ATD and site-specific androgen receptor agonists - AnabolicMinds.com

ATD and site-specific androgen receptor agonists

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    ATD and site-specific androgen receptor agonists


    Can certain aramotase inhibitors demonstrate a higher affinity for the AR in the hypothalamus as compared to the AR peripherally? If you could get a substance to show a higher affinity to the AR than T centrally, but then allow T to preferentially bind in the rest of the body, the effects could be profound. You would have a compound that allows you to elevate T above normal physiological levels with less of a negative impact upon the htpa. Yes, the hypothalamus is not the only element of the feedback loop, but it is a substantial component of that loop. Perhaps you could even potentially bridge between cycles with low levels of T (as proposed and not so universally accepted by USPLabs and others) and dupe the body into believing you are within normal physiological levels.

    ALRI claims to have a compound that does this. They are using ATD (1,4,6-androstatriene-3,17-dione) and claiming that it is a site-specific androgen receptor agonist. How cool would this be if it were to be true. The write-up on ALRI’s site states:

    3,17-dioxo-etiochol-1,4,6-triene is also a site-specific (like the hypothalamus) androgen receptor agonist. Based upon some studies the unique structure of this compound allows for an 80-90% reduction in androgen receptor activity of the hypothalamus, yet only a very small 10% decrease in the rest of the body. So all of that extra testosterone you are now making really works in all the right places!

    However, I must admit, I am still skeptical. Hopefully, now that it looks like Author is going to become a board sponsor, maybe he can help squelch some of my skepticism. I would love to believe this is possible.

    I have read the abstracts (and a couple of the full texts), and have not really found any concrete evidence to support this assertion. I will post the abstracts.

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    Abstract from first study

    Horm Behav. 1989 Mar;23(1):10-26.

    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.


    Second Study

    Estrogen synthesis in fetal sheep brain: effect of maternal treatment with an aromatase inhibitor.

    Roselli CE, Resko JA, Stormshak F.

    Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, Oregon 97201-3098, USA. rosellic@ohsu.edu

    The aim of the present study was to determine whether the fetal lamb brain has the capacity to aromatize androgens to estrogens during the critical period for sexual differentiation. We also determined whether administration of the aromatase-inhibitor 1,4,6-androstatriene-3,17-dione (ATD) could cross the placenta and inhibit aromatase activity (AA) in fetal brain. Eight pregnant ewes were utilized. On Day 50 of pregnancy, four ewes were given ATD-filled Silastic implants, and the other four ewes received sham surgeries. The fetuses were surgically delivered 2 wk later (Day 64 of gestation). High levels of AA (0.8-1.4 pmol/h/mg protein) were present in the hypothalamus and amygdala. Lower levels (0.02-0.1 pmol/h/mg protein) were measured in brain stem regions, cortex, and olfactory bulbs. The Michaelis-Menten dissociation constant (K(m)) for aromatase in the fetal sheep brain was 3-4 nM. No significant sex differences in AA were observed in brain. Treatment with ATD produced significant inhibition of AA in most brain areas but did not significantly alter serum profiles of the major sex steroids in maternal and fetal serum. Concentrations of testosterone in serum from the umbilical artery and vein were significantly greater in male than in female fetuses. No other sex differences in serum steroids were observed. These data demonstrate that high levels of AA are found in the fetal sheep hypothalamus and amygdala during the critical period for sexual differentiation. They also demonstrate that AA can be inhibited in the fetal lamb brain by treating the mother with ATD, without harming fetal development.


    Third Study

    J Steroid Biochem. 1987 Sep;28(3):337-44.

    Studies on aromatase inhibition with 4-androstene-3,6,17-trione: its 3 beta-reduction and time-dependent irreversible binding to aromatase with human placental microsomes.

    Numazawa M, Tsuji M, Mutsumi A.

    Tohoku College of Pharmacy, Sendai, Japan.

