Can we please stop with the borlore - Prolactin DOES NOT INCREASE GYNO

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  1. Quote Originally Posted by justreading View Post
    Actually most won't touch m-1-t or superdrol because they are unproven and show signs of being more toxic than dbol. Track the history of these drugs and their analogs and you will know why real deal users are smart enough to not touch them, for their health.
    Ok, well it's your story, you tell it... I'd take my chance with a GMP certified facility making my M1T vs. a guy in his basement making D-Bol tabs any day. Additionally, that wasn't what I heard, it was that it wasn't "real gear". I think you are really stretching here...


  2. Quote Originally Posted by LegalGear View Post
    No one is saying that prolactin is "good" however having people reduce aspects of their hormonal cascade when there is no indication of higher than normal levels is crazy and pointless. Like anything excess prolactin isn't a positive, but reducing it just because isn't good either.
    It's like anything else- you want to keep levels normalized, and not throw it out of whack- It is ok to lower E, Cortisol, and SHBG to a certain extent, but there is a rebound effect when you start messing around with these entities. Prolactin isn't "bad" in most contexts- but in an atypical state where the T:E or T:C ratio isn't where it should be, it could be an issue, just like decreasing it too much could be an issue as well.....homeostatic mechanisms are pretty delicate things
    Dirk Tanis, BA, MSci
    Chief Operating Officer, Applied Nutriceuticals
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  3. Some choice quotes:

    " Patients in the lowest PRL quartile showed a higher risk of metabolic syndrome , arteriogenic ED , and premature ejaculation."

    That's right drive that prolactin into the ground! Erectile Dysfunction, Metabolic Syndrome, Premature Ejaculation. All great things for a guy.


    J Sex Med. 2009 May;6(5):1457-66. Epub 2009 Feb 10.
    Hypoprolactinemia: a new clinical syndrome in patients with sexual dysfunction.

    Corona G, Mannucci E, Jannini EA, Lotti F, Ricca V, Monami M, Boddi V, Bandini E, Balercia G, Forti G, Maggi M.

    Andrology Unit, Department of Clinical Physiopathology, University of Florence, Florence, Italy.

    INTRODUCTION: The physiological role of prolactin (PRL) in male sexual behavior is poorly understood. Conversely, the association between PRL pathological elevation in both reproductive and sexual behavior is well defined. AIM: The aim of the present study is to assess the correlates of normal PRL (PRL < 735 mU/L or 35 ng/mL), in male subjects consulting for sexual dysfunction. METHODS: A consecutive series of 2,531 (mean age 52.0 +/- 12.9 years) subjects was investigated. Patients were interviewed using the structured interview on erectile dysfunction (SIEDY), a 13-item tool for the assessment of erectile dysfunction (ED)-related morbidities. Middlesex Hospital Questionnaire was used for the evaluation of psychological symptoms. MAIN OUTCOME MEASURES: Several hormonal (testosterone, thyroid stimulation hormone, and PRL) and biochemical parameters (glycemia and lipid profile) were studied, along with penile Doppler ultrasound (PDU) and SIEDY items. RESULTS: After adjustment for confounders anxiety symptoms decreased across PRL quartiles (I: <113 mU/L or 5 ng/mL; II: 113-156 mU/L or 5.1-7 ng/mL; III: 157-229 mU/L or 7.1-11 ng/mL; IV: 229-734 mU/L or 11.1-34.9 ng/mL). Patients in the lowest PRL quartile showed a higher risk of metabolic syndrome (MetS; odds ratio [OR] = 1.74 [1.01-2.99], P < 0.05), arteriogenic ED (peak systolic velocity at PDU < 35 cm/sec; OR = 1.43 [1.01-2.03], P < 0.05), and premature ejaculation (PE; OR = 1.38 [1.02-1.85]; P < 0.05). Conversely, comparing subjects with PRL-secreting pituitary adenomas (N = 13) with matched controls, no significant difference was observed, except for a higher prevalence of hypoactive sexual desire in hyperprolactinemia. CONCLUSIONS: Our findings demonstrate that, in subjects consulting for sexual dysfunction, PRL in the lowest quartile levels are associated with MetS and arteriogenic ED, as well as with PE and anxiety symptoms. Further studies are advisable in order to confirm our preliminary results in different populations.

