ATD instead of HCG?

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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]
    can you translate this into beelzelanguage?

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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?
    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.

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    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.

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    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.
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    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.
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    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
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    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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    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.
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    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.
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    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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    Quote Originally Posted by CEDeoudes59
    Neat Smilies
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    It just seemed right to add this one.
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    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!
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    Doubt it.
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    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?
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    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.
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    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.
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    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
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    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?
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    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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    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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    Quote Originally Posted by bow
    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....
    Bow, I read that article ALR has on readthecore and it does say that its affinity to binding to the hypothalamus is higher than in other tissues. This may very well be the case, but does anybody have a study showing this? The below articles are very informative but dont explicitly state this, unless Im just reading it wrong.
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    I'm just gonna say again that I willl patiently await ALR's further explanation. I know he is busy, but I expect at some time he'll let us know a bit more, since he opened this idea up publicly. However, I'll say in honesty that I wish the ALRI team would be a bit more vocal on the subject. Or perhaps they simply don't know yet either. I've asked repeatedly for info, at least particulars on the ALRI products (HOT/HOTter), yet don't get responses, unfortunately...
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    Not too surprising, from what I've seen, he doesn't explain much of anything, nor use references that actually hold any value.
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    No, but ALRI stuff works. Like him or not (I personally like the guy), his stuff WORKS.
    So I use his stuff.
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    Quote Originally Posted by N4cer
    No, but ALRI stuff works. Like him or not (I personally like the guy), his stuff WORKS.
    So I use his stuff.
    Most of it works, prostan has not been all the rage it was cracked up to be unless stacked with something stronger, but no supplement line is perfect. Just like many other supplement companies who are releasing designer supplements, they are just reinventing the wheel. DMT has been around since the 70's.
    *Not trying to be a smart ass, just stating an observation*
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    Quote Originally Posted by N4cer
    No, but ALRI stuff works. Like him or not (I personally like the guy), his stuff WORKS.
    So I use his stuff.
    And just so you understand, I have a bottle of E-Max at my house, so I use his stuff too.
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    Quote Originally Posted by Onslaught
    Not too surprising, from what I've seen, he doesn't explain much of anything, nor use references that actually hold any value.
    actually I have always found Author to be quite willing to discuss questions and explain things in the past. Same with the ALRI team. This ATD issue, however seems to be an exception. I've been posting queries about ALR's take on ATD and the HCG issue (stemming from the "Core" article), as well as questions on dosing requirements and ATD content of UH/ HOTter for over 2 weeks in a number of threads (and even in PM's). Apparently either nobody knows or nobody's telling!
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    My experience with Author and the ALRI team is that they do not comment on the board on a daily basis. Usually they are not heard from for a number of days and then appear to answer as many of the questions as they can. When they do answer I have found them to be helpful and friendly. I think we were coming to the end of one of their "few day" absent periods when this issue about the reporter contacting them started and since they have not been heard of except in regard to that issue. I imagine that some things will change this week when their new site goes up.



    Quote Originally Posted by milwood
    actually I have always found Author to be quite willing to discuss questions and explain things in the past. Same with the ALRI team. This ATD issue, however seems to be an exception. I've been posting queries about ALR's take on ATD and the HCG issue (stemming from the "Core" article), as well as questions on dosing requirements and ATD content of UH/ HOTter for over 2 weeks in a number of threads (and even in PM's). Apparently either nobody knows or nobody's telling!
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    Quote Originally Posted by Mr.50
    . I think we were coming to the end of one of their "few day" absent periods when this issue about the reporter contacting them started and since they have not been heard of except in regard to that issue. I imagine that some things will change this week when their new site goes up.
    You pretty much hit the nail on the head. You guys just need ti chill til that thing blows over.

    Self preservation...
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    Quote Originally Posted by Lean One
    You pretty much hit the nail on the head. You guys just need ti chill til that thing blows over.

    Self preservation...
    Eh, ok, that sounds reasonable.
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    Quote Originally Posted by Sky9
    Bow, I read that article ALR has on readthecore and it does say that its affinity to binding to the hypothalamus is higher than in other tissues. This may very well be the case, but does anybody have a study showing this? The below articles are very informative but dont explicitly state this, unless Im just reading it wrong.

    There is a study to support the notion that atd demonstrates tissue preference, at least in terms of aramotase activity. I posted this a while back in this thread:

    ATD and site-specific androgen receptor agonists

    ______________________________ ____________________
    J Clin Endocrinol Metab. 1984 Dec;59(6):1088-96.

    Inhibition of aromatization stimulates luteinizing hormone and testosterone secretion in adult male rhesus monkeys.
    Ellinwood WE, Hess DL, Roselli CE, Spies HG, Resko JA.