    The metabolism of 4-androstene-3,6,17-trione (AT), previously described as a suicide substrate for aromatase, and its irreversible binding to aromatase were studied by using human placental microsomes. AT was rapidly converted into 3 beta-reduced metabolite (3-OHAT) with an enzyme other than aromatase in the microsomes in the presence of NADPH under either aerobic or anaerobic conditions. The conversion was efficiently prevented by a steroid 5 alpha-reductase inhibitor. 3-OHAT was characterized as a competitive (Ki = 6.5 microM) and irreversible inhibitor of aromatase. Both 14C-labeled AT and 3-OHAT were demonstrated to be irreversibly bound to aromatase probably through a sulfur atom of the enzyme in time-dependent manners in the presence of NADPH, being accompanied with time-dependent losses of the enzyme activity. It was shown that the process of an apparent time-dependent loss of aromatase activity caused by AT even under conditions allowing its 3 beta-reduction should principally depend on the action of the parent inhibitor AT itself and not on that of the metabolite 3-OHAT.


    Fourth Study

    White button mushroom phytochemicals inhibit aromatase activity and breast cancer cell proliferation.

    Grube BJ, Eng ET, Kao YC, Kwon A, Chen S.

    Division of Immunology, Beckman Research Institute of the City of Hope, Duarte, CA 91010, USA.

    Estrogen is a major factor in the development of breast cancer. In situ estrogen production by aromatase/estrogen synthetase in breast cancer plays a dominant role in tumor proliferation. Because natural compounds such as flavones and isoflavones have been shown to be inhibitors of aromatase, it is thought that vegetables that contain these phytochemicals can inhibit aromatase activity and suppress breast cancer cell proliferation. Heat-stable extracts were prepared from vegetables and screened for their ability to inhibit aromatase activity in a human placental microsome assay. The white button mushroom (species Agaricus bisporus) suppressed aromatase activity dose dependently. Enzyme kinetics demonstrated mixed inhibition, suggesting the presence of multiple inhibitors or more than one inhibitory mechanism. "In cell" aromatase activity and cell proliferation were measured using MCF-7aro, an aromatase-transfected breast cancer cell line. Phytochemicals in the mushroom aqueous extract inhibited aromatase activity and proliferation of MCF-7aro cells. These results suggest that diets high in mushrooms may modulate the aromatase activity and function in chemoprevention in postmenopausal women by reducing the in situ production of estrogen.


    Fifth Study

    J Steroid Biochem. 1986 Oct;25(4):593-600. Related Articles, Links

    Effect of 1,4,6-androstatriene-3,17-dione (ATD), 4-hydroxy-4-androstene-3,17-dione (4-OH-A) and 4-acetoxy-4-androstene-3,17-dione (4-Ac-A) on the 5 alpha-reduction of androgens in the rat prostate.

    Motta M, Zoppi S, Brodie AM, Martini L.

    The present study reports the effects exerted by 1,4,6-androstatriene-3,17-dione (ATD), 4-hydroxy-4-androstene-3,17-dione (4-OH-A) and 4-acetoxy-4-androstene-3,17-dione (4-Ac-A), three steroids known to inhibit the aromatization of androgens to estrogens, on the in vitro metabolism of labelled testosterone (T), dihydrotestosterone (DHT) and androstenedione (delta-4-A) in the ventral prostate of adult male rats. It has been found that ATD, in the concentration tested, does not influence the conversion of labelled T into DHT, but decreases the formation of 5 alpha-androstane-3 alpha,17 beta-diol and 5 alpha-androstane-3 beta,17 beta-diol (diols). On the contrary, 4-OH-A and 4-Ac-A simultaneously decrease the formation of DHT and the diols. When T is used as the substrate, the presence in the medium of these three steroids enhances the formation of delta-4-A and of 5 alpha-androstanedione (5 alpha-A). ATD, but not 4-OH-A and 4-Ac-A inhibits the conversion of labelled DHT into the diols. The transformation of labelled delta-4-A into 5 alpha-A is not modified by either ATD or 4-OH-A, while 4-Ac-A exerts only a small inhibition. These results suggest that the three aromatase inhibitors tested are able to profoundly modify the metabolism of T in the ventral prostate of the rat. In particular: 4-OH-A and 4-Ac-A are able to inhibit the conversion of T into DHT; ATD is able to inhibit the conversion of DHT into the diols; ATD and 4-OH-A do not inhibit the process of 5 alpha-reduction of delta-4-A into 5 alpha-A, while 4-Ac-A exerts only a minor effect. It is suggested that in the ventral prostate of the rat there are two different 5 alpha-reductase isoenzymes, one sensitive to the inhibitory effect of the steroid tested and which is responsible for the conversion of T into the 5 alpha-reduced metabolites of the 17-OH series (DHT and the diols), and a second one, insensitive to the effects of the three steroids, which affects the conversion of delta-4-A into 5 alpha-A.


