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

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  1. 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?


  2. 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.
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  3. 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.

  4. 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.

  5. Sorry, I mistyped it. Big deal, that is splitting hairs dude.
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  6. 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

  7. 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.

  8. LG,

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

  9. 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

  10. Quote Originally Posted by hardknock View Post
    That statement can be considered odd and somewhat ironic bro. Just saying....
    Wow... i didnt read this part. Funny to attack anecdotal evidence when that is all your company is running on LG.
    The Historic PES Legend

  11. Quote Originally Posted by LegalGear View Post
    why then do you have people running around worried all day about their prolactin levels? It's your typical scare tactics.
    OmG!

    PROLACTIN TERRORISTS !!!11!!11!

  12. Quote Originally Posted by DAdams91982 View Post
    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.
    Brought nothing? Whatever, you are obviously not reading anything. Additionally my post is on prolactin, morphing into a discussin about Progestins is interesting but I don't have a ton of time for it. I posted studies showing the potential downside of lowering prolactin. THAT IS THE THREAD! Not progestins...

  13. Brought Nothing

    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.

  14. Quote Originally Posted by LegalGear View Post
    Brought nothing? Whatever, you are obviously not reading anything. Additionally my post is on prolactin, morphing into a discussin about Progestins is interesting but I don't have a ton of time for it. I posted studies showing the potential downside of lowering prolactin. THAT IS THE THREAD! Not progestins...
    I mentioned progestine, and you went off on your little tantrum trying to debunk me. So, maybe it is you that should reread the thread there big guy. Your preteen mentality is very tiresome.
    The Historic PES Legend

  15. Quote Originally Posted by DAdams91982 View Post
    I mentioned progestine, and you went off on your little tantrum trying to debunk me. So, maybe it is you that should reread the thread there big guy. Your preteen mentality is very tiresome.
    You've been a prolactin terrorist this entire thread!!!

  16. You clearly can't read...and obviously neither can Concilliator or whatever his name is...

    He purposefully misuses the literature as usual. I've refuted everything he's said and yet crickets chirp...

    The paper sited shows an affinity for the PR of 8-9% and we are splitting hairs on symantics, the net effect is the same. Additionally, the graph shows specifically that at lower concentrations the net effect of Deca is to NOT be as potent a progestin.

    So, in a nutshell, Deca with a 8-9% affinity and a lower activity level up until high concentrations are reached is a full agonist (your two papers by the way) in your eyes. The net effect is going to be a partial agonist like I was saying in the first place.

    Yes, this is BRINGING NOTHING. I always wonder why the world exists in the way it does, all I need to do is get back on these threads... Reading the papers, responding, showing how the data is being misinterpreted, yes, this is nothing...

  17. I get on showing a presentation and reference from a Doctor that says Prolactin has NO ROLE in gyno. So, it's not MY theory, it's the theory of a Doctor. Where did the other "theory" come from? A bunch of dudes that think progestins and prolactins are interchangable because they both start with P. When you take the counter point to the good Dr. you then take the burden of proving your argument.


    Progesterone is the second or third (I believe the second) highest hormone in the MALE body after testosterone, so it seems pretty likely that it isn't the "progestational" effects.

  18. Quote Originally Posted by LegalGear View Post
    I get on showing a presentation and reference from a Doctor that says Prolactin has NO ROLE in gyno. So, it's not MY theory, it's the theory of a Doctor. Where did the other "theory" come from? A bunch of dudes that think progestins and prolactins are interchangable because they both start with P. When you take the counter point to the good Dr. you then take the burden of proving your argument.


    Progesterone is the second or third (I believe the second) highest hormone in the MALE body after testosterone, so it seems pretty likely that it isn't the "progestational" effects.
    Man... LG... your are better than the sundays paper comic section. Your demeaning nature toward your own consumer base is fascinating. Places you right where LG belongs.
    The Historic PES Legend

  19. Quote Originally Posted by justreading View Post
    LG,

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

    You want the explanation?