  4. Quote Originally Posted by LegalGear View Post
    Ok, well it's your story, you tell it... I'd take my chance with a GMP certified facility making my M1T vs. a guy in his basement making D-Bol tabs any day. Additionally, that wasn't what I heard, it was that it wasn't "real gear". I think you are really stretching here...
    M1T was a weird compound- I have worked with it some- and also used it- didn't really like working with it (really can irritate the nasal passages and eyes, even with protective garbing). As for using it- I have never had that dramatic an effect out of anything I have taken- it was too strong for me, even @ 10 mg/day
    Dirk Tanis, BA, MSci
    Chief Operating Officer, Applied Nutriceuticals

  5. Quote Originally Posted by LegalGear View Post
    Some choice quotes:

    " Patients in the lowest PRL quartile showed a higher risk of metabolic syndrome , arteriogenic ED , and premature ejaculation."

    That's right drive that prolactin into the ground! Erectile Dysfunction, Metabolic Syndrome, Premature Ejaculation. All great things for a guy.


    J Sex Med. 2009 May;6(5):1457-66. Epub 2009 Feb 10.
    Hypoprolactinemia: a new clinical syndrome in patients with sexual dysfunction.

    Corona G, Mannucci E, Jannini EA, Lotti F, Ricca V, Monami M, Boddi V, Bandini E, Balercia G, Forti G, Maggi M.

    Andrology Unit, Department of Clinical Physiopathology, University of Florence, Florence, Italy.

    INTRODUCTION: The physiological role of prolactin (PRL) in male sexual behavior is poorly understood. Conversely, the association between PRL pathological elevation in both reproductive and sexual behavior is well defined. AIM: The aim of the present study is to assess the correlates of normal PRL (PRL < 735 mU/L or 35 ng/mL), in male subjects consulting for sexual dysfunction. METHODS: A consecutive series of 2,531 (mean age 52.0 +/- 12.9 years) subjects was investigated. Patients were interviewed using the structured interview on erectile dysfunction (SIEDY), a 13-item tool for the assessment of erectile dysfunction (ED)-related morbidities. Middlesex Hospital Questionnaire was used for the evaluation of psychological symptoms. MAIN OUTCOME MEASURES: Several hormonal (testosterone, thyroid stimulation hormone, and PRL) and biochemical parameters (glycemia and lipid profile) were studied, along with penile Doppler ultrasound (PDU) and SIEDY items. RESULTS: After adjustment for confounders anxiety symptoms decreased across PRL quartiles (I: <113 mU/L or 5 ng/mL; II: 113-156 mU/L or 5.1-7 ng/mL; III: 157-229 mU/L or 7.1-11 ng/mL; IV: 229-734 mU/L or 11.1-34.9 ng/mL). Patients in the lowest PRL quartile showed a higher risk of metabolic syndrome (MetS; odds ratio [OR] = 1.74 [1.01-2.99], P < 0.05), arteriogenic ED (peak systolic velocity at PDU < 35 cm/sec; OR = 1.43 [1.01-2.03], P < 0.05), and premature ejaculation (PE; OR = 1.38 [1.02-1.85]; P < 0.05). Conversely, comparing subjects with PRL-secreting pituitary adenomas (N = 13) with matched controls, no significant difference was observed, except for a higher prevalence of hypoactive sexual desire in hyperprolactinemia. CONCLUSIONS: Our findings demonstrate that, in subjects consulting for sexual dysfunction, PRL in the lowest quartile levels are associated with MetS and arteriogenic ED, as well as with PE and anxiety symptoms. Further studies are advisable in order to confirm our preliminary results in different populations.
    This relates to what I was saying before: anyone who tends to run into issues with PRL seems to have already had some endocrine disruptive issues- in this case the patients were coming in for erectile dysfunction- and it doesn't really give the #'s for the other hormonal profiles- but I would be willing to make a bet that they were out of whack as well....
    Dirk Tanis, BA, MSci
    Chief Operating Officer, Applied Nutriceuticals

  6. Quote Originally Posted by LegalGear View Post
    Ok, well it's your story, you tell it... I'd take my chance with a GMP certified facility making my M1T vs. a guy in his basement making D-Bol tabs any day. Additionally, that wasn't what I heard, it was that it wasn't "real gear". I think you are really stretching here...
    Were you beaten up by a bodybuilder? Seriously, where did this hatred come from? You are supposed to be a professional in the athletic enhancement field, how can you know so little about something yet speak so definitively?

  7. Quote Originally Posted by LegalGear View Post
    Some choice quotes:

    " Patients in the lowest PRL quartile showed a higher risk of metabolic syndrome , arteriogenic ED , and premature ejaculation."

