went and split all my 25mg caps up into 12.5 mg caps..... question though... typically with any AI or serm i would dose t all at night.... BUT with HDX2 its taken throughout the day at a constant dose, could the same be done with ATD like (3) 12.5mg doses taken spread through the day withh fish oils??? or would it be better to take the 37.5 mg together before bed?
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    Quote Originally Posted by Solitude View Post
    Interesting thread.



    So would you say that 50 mg would be the max recommended dosage?
    Well 75mg or more is a righteous test booster for sure, but yeah if you wanna preserve libido 50mg is the max IME. If you have some MFX or DHEA in PCT that's good libido insurance anyway, but even just 25mg of ATD is a good anti-e with no perceivable anti-a effects on a cycle.

    The test boosting becomes impressive closer to 50mg and 25mg actually increases libido for me. In women, I've seen 25mg send libido through the roof! It does seem to be dependent on the presence of functional ovaries though which tells me it's probably not a central mechanism that explains the low dose libido boost, it's just that too many central ARs get filled up and nullified with higher doses probably.
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    Quote Originally Posted by poopypants View Post
    its funny right after reading this thread i went and split all my 25mg caps up into 12.5 mg caps..... question though... typically with any AI or serm i would dose t all at night.... BUT with HDX2 its taken throughout the day at a constant dose, could the same be done with ATD like (3) 12.5mg doses taken spread through the day withh fish oils??? or would it be better to take the 37.5 mg together before bed?
    I'd split it up if your going for an anabolic effect based on the test boosting properties or an anti-e effect treating gyno, but if it's specifically for PCT purposes right before bed inspires the best gonadotropic surge probably which is good for reestablishing a normal pattern of pituitary secretion.
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    D, throwing out all of these doses and stuff is great but...where are the studies?

    how is it known if taking ATD and blocking the AR is actually GOOD for post cycle therapy? Dont we want the AR to UPregulate during pct? not DOWNregulate?
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    Quote Originally Posted by jomi822 View Post
    D, throwing out all of these doses and stuff is great but...where are the studies?

    how is it known if taking ATD and blocking the AR is actually GOOD for post cycle therapy? Dont we want the AR to UPregulate during post cycle therapy? not DOWNregulate?
    I don't know of any studies in guys like us. Just old blood work from the DS beta days with this stuff and data shared with me from other product developers in the game that have really exploited this property of ATD to make lots of similar compounds.

    As far as PCT, your ARs are way unregulated by the end of a cycle. In PCT you want to downregulate them again and upregulate SHBG at the same time. That's what causes you to lose the tolerance where you can start a new cycle after a month or two and get that strong response all over again. I don't really have any clear-cut studies though, so the doses I stated are just my overall objective impression and personal subjective response to this compound.

    The mechanisms I explained just stand to reason based on studies like you posted and the general, central effects of other anti-androgen, but it is only a guess to try and explain the anecdotal observations. That's the best I got with this one bro, but I'd like to see some studies too if you could find some.
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    Quote Originally Posted by DR.D View Post
    Well 75mg or more is a righteous test booster for sure, but yeah if you wanna preserve libido 50mg is the max IME. If you have some MFX or DHEA in post cycle therapy that's good libido insurance anyway, but even just 25mg of ATD is a good anti-e with no perceivable anti-a effects on a cycle.

    The test boosting becomes impressive closer to 50mg and 25mg actually increases libido for me. In women, I've seen 25mg send libido through the roof! It does seem to be dependent on the presence of functional ovaries though which tells me it's probably not a central mechanism that explains the low dose libido boost, it's just that too many central ARs get filled up and nullified with higher doses probably.

    I see, thanks D!

    Btw did you get the email I sent you?
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    Quote Originally Posted by Solitude View Post
    I see, thanks D!

    Btw did you get the email I sent you?
    I'll check today. My DSL service is in and out so I'm a little behind on PMs.
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    Wow, I didn't realize that ATD use was even still debated. That's definitely not a new study. It says 1989 on it, and I have it saved in my Favorites from 2005. I don't think I've used ATD since.

    I must definitely note though, the last time I did use it, it was accompanied with a welcomed strength increase during PCT, better than while on (granted it was a MOHN/MDHT cutter).
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    Id like to read the full study before making any fa-sure comments. Because Im not exactly sure what the author means by “No agonistic properties of ATD were observed…” Just because ATD is not an agonist of AR activity doesn’t necessarily mean it’s a full antagonist either. For example, its highly unlikely that it blocks negative feedback from the AR. It’s like proposing DHT blocks the negative inhibition on the hypothalamus because it competitively binds for the AR between testosterone. (DHT obviously does not block inhibition)

    Ive always said that using a steroidal-AI for PCT is a bad idea just because it is a steroid which can bind directly to the AR, and inhibit LH/FSH. More over, estrogen is a protector and sensitizer of the leydigs, so keeping estrogen excessively low can actually hurt the testes ability to produce testosterone – eventually.

    The only libido increase or stimulation of testosterone production from the use of ATD (or any steroidal AI) would be from estrogen inhibition and immediate increase in LH/FSH because of reduced suppression at the hypothalamus from estrogen. Thus, the only use for a steroidal AI would be a very short-term application either DURING of an estrogenic steroid cycle, or immediately after. Otherwise, they have no place in PCT.

    -Pp
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    Stopped reading when I got to rats. Although you can extrapolate "possibilities" based on animal testing, you definitely cannot expect a human to respond like an animal.

    Good post anyway; I don't like ATD, kills the Mr. Winky.
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    I have neither studies nor any scientific data to back this up, but I personally would never use ATD during post cycle therapy.

    Remember all those "delayed gyno" complaints that guys were experiencing 2 to 3 months after Superdrol or PP cycles? It seemed as though many of them were using ATD-based products for post cycle therapy (either with a SERM, or sometimes no SERM at all).

    I would consider using ATD as a standalone to boost test, but that’s it.
  

  
 

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