    Experiments were conducted to examine the role of aromatization in the control of LH and testosterone secretion in adult male rhesus monkeys. Treatment of male monkeys (n = 7) with sc Silastic packets containing the aromatase inhibitor 1,4,6-androstatriene-3,17-dione (ATD) resulted in 1.5- to 3-fold elevations in serum LH and testosterone concentrations in six of seven animals. Concurrent treatment of ATD-treated monkeys with small quantities of estradiol-17 beta (n = 4) abolished the stimulatory effect of ATD. During ATD treatment, peripheral estradiol levels were reduced by 30% and hypothalamic aromatase activity, as determined in vitro, was reduced 80-90%. The lack of androgenic or antiandrogenic activity of ATD was demonstrated by its inactivity in either a mouse seminal vesicle bioassay or a highly sensitive penile spine bioassay. Furthermore, ATD did not react with rat prostatic or hypothalamic cytosol androgen receptors. 1,4,6-Androstatriene-17-ol-3-one, a possible metabolite of ATD in vivo, did react with prostatic and hypothalamic androgen receptors, but possessed no antiandrogenic activity in either bioassay. Thus, treatment of adult males with an aromatase inhibitor that inhibits both peripheral and central aromatization, and which has no apparent antiandrogenic activity, results in stimulation of LH and testosterone secretion. These data demonstrate that aromatization of androgens to estrogens plays an important role in negative feedback regulation of LH secretion and maintenance of normal testosterone levels in adult male primates.
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    Another interesting development came to light recently at Avant. The study below was recently posted in this thread:

    http://forum.avantlabs.com/index.php...ic=15482&st=60

    This may explain why some are seeing increased test levels while administering exogenous hormones and experiencing a decrease in LH and FSH. Could ATD be giving a false result for an increase in test? Perhaps this explains Anarchy’s bloodwork and ATD in no way directly stimulates the testies. Its worth discussion.

    Steroids. 1980 Dec;36(6):717-21.

    Immunological interference of the synthetic aromatase inhibitor 1,4,6-androstatriene-3,17-dione (ATD) and its metabolite(s) in the radioimmunoassay for testosterone.

    Donaldson MD, Forest MG.

    Radioimmunoassay (RIA) for testosterone (T) in unchromatographed plasma extracts from ATD-treated rats gave spuriously high values for T. Cross-reaction and chromatographic studies subsequently showed that ATD and, to a much greater extent, its metabolite(s) were responsible for this overestimation. Celite column chromatography proved to be an effective way of separating T from ATD and its product(s) of metabolism.
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    bow, you highlighted the least interesting part of the last study you posted, as far as this discuss goes, the following is of way more interest to us:

    The lack of androgenic or antiandrogenic activity of ATD was demonstrated by its inactivity in either a mouse seminal vesicle bioassay or a highly sensitive penile spine bioassay.
    Granted, these are rat studies and done in vitro, take this together with another study showing anti-androgenic activity in the brain and we have ourselves a SARM.
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    Quote Originally Posted by Onslaught
    bow, you highlighted the least interesting part of the last study you posted, as far as this discuss goes, the following is of way more interest to us...

    I highlighted the part of the study that addresses the question asked (with regards to preferential tissue sensitivity).

    There is no question (as emphasized by the section of the study you posted) that we are far from proving ATD is a hypothalamic site specific ar agonist. My argument with the thread I linked above is exactly that the studies are contradictory and far from being conclusive.
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    But the problem here is that it appears there is at least the possibility that ATD is not really raising Test at all but just giving a false positive???? That is how I read it but maybe I am missing something. I can say though that the boys really felt much fuller to me when I was on Ultra Hot. I know tha is subjective but it was quite noticable.
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    Quote Originally Posted by milwood
    actually I have always found Author to be quite willing to discuss questions and explain things in the past. Same with the ALRI team. This ATD issue, however seems to be an exception. I've been posting queries about ALR's take on ATD and the HCG issue (stemming from the "Core" article), as well as questions on dosing requirements and ATD content of UH/ HOTter for over 2 weeks in a number of threads (and even in PM's). Apparently either nobody knows or nobody's telling!
    You are aksing questions in wihch the leading endocrinologists don't evne have answers to. The majority of ALL of this is theoretical so if you want "answers" that there is proof of any kind you will never get it. You can ask Dr. Crisler the same questions and he simply won't know. His HCG treatment that most of you take as "law" was criticized heavily within the medical community. Most of their comments are based on clinical results, not published work. HRT and its effects are in its infancy. Most of the answers you will ever get are based on SOME studies and theory.


    And I doubt he is going to answer anything in the near future...
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    Thanks Bow, I appreciate the literature.
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    Quote Originally Posted by Bobo
    You are aksing questions in wihch the leading endocrinologists don't evne have answers to. The majority of ALL of this is theoretical so if you want "answers" that there is proof of any kind you will never get it. You can ask Dr. Crisler the same questions and he simply won't know. His HCG treatment that most of you take as "law" was criticized heavily within the medical community. Most of their comments are based on clinical results, not published work. HRT and its effects are in its infancy. Most of the answers you will ever get are based on SOME studies and theory.


    And I doubt he is going to answer anything in the near future...
    So whats your take on ATD vs HCG Bobo??? Is it as effective for keeping the boys pumping while on cycle?
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    Quote Originally Posted by Sky9
    Most of it works, prostan has not been all the rage it was cracked up to be unless stacked with something stronger, but no supplement line is perfect. Just like many other supplement companies who are releasing designer supplements, they are just reinventing the wheel. DMT has been around since the 70's.
    *Not trying to be a smart ass, just stating an observation*
    And how do you make this judgement? I could smell this one from a mile away. People expect gains similar to the rest of their compunds without even understand that its "winny like effects" would probably produce VERY little in terms of LBM. Its a cutting agent.

    Once again, the results are coming form inexperienced users who probably shouldn't be using it in the first place.
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    Quote Originally Posted by Sky9
    So whats your take on ATD vs HCG Bobo??? Is it as effective for keeping the boys pumping while on cycle?
    As I said before they were a sponsor and to this day I don't think it will be as effective as HCG. THat doens't mean it doesn't work but there isn't enoug evidence that I see. But Author usually has bloodwork that supports his arguements....He posted them earlier with Ulta Hot and they were pretty impressive but thats gone now...
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