    That's right drive that prolactin into the ground! Erectile Dysfunction, Metabolic Syndrome, Premature Ejaculation. All great things for a guy.
    Looks like somebody still needs to learn basic concepts, like correlation does not imply causation.

  8. Quote Originally Posted by LegalGear View Post
    No one is saying that prolactin is "good" however having people reduce aspects of their hormonal cascade when there is no indication of higher than normal levels is crazy and pointless. Like anything excess prolactin isn't a positive, but reducing it just because isn't good either.
    there is not a single positive reason for a male to have prolactin at all, so what would be the negative of reducing it. it seems that bromo is popular for it's sex benefits as well as overall well being that users report. prolactin also reduces production of testosterone and dopamine, so i don't think there is a 'however'. prolactin is just plain bad for males period.
    WELL DONE IS BETTER THAN WELL SAID

  9. Quote Originally Posted by LegalGear View Post
    Prolactin has NO effect on gyno according to:

    Anastassia Amaro, MD Fellow, Endocrinology and Metabolism
    Washington University School of Medicine December 15, 2005

    Sited also in Griffin and Wilson, Williams Textbook ofEndocrinology, Tenth Edition,18:709-769, 2003
    Why don't you give a link to the PDF where you found this? http://endo.wustl.edu/conferences/PD...necomastia.pdf (slide 19)

    The basis of your argument is an appeal to authority (Dr. Amaro), who in turn appeals to another authority (Griffin and Wilson). What we need to know is what exactly it says in Williams Textbook of Endocrinology between pages 709 and 769. You need to investigate whether Dr. Amaro paraphrased correctly. Did Griffin and Wilson give primary references to support their claim? What were they and how strong are they? You've barely scratched the surface.

  10. Quote Originally Posted by LegalGear View Post
    I just posted a link by a doctor specializing in this field who said in his presentation and cited an advanced medical text saying "prolactin has no effect on gynocomastia" in his presentation on the subject.
    First, you didn't post a link. You gave a reference. Second, you misquoted him, which is you just being lazy. Don't put quote marks around a paraphrase.
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  11. Quote Originally Posted by LegalGear View Post
    Progesterone REDUCES gyno.
    According to what?
    Quote Originally Posted by LegalGear View Post
    The thing about progesterone is that things like Deca are natural progesterone agonists, meaning they bind to the PR but only have 30% of the effect of pregesterone, which means that they LESSEN the progesterone effect being a possible CAUSE for gyno.

    Progesterone reduces estrogen receptor activity and something like Deca that reduces progesterone makes estrogen stronger.
    You're obviously confused. Just because deca and tren and other progestogenic steroids have a lower affinity for the PGR than progesterone itself does not mean they lessen the effect of progesterone. They're agonists that will increase progestational activity. Testosterone has a lower affinity for the androgen receptor than trenbolone, but that doesn't mean that testosterone reduces the anabolic/androgenic effect of trenbolone. Think about it.

  12. Quote Originally Posted by LegalGear View Post
    Progesterone REDUCES gyno.
    EXCUSE ME ?
    I had some "progesterone gyno" (i.e. it involved darkening and widening of areolas) from rebound, stress-induced or hell-knows-what progesterone. Blood tests showed normal E2 and crazy progesterone numbers. ATD had no effect. Proviron slowly brought it under control.

  13. They will absolutely lessen the effect of progesterone. They are PARTIAL AGONISTS. Testosterone is NOT a partial agonist, it is a full agonist

    "Partial agonists (such as buspirone, aripiprazole, buprenorphine, or norclozapine) bind and activate a given receptor, but have only partial efficacy at the receptor relative to a full agonist. They may also be considered ligands which display both agonistic and antagonistic effects - when both a full agonist and partial agonist are present, the partial agonist actually acts as a competitive antagonist, competing with the full agonist for receptor occupancy and producing a net decrease in the receptor activation observed with the full agonist alone. Clinically partial agonists can activate receptors to give a desired submaximal response when inadequate amounts of the endogenous ligand are present, or they can reduce the overstimulation of receptors when excess amounts of the endogenous ligand are present."

    Your test/deca/tren analogy makes absolutely no sense considering that both Deca and Tren are higher affinity steroids. So, test is a 100, deca 120 and tren a 400 any of these will work as an agonist. Deca has a lower activity level than progesterone so, with it binding it displaces progesterone therefore it will be a partial agonist. You'd have to take far higher doses to get the same activity level. Since testosterone is at 100% activity, it's not really a comparison with something with 30% activity. Think about it.