    Fine, as I've said numerous times. "heresay" isn't proof. Two things could be going on. All nipple tissue will produce fluid if squeezed, there are sweat and oil ducts that have fluid. Try it now, go squeeze your nipples for 2-3 minutes and see the fluid come out. How did I find this out, I got a panic stricken call from my sales rep saying that M1P caused a guy to leak. He was also on M1P and after squeezing his nips for a minute or two some fluid came out. So, then I for science sake squeezed mine (I was not taking M1P) and guess what? Yep, fluid.

    Breast tissue in general is very sensitive. If you keep touching it and playing with it, they tend to get very irritated and sore. So, of course human nature is to keep playing with it to "check". This accounts for 99% of the pain, swelling that people feel.

    Finally, I reread the posts and Concilliator said that Tren and Deca are not as strong progestins as Progesterone, then sites a study showing Tren to be as potent. This will be lost on the masses.

    The point is to challenge the Dr. and the medical text book...great argument. I am officially done with this thread, it's clearly pointless.

  20. Quote Originally Posted by DAdams91982 View Post
    Man... LG... your are better than the sundays paper comic section. Your demeaning nature toward your own consumer base is fascinating. Places you right where LG belongs.
    I wasn't specifically talking to you anyway. You're points about it being ESTROGEN are 99% on point. However, still when you make statements like "brought nothing" it gets me irritated.

  21. Quote Originally Posted by LegalGear View Post
    You want the explanation?

    Fine, as I've said numerous times. "heresay" isn't proof. Two things could be going on. All nipple tissue will produce fluid if squeezed, there are sweat and oil ducts that have fluid. Try it now, go squeeze your nipples for 2-3 minutes and see the fluid come out. How did I find this out, I got a panic stricken call from my sales rep saying that M1P caused a guy to leak. He was also on M1P and after squeezing his nips for a minute or two some fluid came out. So, then I for science sake squeezed mine (I was not taking M1P) and guess what? Yep, fluid.

    Breast tissue in general is very sensitive. If you keep touching it and playing with it, they tend to get very irritated and sore. So, of course human nature is to keep playing with it to "check". This accounts for 99% of the pain, swelling that people feel.

    Finally, I reread the posts and Concilliator said that Tren and Deca are not as strong progestins as Progesterone, then sites a study showing Tren to be as potent. This will be lost on the masses.

    The point is to challenge the Dr. and the medical text book...great argument. I am officially done with this thread, it's clearly pointless.
    Yes if poked enough! But what about swollen nipples with instant lactation with light preasure from people with no history of overactive sweat glands?

    I know from personal experience that prolactin causes gyno in me, I don't want to go into full detail but some Rec drugs lower dopamine and cause an increase in prolactin and they definitely cause gyno.

  22. Not sure about recreation drugs, so again anything is possible when you mess with your endocrine system and mix compounds. Also, it's not overactive sweat glands, it's normal oil ans sweat.

    DAdams, since I might have been kind of a ****, let me send you some free products. I try to make amends when I am overly harsh. PM me your address and what you want to try...

  23. One thing I will say first. You can find one or two studies to backup basically anything you want to say. But if you have any experience in and have been around people who have you will know a few things to be true.

    There are some who are sensitive to progesterone's and some who aren't. I myself, and many others that I know - and I would go as far as to say the majority get gyno while on things like Tren and Deca. That isn't ridiculous to say or some groundbreaking news - it's well known, and has been among people who don't sit behind a keyboard arguing on forums. Rather, the ones who are actually using these compounds and lifting weights to boot. I can also say that running dostinex while on either of these completely prevents it, and again that's not just me - a very widely known fact.

    One thing I do know is that heavy doses of B6, Dostinex(Caber), p-5-p, dopamine (I think?), and a couple others all lower prolactin and all have been shown to help with things like Tren/Deca/etc...

    So bring all your studies, everything else you need to make you feel better and I will find a couple bunk ones myself to "prove" the antithesis. Just goes to show you all these "scientists and doctors" really for the most part don't know wtf they are doing and have never actually got out there and tried anything for themselves. Its like a politician telling you what the war is like over in Afghanistan/Iraq, then the ACTUAL soldiers come back and are like wtf?...no - same concept.

  24. Hey LG,

    You bug-eyed, side-steppin' sand crab, you...

    Let's have a go at it, I want some of those free samples, too.
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