    Sixth Study

    J Steroid Biochem Mol Biol. 1992 Oct;43(4):281-7. Related Articles, Links

    In vitro potency and selectivity of the non-steroidal androgen aromatase inhibitor CGS 16949A compared to steroidal inhibitors in the brain.

    Wozniak A, Holman SD, Hutchison JB.

    MRC Neuroendocrine Development and Behaviour Group, Institute of Animal Physiology and Genetics Research, Babraham, Cambridge, England.

    A sensitive in vitro 3H2O microassay for aromatase activity was used to evaluate the potency and selectivity of three aromatase inhibitors in mammalian (gerbil) and avian (ring dove) hypothalamus. The steroidal inhibitors, 1,4,6-androstatrien-3,17-dione (ATD) and 4-hydroxy-androstenedione (4-OH-A) were compared with a new non-steroidal imidazole inhibitor, CGS 16949A [4-(5,6,7,8-tetrahydroimidazo-[1,5-a]-pyridin-5-yl)benzonitrile HCl]. Adult male dove hypothalamic aromatase is highly active [Vmax = 5.3 pmol testosterone (T) converted/h/mg protein], has high substrate binding affinity (Km = 4.0 nM), and direct involvement in control of sexual behaviour. With [1 beta-3H]T or [1 beta-3H]A as substrate, male dove preoptic aromatase activity was inhibited more effectively and selectively by CGS 16949A. Thus, Kis and IC50s for aromatization were approximately 50 times lower for the non-steroidal inhibitor, and inhibition of the other major androgen-metabolizing enzymes (5 alpha/beta-reductase) occurred at concentrations at least one order of magnitude greater than for ATD and 4-OH-A. Neonatal male gerbil hypothalamic aromatase activity (Vmax = 1.3 pmol T converted/h/mg protein) was lower than in the dove. Aromatase inhibition by CGS 16949A is more potent in the neonatal gerbil than in the dove (Kis of 0.03 and 0.60 nM, respectively, with A as substrate). We conclude that the imidazole is an effective aromatase inhibitor in both the adult and developing brain.
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    Nice post bow. I'm def. interested in this too. I admit that at first L. Rea didn't really do it for me and I totally disrespected him due to his principles/theories, but now I'm starting to like him/his theories more and more every time I hear or read about it. I guess you could call me a convert...lol. Or maybe just an *******...

    This product would be incredibly useful to the AAS user for bridging like you said. Although every thing I've ever read proves otherwise.....this way sounds like it could hold more water than other typical "bridging protocols."
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    Quote Originally Posted by lifted
    Although every thing I've ever read proves otherwise.....this way sounds like it could hold more water than other typical "bridging protocols."

    Agreed. Very interested to see what they and other have to say. I would really be interested to see someone bridge with a low weekly test dosage, say 200 mg's week for a couple of weeks during PCT while taking Ultra Hot. Then immediate cease adminstration and about two days later (after the test base has systematically cleared), get a blood test. That would go a really long way to determining if this at least has a stronger binding affinity (ki) than T in the hypothalamous.