    By the way, I didn't paraphrase, I took the QUOTE right from his presentation. I stand by my point that reducing hormone levels in healthy men below normal levels isn't a good idea. That was my point...

    There is a ton that we don't know. However, I doubt messing with every hormone in your body at once is a good idea. The point is that for normal people to try and drop their prolactin levels is potentially harmful. If you have higher than normal, by all means...however, I keep reading these threads where guys are worried about reducing prolactin when there is no indication that they have high levels. By the way, my wife has hyper prolactemia and at the risk of TMI, she has no lactation, but somehow 100's of BRO's have this issue...

    Clin Pharmacol Ther. 1995 Sep;58(3):354-9.
    Restoration of normal sperm characteristics in hypoprolactinemic infertile men treated with metoclopramide and exogenous human prolactin.

    Ufearo CS, Orisakwe OE.

    Department of Physiology, Faculty of Medicine, Nnamdi Azikiwe University, Nigeria.

    We investigated the effects of induced increase in prolactin levels on spermatogenesis in 20 infertile men with hypoprolactinemia using exogenous human prolactin (hPRL) and metoclopramide. The subjects were selected from a population of 175 infertile men in whom the prevalence of hypoprolactinemia was 33.14%. Mean basal plasma prolactin was 2.79 +/- 0.62 ng.ml-1 in the infertile men and 9.57 +/- 2.14 ng.ml-1 in the normal control subjects. At the sixteenth week, mean plasma prolactin was 9.41 +/- 1.3 ng.ml-1 in subjects treated with exogenous hPRL and 5.2 +/- 0.7 ng.ml-1 in subjects treated with metoclopramide. Mean basal sperm concentration was approximately 8.8 million per milliliter in the infertile men and 41.5 million per milliliter in the normal control subjects. Mean sperm concentration was approximately 37 million per milliliter in subjects treated with exogenous hPRL, whereas the peak mean value was 23 million per milliliter in subjects treated with metoclopramide for 16 weeks. At basal conditions, the mean percentages of abnormal sperm were 66.75% +/- 14.93% and 21.36% +/- 4.78% in infertile and normal subjects, respectively. In subjects treated with exogenous hPRL and metoclopramide, the mean percentage of abnormal sperm were 24.7% and 31%, respectively, at week 16. Mean plasma prolactin, mean sperm concentration and the mean percentage of abnormal sperm were 3.3 +/- 1.4 ng.ml-1, 7 million per milliliter, and 60.5, respectively, in the infertile subjects after drug withdrawal at week 14. In normal control subjects, there was no significant difference (p = 0.01) in the plecebo effect. We therefore conclude that the low prolactin levels in this group of infertile men may be one of the primary causes of their infertility.

    J Androl. 1985 Jan-Feb;6(1):10-4.
    Induced hypoprolactinemia and testicular steroidogenesis in man.

    Suescun MO, Scorticati C, Chiauzzi VA, Chemes HE, Rivarola MA, Calandra RS.

    The effects of short-term hypoprolactinemia on the pituitary-gonadal axis were evaluated in a group of patients with untreated prostatic carcinoma. Each patient was studied prior to and during 7-day oral administrations of bromocriptine (2.5 mg q.i.d.). Serum LH, prolactin (PRL), androst-4-ene-3,17 dione (androstenedione), testosterone, and 5 alpha-androstane-3 alpha, 17 beta-diol (5 alpha-Diol) levels, as well as intra-testicular testosterone, dihydrotestosterone (DHT), 5 alpha-Diol and zinc (Zn) concentrations, were determined. Daily administration of bromocriptine caused a marked suppression of serum PRL (mean +/- SEM, 23.8 +/- 2.5 vs. 6.4 +/- 1.0 ng/ml) without concomitant changes in serum LH levels (mean +/- SEM, 8.3 +/- 1.6 vs. 8.9 +/- 2.1 ng/ml). Hypoprolactinemia induced a significant decrease (P less than 0.05) in the mean peripheral testosterone levels; but 5 alpha-Diol and androstenedione remained unchanged. However, in testicular tissues, bromocriptine treatment resulted in significant increases in mean concentrations of total androgens (P less than 0.001), testosterone (P less than 0.001) and DHT (P less than 0.02). Testicular levels of 5 alpha-Diol were not significantly altered. There was no change in Zn levels in basal conditions and during bromocriptine administration. These results indicate that short-term suppression of serum PRL levels in man affects basal testicular function without altering serum LH. However, a direct action of bromocriptine on the human gonad cannot be excluded.

