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

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

Invalid Link Removed (from March of this year) tested the transactivational activity of nandrolone in the human progesterone receptor. See Invalid Link Removed, 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, Invalid Link Removed 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 10–8 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 Invalid Link Removed from 2004, they performed a human progesterone receptor bioassy. Tren was compared to a progesterone standard. As you can see in Invalid Link Removed, tren produced a 100% (full agonist) response.

You don't get a full response from partial agonists, do you?
 
LegalGear said:
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.
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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.
 
LegalGear said:
By the way, I didn't paraphrase, I took the QUOTE right from his presentation.
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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.
 
thebigt said:
there is not a single positive reason for a male to have prolactin at all, so what would be the negative of reducing it.
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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.
 
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.
 
LG,

Explain male lactation on tren then (or even just in general). If prolactin has no effect how can men get gyno while lactating?
 
LegalGear said:
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.
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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.
 
DAdams91982 said:
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.
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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...
 
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.
 
LegalGear said:
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...
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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 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...
 
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.
 
LegalGear said:
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.
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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.
 
justreading said:
LG,

Explain male lactation on tren then (or even just in general). If prolactin has no effect how can men get gyno while lactating?
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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.
 
DAdams91982 said:
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.
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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.
 
LegalGear said:
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.
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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.
 
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...
 
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.
 
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. :twak:
 
bLacKjAck. said:
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.
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I'd agree with that statement, but I will tell you, that I've tried Progesterone cream when I had estrogen issues and it worked like a champ. I've had other people try it and it also worked. I agree that studies are a small part, however I will also say that people throw these things around too without anything to back it up, which is what irritates me.
 
LegalGear said:
I think we can say with safety that "No effect" and "No role" are pretty much the same thing.
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I think we can also say with safety that you were retarded to say "By the way, I didn't paraphrase, I took the QUOTE right from his presentation."
LegalGear said:
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.
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LegalGear, you seriously need to learn the difference between affinity and activation. You're still mixing them up.

Just because something is at a concentration that does not produce full activity does not make it a partial agonist. Those are two different things. Test is a full agonist of the AR. If you're taking 200mg/wk and getting less than full activity, it doesn't change the fact that test is still a full agonist, does it? Rather, something is a full agonist if it is capable of producing maximal activity when the receptor is saturated with the ligand, at whatever concentration that might be. All the data I provided shows that deca is a full agonist. Accordingly, it will NOT be blocking or reducing the effect of endogenous progesterone. It will only be adding to the overall progestational activity, which directly contradicts your unsupported argument earlier in this thread. The data shows that deca and tran have the same activity as progesterone, producing a 100% response. It just takes a higher concentration to saturate the receptor, since as ligands they have lower affinity.
 
LegalGear said:
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.
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Probably not. The other study, in a different cell line, however, found a maximal response from nandrolone at 10–8 M. Invalid Link Removed found that even a single, 100mg shot of deca produced plasma levels that high (>10 nM).

What we know is that there's definitely progestational activity from deca. The question is how much. We can only guess what happens in vivo, in cells that matter in human males.
LegalGear said:
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".
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Sorry. You should start to do your own research.
 
LegalGear said:
You look through the literature and cherry pick to support your opinion yet don't provide any counter to proof.
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I didn't cherry pick anything. Those are the only studies I could find that even addressed the question of whether nandrolone is a full or partial agonist. Don't use red herrings to change the topic to how I'm not providing evidence for your position. Do yourself a favor and post the counter evidence if you want to imply that it's out there and that I'm ignoring it. Retarded.
LegalGear said:
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.
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Really? What obvious information did I avoid? People can go read the thread themselves: Invalid Link Removed

I actively posted and debated in that thread for pages and pages. Of course, you didn't like that thread because it exposed your marketing claims for what they clearly were, bull****.
 
LegalGear said:
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...
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Apparently, it's "misusing" the literature to post several studies that contradict LG's position, LOL. You refuted nothing because you posted no counter evidence. Crickets are not chirping... I'm posting. You haven't posted a shred of support for your claim that deca is a partial agonist. However, you have demonstrated that it's a concept that you don't understand.
LegalGear said:
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.
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Yes, that study found nandrolone to have a relative affinity of 8-9%. That's relative to progesterone. If we used tren as the standard, deca could have a relative affinity of 100%. The percentage tells you nothing about activation potential. What the data shows is that nandrolone and tren are full agonists, capable of producing maximal transactivation. My point with all the references is that you are incorrect to state that "They [deca/tren] will absolutely lessen the effect of progesterone. They are PARTIAL AGONISTS." Everything I've posted contradicts that. You've posted nothing to support it.