    Anyway, I think I found the study where ALRI may have come up with their numbers regarding the preferential binding rates. Only problem is it has less to do with AR binding and more to do with varying aramotase activity in the body.

    .............................. .............................. .............................. .............................. .............................. ...............

    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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    Im about to start post cycle and am all about trying a bridge with 200mg/week of test, if ALRI wants to pay for the Ultra HOT and my blood tests (really not wanting to come off yet lol)
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    What about selective androgen receptor modulators?
    Anyone knows any substances in specific?
    I think it´s gona be the new sh*t in futer if it isn´t already in olympic sports.
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    There are a couple of really interesting statements made in the abstract above. First:

    "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."

    From this statement we can conclude that neither ATD or its metabolites, even if they do show a binding affinity to the AR, do not show any antiandrogenic effects in the hypothalamus.

    They go on to say:

    "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."

    Essentially, what this says is that ATD is effective as suicide inhibitor in preventing the aromatization of T to E. We have known for some time that preventing the aromatization of T is strong variable in the feedback loop. This is nothing new.

    So, unless I am misinterpreting this, this study really refutes the claim that ATD is going to block the androgenic effects of T in the hypothalamus and thus the negative effects it exerts on the htpa. Although I must admit I have not had a chance to read the full text of the study, so I may be jumping to conclusions.
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    I'm reading it as saying that ATD doesnt bind/interact with the hypothalymus AR but that one of its metabolites does.
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    bump

    anyone else want to take a shot at some laymans terms.
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    I think you are forgetting lots of things. 1) test does more than make you more muscular 2) lots of the effects of test depend upon its conversion to estrogen or DHT in cytosol of certain tissues 3) the effects of SHBG and inhibin from the sertoli cells in response to increased test which are major mechanisms of control, not just direct negative feedback but indirect also. Beware of 'pub med' voodoo
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    Quote Originally Posted by Jay Mc
    I think you are forgetting lots of things. 1) test does more than make you more muscular 2) lots of the effects of test depend upon its conversion to estrogen or DHT in cytosol of certain tissues 3) the effects of SHBG and inhibin from the sertoli cells in response to increased test which are major mechanisms of control, not just direct negative feedback but indirect also. Beware of 'pub med' voodoo

    Understood. Which is why prefaced this thread by stating "Yes, the hypothalamus is not the only element of the feedback loop." All of which you state is true. Yet the implications, if valid, still hold great merit with respect to bodybuilding.
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    The idea that preferentially decreasing androgen binding in the hypothalamus vs the periphery (specifically muscle) could be a very good thing is not at all new. Pat Arnold and I discussed it on the MFW newsgroup like 4 years ago.

    The rub is getting it done, and looking at these abstracts, I don't see where the idea that ATD is doing this is coming from. The only thing I can think of is that one of the studies in the hypothalamus shows it to be an antagonist, while that other study shows it not to have activity (peripherally, but also in the hypothalamus)

    The other thing that might be noteworthy is that it more strongly inhibited aromatase in the hypothalamus than periphery in that last study, but 1) it is in vitro and 2) that is not at all the same a selective AR modulation.

    Maybe there are others studies they are hiding (or maybe the abstract greatly misrepresents the full text), but from the abstracts shown, the claims seem like a stretch at best.
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    Quote Originally Posted by Par Deus
    Maybe there are others studies they are hiding (or maybe the abstract greatly misrepresents the full text), but from the abstracts shown, the claims seem like a stretch at best.
    That is basically that same conclusion I came to after reading the abstracts. However, it looks like in this case ALRI has done their homework. When I questioned the claim in ALRI's section, Author's comment was:


    Quote Originally Posted by Author L. Rea
    To put this belief to the real world test, we used 16 trained test subjects. (Done last year in Mexico)

    1) 4 were given a placebo
    2) 4 were given an ATD analog daily
    3) 4 were given 100mg methyl testosterone/1.5mg anastrolzol daily
    4) 4 were given 100mg methyl testosterone/ATD analog daily.