    Andrologia. 1985 Mar-Apr;17(2):172-7.
    Bromocriptine, a dopamine agonist, directly inhibits testosterone production by rat Leydig cells.

    Chambon M, Grizard G, Boucher D.

    We investigated the direct effects of bromocriptine (BR) on both basal and hCG-stimulated testosterone production by rat collagenase-dispersed Leydig cells. In a final volume of 2.2 ml, 2.10(6) Leydig cells were incubated at 33 degrees C for 3 h either alone or with various amounts of hCG (1. 10. 10(2). 10(3). 10(4) mUI/vial) and BR (1.5 10(-9), 1.5 10(-7), 1.5 10(-5) M); BR was dissolved in 20 microliters of ethanol. BR (1.5 10(-5) M) decreased significantly both basal and hCG-stimulated testosterone production whereas at lower doses, BR had no effect. These results suggest that the dopamine itself may regulate rat Leydig cell function and that there is room for criticism of BR-induced hypoprolactinemia as an experimental model to study the effect of prolactin on the androgenic function.

    Fertil Steril. 1991 Feb;55(2):355-7.
    Effects of chronic bromocriptine-induced hypoprolactinemia on plasma testosterone responses to human chorionic gonadotropin stimulation in normal men.

    Oseko F, Nakano A, Morikawa K, Endo J, Taniguchi A, Usui T.

    Department of Medicine, Shimane Medical University, Japan.

    To study the role played by normal levels of plasma prolactin (PRL) in the secretion of testosterone (T) in the testes, we induced hypoprolactinemia with a daily dose of 5 mg bromocriptine administered orally in five normal men 20 to 35 years of age for 8 weeks. The basal PRL, T, luteinizing hormone, follicle-stimulating hormone, and maximum responses of plasma T to human chorionic gonadotropin (hCG) stimulation were measured every 2 weeks. Basal levels of plasma T were reduced in the 1st 2-week-long period of hypoprolactinemia. In the 4-week-long period of hypoprolactinemia, the maximal response of plasma T to hCG stimulation was significantly reduced. The findings suggest that normal levels of plasma PRL may play an important role in the secretion of T in the human testes in vivo.

  14. Quote Originally Posted by Conciliator View Post
    First, you didn't post a link. You gave a reference. Second, you misquoted him, which is you just being lazy. Don't put quote marks around a paraphrase.
    How is the exact word a paraphrase? Please tell me how I paraphrased slide 19 which says the exact words I quoted... why do I even bother.

    Yeah, have at it. Lower that prolactin down to the floor and while you're at it take progesterone down with it too. Have fun...

  15. Quote Originally Posted by chemistclear View Post
    I've seen some great dialog in this thread. Here are a few quotes to chew on.
    Great quotes and dialogue- and there are a ton of inter-relations among Pregnenolone, Progesterone, testosterone, estrogen, and all of their subsequently reduced forms. Mess with one, you mess with all of them, at least somewhat.....

    Throw in some of the crazy stacks that I (and I am sure all of you) have seen nowadays, and the resulting hormonal alterations/permutations can be staggering, and there is really no way to accurately account for all of the different variables. In a lot of cases, this forces us to rely, at least somewhat, on anecdotal evidence. Personally, I don't see an IRB ever approving a study where nandrolone is stacked with methandienone, yet we know "it works", at least for physique-enhancement purposes.....
    Dirk Tanis, BA, MSci
    Chief Operating Officer, Applied Nutriceuticals

  16. Quote Originally Posted by LegalGear View Post
    Yeah, have at it. Lower that prolactin down to the floor and while you're at it take progesterone down with it too. Have fun...
    Dude, calm down and quit being so defensive. You read something you took as gospel and came here playing cowboy talking down to the collective. If you cannot take criticism about things, then don't post.
    The Historic PES Legend

  17. I am prone to gyno, and I seem to get two TYPES of gyno

    1) estrogen gyno - while on testosterone I get estrogen induced gyno; this is a slow process where both my nips will get sensitive and I can feel the lump of gyno tissue under them (usually "dormant") activating, becoming puffier, and painful when pressure is applied

    Taking an AI will reduce the estrogen gyno immediately, a small amount of letro is sufficient to reduce the sensitivity and puffiness to nothing

    2) "Progestin gyno" - I have gotten this from two PH's Max LMG and the 19-nor "tren." In the first case i was running it standalone, in the second case it was stacked with testosterone.
    In both cases, gyno appeared in the first week of use of that steroid, AND WAS LOCALIZED TO ONE NIPPLE. In the first case it targetted my left nipple, and in the second case my right nipple was targetted. The other nip would be very mildly sensitive, but the targetted nip would be extremely sore, VERY puffy, with a noticable lump underneath that was... Well, trying to grow i suppose.