Not to mention that there are other references for nandrolone, showing that it may have a 20-30% RBA compared to progesterone. At 10%, it means that if you have 10x more nandrolone in your body than natural progesterone (which would be easy with the doses guys are injecting), you would double the progestogenic action in the body. If nandrolone has 30% the affinity of progesterone, that same dose would quadruple the progestogenic effects in the body. That could easily have physiological significance.
 
As stated numerous times, increased AR's in immature cells would make logical sense since they are turning into androgen dependent cells.


There are conflicting papers on this subject and your paper doesn't even site the activity of Deca, it says "similar" results.

Fertil Steril. 1979 May;31(5):552-61.
Competitive progesterone antagonists: receptor binding and biologic activity of testosterone and 19-nortestosterone derivatives.

Reel JR, Humphrey RR, Shih YH, Windsor BL, Sakowski R, Creger PL, Edgren RA.

Testosterone and 19-nortestosterone derivatives were evaluated in a developmental scheme designed to identify competitive progesterone antagonists having abortifacient activity. Compounds that displayed significant binding to the rabbit uterine progesterone receptor were followed in biologic tests for progestational, antiprogestational, and abortifacient activities. Of the seven compounds tested for both progestational and antiprogestational activity, only one, 5 alpha-dihydronorethindrone, behaved exclusively as an antagonist. Five other 19-nortestosterones (19-nortestosterone, 17 beta-hydroxyestra-4, 9(10)-dien-3-one, norethindrone, norethindrone acetate, and R 2323) proved to be mixed agonists/antagonists. 5 alpha-Dihydronorethindrone, norethindrone, and 19-nortestosterone terminated pregnancy during the postnidatory period in rats; in addition, the latter two compounds inhibited progesterone-supported pregnancy in spayed rats and curtailed pregnancy during the postnidatory period in hamsters. These results demonstrate that several 19-nortestosterone derivatives bind to the uterine progesterone receptor and behave either as antagonists or mixed agonists/antagonists.

At some point it would seem that any concentration androgens can stimulate the PR, as shown in this article so, showing activity at a high concentration isn't reserved to deca.

Methods Find Exp Clin Pharmacol. 1997 May;19(4):215-22.
Estrogenic and progestagenic activities of physiologic and synthetic androgens, as measured by in vitro bioassays.

Markiewicz L, Gurpide E.

Mount Sinai School of Medicine (CUNY), Department of Obstetrics, Gynecology and Reproductive Science, NY, USA.

Estrogenic activities of testosterone (T) and 5a-dihydrotestosterone (DHT) were detected and measured by using their specific stimulatory effects on alkaline phosphatase (AP) activity in human endometrial adenocarcinoma cells of the Ishikawa Var-1 line. These two physiologic androgens were able to induce, at microM concentrations, estrogenic effect believed to be mediated by the estrogen receptor (ER) since the antiestrogens ICI-164384 and 4-hydroxytamoxifen (OHTam), but not the antiandrogens hydroxyflutamide (OHFl) or cyproterone acetate (CPA), reversed that effect. By using another in vitro bioassay, based on the progestin-specific stimulation of AP activity in cells of the T47D human breast cancer line, progestagenic activity was detected and measured in T, DHT and three synthetic androgens: nandrolone (19-nortestosterone). 7 alpha-methyl 19-nortestosterone (MENT) and mibolerone (7 alpha, 17 alpha-dimethyl 19-nortestosterone) (DMNT). While progestagenic effects of T and DHT required relatively high concentrations (microM levels), the synthetic androgens stimulated AP activity at nM or pM levels. These effects seem to be mediated by the progesterone receptor (PR), since they are completely abolished by the antiprogestins RU-486, ZK-98299 and ZK-112993, but not by the antiandrogen OHFl. These simple in vitro bioassays, expressing biological effects of the test compounds in human cells in culture, revealed dual or multiple hormonal activities coexisting in a single compound and provide quantitative information of considerable pharmacological importance concerning the complex actions of drugs.

Even so, where is the paper showing that progestational activity is partly the cause of gyno, even more so, where is the proof that normal prolactin levels or even higher than normal cause gynocomastia.
 
LegalGear said:
There are conflicting papers on this subject and your paper doesn't even site the activity of Deca, it says "similar" results.
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What paper? Where?
LegalGear said:
Fertil Steril. 1979 May;31(5):552-61.
Competitive progesterone antagonists: receptor binding and biologic activity of testosterone and 19-nortestosterone derivatives.

Reel JR, Humphrey RR, Shih YH, Windsor BL, Sakowski R, Creger PL, Edgren RA.
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Good to see you finally post some evidence. I would love to get the full text of this paper, but it's 30 years old and unavailable. They apparently tested the progestational activity in vivo with the McPhail Index and a pregnancy maintenance test. The abstract gives you little to go off of, though. For example, was the nandrolone given parenterally or enterally? At what concentrations? How were the tests performed? Did they do any testing with the human progesterone receptor, or just rabbit PR?