    1) Obviously the first 4 realized no significant changes in LH/FSH/estradiol/testosterone at 2, 4 and 8 week retesting periods.

    2) The ATD analog only group showed an average 50% decrease in estradiol, and a significant increase in LH/FSH/testosterone.

    3) The anastrolzol/methyl testosterone group all showed a significant increase in testosterone (gee, are you surprised?) and a decending decrease in LH/FSH over the 8 week period until near 0, and estradiol levels increased an average of 1.6 times normal.

    4) The ATD analog/Methyltestosterone group of course had a major increase in testosterone. LH/FSH decreased after the first 2 weeks an average of 34% but remained constant until termination of the project at week 8. Estradiol was an average of 1.9 times normal.

    What does this mean? Well, if in the latter two groups estradiol were near the same then the estrogen negative feed back loops were as well. However the continued endogenous (made in the body) production of LH/FSH STRONGLY suggests that the findings in the research above is applicable in that the androgen negative feed back loop was inhibited by the ATD analog.
    Looks like there may be some promise with respect to the ATD analog he is using. If estrogen was 1.9 times normal, that alone could be enough to desensitize the pituitary into a 34% reduction in LH/FSH. However, I am dying to see some bloodwork from independend users (kinda like what Kneller did with Dio) after a cycle with ARLI's ATD analog and a moderate aas cycle.

    Any takers?
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    Quote Originally Posted by bow
    That is basically that same conclusion I came to after reading the abstracts. However, it looks like in this case ALRI has done their homework. When I questioned the claim in ALRI's section, Author's comment was:




    Looks like there may be some promise with respect to the ATD analog he is using. If estrogen was 1.9 times normal, that alone could be enough to desensitize the pituitary into a 34% reduction in LH/FSH. However, I am dying to see some bloodwork from independend users (kinda like what Kneller did with Dio) after a cycle with ARLI's ATD analog and a moderate aas cycle.

    Any takers?
    I am goign to try ultra hot and get some blood work done and I will let you guys know
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    Quote Originally Posted by Funny Monkey
    I am goign to try ultra hot and get some blood work done and I will let you guys know
    Cool. What are you stacking it with?
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    Quote Originally Posted by bow
    Cool. What are you stacking it with?
    Some fenugreek, avena sativa, gingko, tribulus, hawthorne berry, milkthistle. It's basically just a blend I cap myself.

    I am probably going to start it monday or next wednesday. I am graduating this Saturday and throwing a keg party and then I have a bachelor party on the 21st so I at least want to get one of those out of the way before I start trying to bring my natty test back up. If your interested in my previous blood work I have a post in the anabolics section.
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    Quote Originally Posted by Funny Monkey
    Some fenugreek, avena sativa, gingko, tribulus, hawthorne berry, milkthistle. It's basically just a blend I cap myself.

    I am probably going to start it monday or next wednesday. I am graduating this Saturday and throwing a keg party and then I have a bachelor party on the 21st so I at least want to get one of those out of the way before I start trying to bring my natty test back up. If your interested in my previous blood work I have a post in the anabolics section.

    That's cool. Hope it goes well for you for getting your natural test back. The only problem is*that to test the theory of preferential binding to the ar in the hypothalamous, we really need to see post cycle blood results from people stacking Ultra Hot with an aas.
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    Quote Originally Posted by bow
    That is basically that same conclusion I came to after reading the abstracts. However, it looks like in this case ALRI has done their homework. When I questioned the claim in ALRI's section, Author's comment was:

    "omitted"

    Looks like there may be some promise with respect to the ATD analog he is using. If estrogen was 1.9 times normal, that alone could be enough to desensitize the pituitary into a 34% reduction in LH/FSH. However, I am dying to see some bloodwork from independend users (kinda like what Kneller did with Dio) after a cycle with ARLI's ATD analog and a moderate aas cycle.