    Both these compounds are known as "progestins" and kill sex drive so prolactin is almost assuredly being elevated.

    In both these cases, taking letrozole did not stop the gyno, even in high doses (up to 2.5mg/day) the letrozole would only reduce sensitivity and swelling marginally, however the gyno was still visually apparent.


    So i think there is clearly some interaction going on with steroids that are known to increase prolactin.
    Mostly answered PM's
    Don't post on my profile, I don't read that stuff, PM me instead
    <------ Hard to believe, but I wasn't on any anabolics in the avatar shot

  18. Quote Originally Posted by UnrealMachine View Post
    I am prone to gyno, and I seem to get two TYPES of gyno

    1) estrogen gyno - while on testosterone I get estrogen induced gyno; this is a slow process where both my nips will get sensitive and I can feel the lump of gyno tissue under them (usually "dormant") activating, becoming puffier, and painful when pressure is applied

    Taking an AI will reduce the estrogen gyno immediately, a small amount of letro is sufficient to reduce the sensitivity and puffiness to nothing

    2) "Progestin gyno" - I have gotten this from two PH's Max LMG and the 19-nor "tren." In the first case i was running it standalone, in the second case it was stacked with testosterone.
    In both cases, gyno appeared in the first week of use of that steroid, AND WAS LOCALIZED TO ONE NIPPLE. In the first case it targetted my left nipple, and in the second case my right nipple was targetted. The other nip would be very mildly sensitive, but the targetted nip would be extremely sore, VERY puffy, with a noticable lump underneath that was... Well, trying to grow i suppose.

    Both these compounds are known as "progestins" and kill sex drive so prolactin is almost assuredly being elevated.

    In both these cases, taking letrozole did not stop the gyno, even in high doses (up to 2.5mg/day) the letrozole would only reduce sensitivity and swelling marginally, however the gyno was still visually apparent.


    So i think there is clearly some interaction going on with steroids that are known to increase prolactin.
    How did you stop or got rid of the gyno ?

  19. Quote Originally Posted by Problem View Post
    How did you stop or got rid of the gyno ?
    Had to stop taking the PH in question and then it took about 2 weeks to go away
    Mostly answered PM's
    Don't post on my profile, I don't read that stuff, PM me instead
    <------ Hard to believe, but I wasn't on any anabolics in the avatar shot

  20. Quote Originally Posted by LegalGear View Post

    Anecdotal information is the worst kind because juice heads are morons and the people making juice are even worse. You really think an underground lab that is a little low on a compound won't just throw in whatever they have laying around to get a run out?
    That statement can be considered odd and somewhat ironic bro. Just saying....
    ---The internet is the father of the electronic lynch-mob---

  21. Quote Originally Posted by LegalGear View Post
    They will absolutely lessen the effect of progesterone. They are PARTIAL AGONISTS. Testosterone is NOT a partial agonist, it is a full agonist
    It's easy to make the unsupported claim that nandrolone and trenbolone are partial agonists. I disagree. I'm also able to back up the alternative position with very recent research:

    This recent study (from March of this year) tested the transactivational activity of nandrolone in the human progesterone receptor. See figure 2, where it clearly shows that 19-norTestosterone produced a 100% (full agonist) response, right on par with progesterone itself, at a concentration of 10-6 M.

    In corroboration with that, this study from 2006 examined the "Stimulation of progestational transcriptional activity" in a different cell line. It found that 19-nortestosterone (19-NT) "increased transcriptional activity to the same extent as the progestin standard, R5020, at 108 M." R5020 is an extremely potent full agonist. The conclusion states that "as we have shown here, 19-norandrogens exhibit considerable progestational activity both in vitro and in vivo."

    Finally, in this study from 2004, they performed a human progesterone receptor bioassy. Tren was compared to a progesterone standard. As you can see in figure 2, tren produced a 100% (full agonist) response.

    You don't get a full response from partial agonists, do you?