What we do know is that there are newer papers from the same researcher. The lead author, J.R. Reel, is actually the author of Invalid Link Removed I linked to here.

First, looking at progestational transcriptional activity, they found that nandrolone "at 10–8 M, increased transcriptional activity to the same extent as the progestin standard, R5020, at 10–8 M." Second, they performed a functional reporter assay and looked at alkaline phosphatase activity, which is produced in response to progestins in T47DCO cells. At 10-8 M, nandrolone "produced substantial increases in alkaline phosphatase activity." The conclusion states that "as we have shown here, 19-norandrogens exhibit considerable progestational activity both in vitro and in vivo."
 
To add to that, I located Invalid Link Removed on nandrolone in which they performed a bioassay for transactivation of the human progesterone receptor. Again, this is a very recent study, 2007. It explains, "All steroids showed full agonist activity in the AR bioassay, reaching close to 100% of maximal T apart from nilutamide which was a partial agonist, reaching a plateau of 30% of maximal bioactivity (not shown). Significant deviation from maximum values in the PR bioassay was seen only with the PR antagonist, mifepristone (53% of maximal, Fig. 1B) and the prodrug, ethylestrenol (63% of maximal, not shown)." Here's a copy of Invalid Link Removed. As you can see, nandrolone produced a full agonist response in both assays.

The paper also explains that "Currently marketed progestins fall into two main classes according to their structural relatedness to progesterone or 19-nortestosterone [7]. Historically, this split arose from the finding that, whereas 19-nortestosterone (nandrolone) was a more potent androgen than testosterone, it was orally inactive and the introduction of a 17a-ethynyl group to render 19-nortestosterone orally active, as it does for estradiol, produced unexpected but highly potent progestin activity [8]." Historically, several synthetic progestins used for birth control have been 19-nortestosterone derivatives (which is their class name).

Based on these three studies I think it's safe to say that 1) nandrolone definitely has progestational activity, both in vitro and in vivo, and 2) nandrolone is likely a full agonist, capable of producing maximal bioactivity, as shown independently in 3 recent studies.
 
LegalGear said:
At some point it would seem that any concentration androgens can stimulate the PR, as shown in this article so, showing activity at a high concentration isn't reserved to deca.

Methods Find Exp Clin Pharmacol. 1997 May;19(4):215-22.
Estrogenic and progestagenic activities of physiologic and synthetic androgens, as measured by in vitro bioassays.
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Unbelievable. Did you read what the abstract said? "While progestagenic effects of T and DHT required relatively high concentrations (microM levels), the synthetic androgens stimulated AP activity at nM or pM levels." How can you twist that to say that deca is like test in requiring a
"high concentration"? Hell no. It's says that nandrolone has progestational activity at 6 to 9 orders of magnitude lower than that of testosterone, mM (10-3) compared to nM (10-9) or pM (10-12). According to this paper, that means nandrolone produces progestational effects at one millionth to one billionth the concentration of testosterone. Yep, deca is just like test, lol.

To top it off, Nandi once referenced this study, saying "The second reason Deca may be so suppressive is that besides being an androgen, it also has progestigenic properties, meaning it binds to the human progesterone receptor at relatively low concentrations where it acts as an agonist (1)."

Who's "misusing the literature" now?
 
Your graph (full agonist) is a little misleading to your point, the transctivation graph is showing testosterone being a partial agonist at roughly 70% the activity. Additionally, it is showing that relative to progesterone Deca has lower activity which would make it a partial agonist. So, the data based on two graphs isn't conclusive by any stretch since "fullagonist.jpg" doesn't show deca (nortest) achieving the same levels of activation as progesterone. One can clearly see a large gap between progesterone and deca (nortestosterone) at almost every concentration, so to say that it has full agonist potential isn't 100% true based on this graph. In these experiments deca(nortestosterone) has a lower transcription activity level than progesterone.

However I would say you are probably right on this one, I reread the posts. I would agree with your statements that "Based on these three studies I think it's safe to say that 1) nandrolone definitely has progestational activity, both in vitro and in vivo, and 2) nandrolone is likely a full agonist, capable of producing maximal bioactivity, as shown independently in 3 recent studies." Looks like you found some good references to back up it being a full agonist. No one is denying that deca has progestational activity, the issue in question is whether it is a full agonist or partial agonist. Even then it isn't really at all part of the original discussion. So, ok it's looks like it has full transcription activity or pretty close to it. I am fine with being wrong occasionally, no big deal. It's cool to learn and I discovered something new, I had been under the impression that deca was not a full agonist, that it was only a partial agonist. I knew it had a low RBA, since the references were relatively obscure I hadn't bothered to look to see if it had full transcriptional activity. This is how we learn new things by discussing it. It's 100% not clear to me from your data that they do indeed have the same activity level but I would say it is probably the case.
 