    Any takers?
    Am I missing something??

    If the AR was blocked both peripherally and centrally, it is not going to diminish the antagonism of the negative feedback loop on the HPTA.

    Now, if we were to see an attenuation of LH/FSH decrease and say an increase in post-AR transcription in skeletal muscle, I would be Way Impressed(tm)
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    Quote Originally Posted by Par Deus
    Am I missing something??

    If the AR was blocked both peripherally and centrally, it is not going to diminish the antagonism of the negative feedback loop on the HPTA.

    Now, if we were to see an attenuation of LH/FSH decrease and say an increase in post-AR transcription in skeletal muscle, I would be Way Impressed(tm)


    One of is......and very likely it is me

    So, help straighten me out. The hope is that the ATD analog preferentially binds centrally at a higher rate than T and peripherally at a low rate. We do know that certain compounds can preferentially bind at certain tissues in favor of others (as Author pointed out with tamoxifen and breast tissue). If the binding rate was higher the next hope is that it doesn’t activate the signaling pathways that inhibit GnRH transcription with the same amplitude as T. If this was the case, GnRH production would increase and the rest is history.

    I don’t believe the atd analog is an antagonist. I don’t think its blocking anything either peripherally or centrally from attaching to the receptor. It’s is just attaching at a higher rate and then blocking (or decreasing) the signaling pathways to the GnRH neurons that decrease production and thus the negative feedback.

    I often times have a talent for steering off a cliff, so help get me back on path.
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    In your last paragraph are you speaking of aromatase or the androgen receptor??

    Regardless, we can talk science 'til the cow come home and fly with the pigs on their backs, but the data is clearly limited and a bit conflicting. I have a case of Attack, so I'm gonna get on it and see WTF it does, subjectively and empirically.
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    Quote Originally Posted by Par Deus
    In your last paragraph are you speaking of aromatase or the androgen receptor??
    AR

    BTW, Par-Diggity, check out this thread thread if you get a chance. There is some interesting discussion with regards to bridging and even Nadi chimes in. Both attack and ALRI’s products are not technically using ATD, they are using an analog. Anywhoo, yes, ATD is also purported to have preferential aramotase activity centrally (at least here there is some supporting documentation). Suppose time will tell. I too will be giving it a go in the near future.
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    Quote Originally Posted by lifted
    Nice post bow. I'm def. interested in this too. I admit that at first L. Rea didn't really do it for me and I totally disrespected him due to his principles/theories, but now I'm starting to like him/his theories more and more every time I hear or read about it. I guess you could call me a convert...lol. Or maybe just an *******...

    This product would be incredibly useful to the AAS user for bridging like you said. Although every thing I've ever read proves otherwise.....this way sounds like it could hold more water than other typical "bridging protocols."
    Lifted:

    Thank you for your integrity. Most would lack your strength in simply being honest. I realize that at times I am a "bit", okay a lot, controversial, but if I piss you off at least I know I have done my job in getting you to think...agree or not. I taught for a short period and found it anything but rewarding because few would allow truely open forums in academia circles. Now, and for many years, I have been free to enjoy being quite honest and the rewards of the interaction with those like yourself.

    As to the androgen feed back loop and durring protocols...it works. We use it in HRT clinics as a supplement to maintain functional HPTA activity with respectable success.
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    I keep seeing this posted

    ''3,17-dioxo-etiochol-1,4,6-triene is also a site-specific (like the hypothalamus) androgen receptor agonist. Based upon some studies the unique structure of this compound allows for an 80-90% reduction in androgen receptor activity of the hypothalamus, yet only a very small 10% decrease in the rest of the body. So all of that extra testosterone you are now making really works in all the right places! ''

    apparently its from here

    http://www.ncbi.nlm.nih.gov/pubmed/2...?dopt=Abstract

    which has been posted, but not the full article. can anyone get the full article?
  24. PESCIENCE.com
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    It is an anti androgen in the brain. What more do you need to know?
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