  22. Quote Originally Posted by LegalGear View Post
    Your test/deca/tren analogy makes absolutely no sense considering that both Deca and Tren are higher affinity steroids. So, test is a 100, deca 120 and tren a 400 any of these will work as an agonist. Deca has a lower activity level than progesterone so, with it binding it displaces progesterone therefore it will be a partial agonist. You'd have to take far higher doses to get the same activity level. Since testosterone is at 100% activity, it's not really a comparison with something with 30% activity. Think about it.
    Wow. You're really confused if you think that binding affinity and receptor activation are the same thing, LOL. They're two separate concepts. One is how strong of an attraction a ligand has for the receptor. The other is how much activity occurs once that binding takes place. If something has an RBA (relative binding affinity) of 30%, it only tells you that you need about three times the ligand to saturate the receptor compared to something else. RBA's are relative. Depending on the standard you choose to use, the exact same substance can have an RBA of 1% or 1000%. If we use tren as a standard for AR affinity (at 100), test would have an RBA of 25%. That doesn't make test a partial agonist. The absolute affinity is always the same, and it has nothing to do with activity.

    Once the receptor is saturated, what happens (activity) is something else entirely. You could have a maximal response (full agonist), no response (full antagonist), or somewhere in between (mixed response). Going off your logic (where they're the same thing), receptor antagonists must have an RBA of 0%, since they have 0 activity. But if they had an RBA of 0, that would mean they have 0 affinity for the receptor, so they wouldn't even be ligands and wouldn't even bind to the receptor where they could do any blocking. Think about it.

    You need to learn some of the basics before getting into arguments like this.

  23. Quote Originally Posted by LegalGear View Post
    By the way, I didn't paraphrase, I took the QUOTE right from his presentation.
    From slide 19: "Prolactin has no role in Gynecomastia".
    What you said: "prolactin has no effect on gynocomastia".

    Those are not the same thing, are they? So you didn't quote him. You took what he said and put it into your own words. That's called a paraphrase. You don't put quote marks around a paraphrase and attribute it to someone else, even when it's materially equivalent. That's just lazy and rude.

  24. Quote Originally Posted by thebigt View Post
    there is not a single positive reason for a male to have prolactin at all, so what would be the negative of reducing it.
    No. For one, prolactin is involved in immune function. Prolactin receptors are expressed in immune cells and lymphocytes are known to synthesize and secrete prolactin.

  25. Sorry, I mistyped it. Big deal, that is splitting hairs dude.

  26. Quote Originally Posted by LegalGear View Post
    Sorry, I mistyped it. Big deal, that is splitting hairs dude.
    That is what these debates are all about, splitting hairs and developing the facts. You posted your fact, then your fact was turned against you.
    The Historic PES Legend

  27. I posted a fact that used effectively the same language. How was that turned against me? This is why I find these discussions to be pointless and I rarely invest in them (which is why you won't see me spending nearly the time I should). I think we can say with safety that "No effect" and "No role" are pretty much the same thing. So, please explain how was that "turned against me"...waiting with the utmost patience.

    Also, I know Tren is a full agonist and I explained how Tren might be causing issues above and you don't typically see similarities in Tren and Deca. The graph for nandrolone shows a transactivation response for nortest similar to progesterone buy only at 10-6 molar which is likely not going to be achieved in the body. So, even though the data does not show deca to technically be a partial agonist, at relavent concentrations it will act like one even from your graph. Look at the response, showing it doesn't achieve full activity until high concentrations. Additionally from your graph sited in your second paper shows the RBA to be between 8% and 9% for Deca unless I am missing something.

    Finally the bro-logic to blame the progestational activity of Deca for "Deca **** and gyno" is in my opinion an error this then gets extrapolated to Tren and other androgens.

    Also, since you have time to look through the literature Big C. Find me a reference showing Anadrol to have progestational activity. I've never looked but I seriously doubt it is in there. Still, I'd love to see it since this is the common "bro-logic".

    So whether the issue is from poor transcription or low binding affinity seems like the effect would be the same wouldn't it? The point of the thread again is to challenge popular BROLOGIC which has not proven itself to be at all conclusive. No matter that thousands of guys are running around extolling the problems with M1T's progestational activity when there is absolutely nothing structurally that would lead us to believe that it is progestational and doubtfully anything in the literature showing that...

    You look through the literature and cherry pick to support your opinion yet don't provide any counter to proof. Just like in the AR receptor discussion you completely avoid obvious information and refuse to comment on it. This is why it is pointless you refuse to learn anything. The saddest part is that the answer from Pat Arnold is truthful most cases "we don't know" so to run around saying "prolactin causes gyno" as gospel or "progestins cause gyno" as gospel is stupid. I put up these strong statements not because I know everything, just to balance out the absolute stupid belief that someone educated or uneducated on these boards have a freaking clue what is going on and "knows everything".