The original point is to A) not automatically lower prolactin when you have no reason to suspect prolactin is your issue other than you can "feel it". I never said that high prolactin is a good thing, just that it doesn't appear to cause gyno and that there is a need for it in the body. Finally, messing with every hormone in the body because you "feel" it is going to cause more problems. So, everyone running around saying "I need to lower prolactin because I can feel mine is elevated" is idiotic.

As for progesterone, ok I concede it might be a full agonist at high concentrations, yet that doesn't make it causative in gyno when in fact it may actually prevent gyno and four studies on it don't seem to be conclusive when the data is not precise.

This was a good discussion where recent research was brought to light showing Deca to be a full agonist vs. my belief that it was a partial agonist. So, I learned something and I think we've debunked some brolore here saying that prolactin has no role in males and should be beaten down.
 
blind12 said:
I had some gyno and all other hormones except progesterone were in normal range. The gyno was AI-resistant.
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That looks like you had the cause of the gyno cornered - checkmate

What cycle was this from?
 
This is an interesting point about a possible cause for resistant tissues.

Anticancer Res. 2009 Jun;29(6):2167-71.
Differential effects of aromatase inhibitors and antiestrogens on estrogen receptor expression in breast cancer cells.

Smollich M, Götte M, Fischgräbe J, Radke I, Kiesel L, Wülfing P.

Department of Obstetrics and Gynecology, University of Münster, 48129 Münster, Germany.

BACKGROUND: Estrogen receptors (ER) alpha and beta play an important role in breast cancer. Recently, systemic adjuvant endocrine therapy with selective estrogen receptor modulator (SERM) tamoxifen has been challenged by aromatase inhibitors. Compared to antiestrogens, third-generation aromatase inhibitors (anastrozole and letrozole) exhibit an improved efficacy and tolerability. MATERIALS AND METHODS: Using real-time PCR analysis, 21 breast cancer tissue samples were analysed for a change of the ERalpha/ERbeta ratio during malignant progression. In stimulation experiments, differential effects of SERMs, ER antagonists and aromatase inhibitors have been investigated. RESULTS: Transition from normal breast to grade 1 tumors was characterized by down-regulation of ERbeta (relative quantification [RQ]=0.83, p=0.019), while transition from grade 1 to grade 3 tumors was associated with the decrease of ERalpha expression (RQ=1.14 vs. RQ=0.65, p<0.001). In stimulation assays, tamoxifen and fulvestrant increased ERalpha expression to RQ=1.51 (p=0.01) and RQ=1.42 (p<0.001), respectively, and left ERbeta unchanged. In contrast, aromatase inhibitors up-regulated ERbeta to RQ=1.23 (anastrozole, p=0.029) and RQ=1.38 (letrozole, p=0.048). CONCLUSION: Taken together, data indicate that SERMs/antiestrogens and aromatase inhibitors exhibit opposed effects on the ER expression of breast cancer cells: tamoxifen and fulvestrant up-regulate ERalpha expression, while aromatase inhibitors increase ERbeta expression, which may contribute to the aromatase inhibitors' therapeutic superiority over antiestrogens.
 
nattydisaster said:
LegalGear is getting his info from Seth Robets book Anabolic Pharmacology, i'm educationally guessing.

Take trenbolone for example. I have seen a handful of peopl run fina-only cycles and develop gyno. Since tren is a 19-nor compound that doesnt aromatase, then there is no increased estrogen. Yet these people still are getting gyno.

And don't tell me its from estrogen cleaving off from SHBG. That amount of estrogen is very minimal.

You could argue that it is because progestins take a huge hit on the HPTA and shutdown testosterone production easily, then estrogen is increased, but that would contradict your point.

Also, don't let 1-2 studies saying one thing make you assume it is fact. There's plenty of studies testing the same things giving opposite conclusions in science. Even Seth says in his section on pregestins that it is all relatively new research. He also only references 2 studies on this specific topic.

Also, there are PR receptors in gynecomastia. So if you have even the slightest bit of pre-existing gynecomastia from puberty or a previous cycle, progestins can cause increased gyno growth.
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....................
 
UnrealMachine said:
What cycle was this from?
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I don't know the exact cause. Could have been a rebound after a 'var cycle, but I've had no issues after the next one. Progesterone can also rise due to inflammations and depression, I've heard, and I had both. And it could've been something in those recalled Nutra trione caps.
 
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