    No offense Unreal Machine, but honestly do you really have any idea what caused your symptoms? You just work on the assumptions given to you when in fact you really might not have a clue why you have gyno? Also this statement

    "Both these compounds are known as "progestins" and kill sex drive so prolactin is almost assuredly being elevated.

    In both these cases, taking letrozole did not stop the gyno, even in high doses (up to 2.5mg/day) the letrozole would only reduce sensitivity and swelling marginally, however the gyno was still visually apparent.


    So i think there is clearly some interaction going on with steroids that are known to increase prolactin."

    You move from steroids having progestational activity to steroids "KNOWN to increase prolactin". Those kind of statements are what I get upset about. It's rampant. Younger kids read that and then repeat it, giving us the popular "brologic" of today. I'd love to be wrong, but show me papers or anything that show Max LMG and Dienedione to increase prolactin (or even similar androgens, that is fine) thus proving that your gyno is prolactin induced.

  28. LG,

    Explain male lactation on tren then (or even just in general). If prolactin has no effect how can men get gyno while lactating?

  29. Quote Originally Posted by LegalGear View Post
    I posted a fact that used effectively the same language. How was that turned against me? This is why I find these discussions to be pointless and I rarely invest in them (which is why you won't see me spending nearly the time I should). I think we can say with safety that "No effect" and "No role" are pretty much the same thing. So, please explain how was that "turned against me"...waiting with the utmost patience.

    Also, I know Tren is a full agonist and I explained how Tren might be causing issues above and you don't typically see similarities in Tren and Deca. The graph for nandrolone shows a transactivation response for nortest similar to progesterone buy only at 10-6 molar which is likely not going to be achieved in the body. So, even though the data does not show deca to technically be a partial agonist, at relavent concentrations it will act like one even from your graph. Look at the response, showing it doesn't achieve full activity until high concentrations. Additionally from your graph sited in your second paper shows the RBA to be between 8% and 9% for Deca unless I am missing something.

    Finally the bro-logic to blame the progestational activity of Deca for "Deca **** and gyno" is in my opinion an error this then gets extrapolated to Tren and other androgens.

    Also, since you have time to look through the literature Big C. Find me a reference showing Anadrol to have progestational activity. I've never looked but I seriously doubt it is in there. Still, I'd love to see it since this is the common "bro-logic".

    So whether the issue is from poor transcription or low binding affinity seems like the effect would be the same wouldn't it? The point of the thread again is to challenge popular BROLOGIC which has not proven itself to be at all conclusive. No matter that thousands of guys are running around extolling the problems with M1T's progestational activity when there is absolutely nothing structurally that would lead us to believe that it is progestational and doubtfully anything in the literature showing that...

    You look through the literature and cherry pick to support your opinion yet don't provide any counter to proof. Just like in the AR receptor discussion you completely avoid obvious information and refuse to comment on it. This is why it is pointless you refuse to learn anything. The saddest part is that the answer from Pat Arnold is truthful most cases "we don't know" so to run around saying "prolactin causes gyno" as gospel or "progestins cause gyno" as gospel is stupid. I put up these strong statements not because I know everything, just to balance out the absolute stupid belief that someone educated or uneducated on these boards have a freaking clue what is going on and "knows everything".

    No offense Unreal Machine, but honestly do you really have any idea what caused your symptoms? You just work on the assumptions given to you when in fact you really might not have a clue why you have gyno? Also this statement

    "Both these compounds are known as "progestins" and kill sex drive so prolactin is almost assuredly being elevated.

    In both these cases, taking letrozole did not stop the gyno, even in high doses (up to 2.5mg/day) the letrozole would only reduce sensitivity and swelling marginally, however the gyno was still visually apparent.


    So i think there is clearly some interaction going on with steroids that are known to increase prolactin."

    You move from steroids having progestational activity to steroids "KNOWN to increase prolactin". Those kind of statements are what I get upset about. It's rampant. Younger kids read that and then repeat it, giving us the popular "brologic" of today. I'd love to be wrong, but show me papers or anything that show Max LMG and Dienedione to increase prolactin (or even similar androgens, that is fine) thus proving that your gyno is prolactin induced.
    If you don't invest in discussion like this ... then why bring it up? Being the starter of this thread, you have the burden of proof on you. C brought information that is pertinent to this thread, and you bring nothing but what you believe to be fact. You keep asking others to prove themselves, yet you have nothing backing you up. Your constant talking down to others because apparently they have the "Time" to research such things is asinine and consequently incongruous with your time here at AM. You are trying to cover up brologic with your own brologic.
    The Historic PES Legend
  

  
 

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