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You do not need "prolactin control" on a Deca/NPP cycle

I think that 7 weeks is not enough to tell anything. If something bad were to happen to your testes it would most likely be after ten or sixteen weeks, especially considering your supposed condition up to now.

Also, T4 why? Surely you do know that it’s not active until it converts to t3, and that in the field it is not 100% effective as it does not always convert at a predictable rate in a patient. Even though most doctors use it as their cure all for hypothyroid, the best would all agree active t3 is the more effective and overall safer drug.

1. High-dose T4 allows one to maintain high levels of thyroid hormones without entering a hyperthyroid state. Once T3 levels get too high, T4 is converted to rT3.

2. T3 has a short half life and requires multiple doses per day. The half life of T4 is several days.

3. T4 is important in its own right and is not just a pro-hormone to T3
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Haven't you yet figured out that I know what I'm doing?
 
Personally I don’t care enough to put in that kind of effort, but that’s just me. I retain my reading material fairly effortlessly. Once in a blue moon I get a detail wrong. And it drives me crazy when I do.
 
Personally I don’t care enough to put in that kind of effort, but that’s just me. I retain my reading material fairly effortlessly. Once in a blue moon I get a detail wrong. And it drives me crazy when I do.

Yeah, but if your sources are garbage, then your data is garbage.
 
1. High-dose T4 allows one to maintain high levels of thyroid hormones without entering a hyperthyroid state. Once T3 levels get too high, T4 is converted to rT3.

2. T3 has a short half life and requires multiple doses per day. The half life of T4 is several days.

3. T4 is important in its own right and is not just a pro-hormone to T3
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Haven't you yet figured out that I know what I'm doing?

and, a hyperthyroid state increases SHBG, which has already been increased by clomid.

great plan.



T3 increases metabolic rate much more effectively than T4, which still causes TRH suppression. it's like you're taking HCG instead of testosterone..... without dealing with E2 (which you aren't btw)


LOL




.
 
Because DHT works downstream to stop E2-evoked gene transcription which has already been triggered by E2. Lowering E2 at this point will accomplish very little, since the signal cascade has already started.

what? then why are AIs even a thing? because they work to decrease systemic E2, that's why....

why allow the signal to occur when you don't need to even worry about blocking it?
 
and, a hyperthyroid state increases SHBG, which has already been increased by clomid.

great plan.

You never reach a hyperthyroid state with T4. I already explained this. Keep up.

T3 increases metabolic rate much more effectively than T4, which still causes TRH suppression. it's like you're taking HCG instead of testosterone..... without dealing with E2 (which you aren't btw)

Taking high-dose T4 allows you to reach the limits of what your body considered high-but-not-hyperthyroid-T3, any excess T4 is converted to rT3, and a hyperthyroid state is prevented.

I gave a very detailed explanation where I already covered all this. Try and keep up.
 
Tell you both what, though, I’m going to start bookmarking my reading for future reference on here so I can feel like a smarty pants too.
 
what? then why are AIs even a thing? because they work to decrease systemic E2, that's why....

why allow the signal to occur when you don't need to even worry about blocking it?

Because AIs were new, patentable drugs, which never demonstrated efficacy greater than SERMs or Masteril (drostanolone).

Same as MAOIs ---> TCAs ---> SSRIs. Of these drugs, the MAOIs are the most efficious in the treatment of depression, followed by TCAs, and then SSRIs being the least effective.

You've never been involved in drug discovery or development, so of course you're going to assume that newer is better. You're a consumer, not a researcher. Learn the difference.
 
Oh hey... wait a second... didn’t you try to dismiss permanent testicular damage as myth?
 
Because AIs were new, patentable drugs, which never demonstrated efficacy greater than SERMs or Masteril (drostanolone).

Same as MAOIs ---> TCAs ---> SSRIs. Of these drugs, the MAOIs are the most efficious in the treatment of depression, followed by TCAs, and then SSRIs being the least effective.

You've never been involved in drug discovery or development, so of course you're going to assume that newer is better. You're a consumer, not a researcher. Learn the difference.

Lol.... it's pretty clear that your scientific background is lacking quite a bit, regardless of your untoward insults.
 
Because AIs were new, patentable drugs, which never demonstrated efficacy greater than SERMs or Masteril (drostanolone).

Same as MAOIs ---> TCAs ---> SSRIs. Of these drugs, the MAOIs are the most efficious in the treatment of depression, followed by TCAs, and then SSRIs being the least effective.

You've never been involved in drug discovery or development, so of course you're going to assume that newer is better. You're a consumer, not a researcher. Learn the difference.

I design and build tube amplifiers. I understand newer is not better. But I also understand the merit of aromatase inhibitors.
 
Lol.... it's pretty clear that your scientific background is lacking quite a bit, regardless of your untoward insults.

Yeah, it's lacking in high-level cardiopulmonary knowledge, it's lacking in high-level vascular and endothilial knowledge, and my gastrointestinal knowledge is pretty thin.
 
You never reach a hyperthyroid state with T4. I already explained this. Keep up.



Taking high-dose T4 allows you to reach the limits of what your body considered high-but-not-hyperthyroid-T3, any excess T4 is converted to rT3, and a hyperthyroid state is prevented.

I gave a very detailed explanation where I already covered all this. Try and keep up.

well, how much T4?


it's funny how the longer this thread goes, the more you mention various compounds you "forgot" to mention you were on...…
 
Oh hey... wait a second... didn’t you try to dismiss permanent testicular damage as myth?

No. I specifically stated in other posts that 19-nors can damage Leydig cells. The method is malondialdehyde generation causing free-radical oxidation. 19-nors also increase the risk of testicular cancer.
 
well, how much T4?


it's funny how the longer this thread goes, the more you mention various compounds you "forgot" to mention you were on...…

I take T4 daily at 200 mcg as I have for more than a year. It's not part of my cycle.
 
So, in your hypothesis, what’s going to happen to your hpta when you stop the drugs; in what order will you stop them; at what time; and how much time will have elapsed from cycle start to total cessation of treatment?

Everything I have read and understand leads me to think that you will have low test, high e2 and excessive aromatase throughout pct, unless there is a detail in your plan I missed amidst the onslaught of recent replies.
 
Yeah, it's lacking in high-level cardiopulmonary knowledge, it's lacking in high-level vascular and endothilial knowledge, and my gastrointestinal knowledge is pretty thin.

well, it's like this.

if you were literally so much smarter than everybody else here, then nobody would struggle to understand your theories after you proposed them, or be able to consistently produce information that directly refutes information that you post.

it should be so clear that nobody here would struggle with it.

if you're smarter than everybody else, you should be able to break it down so they understand it..... as someone who has taught a lot of people a lot of things, this is something I've understood for a while. makes me wonder why you, as an "instructor of grad students," don't understand how this is done.



.
 
So, in your hypothesis, what’s going to happen to your hpta when you stop the drugs

I'm assuming it's active right now, since all signs point to having pulsatile LH (testicle size, weight, and firmness) and FSH (large volume of thick ejaculate). When I come off cycle, I'll be staying on Clomid at 25 mg/day and Naltrexone at 25 mg/day, and may run Mast E at 200 mg/week as well, depending on how I feel.

in what order will you stop them; at what time; and how much time will have elapsed from cycle start to total cessation of treatment?

I don't set my cycles in stone, I make an outline and then deviate if I feel it's beneficial or necessary. Right now the plan is to continue to run 875 mg/week of TE with 600 mg/week of NPP and probably 300 mg/week of Mast E (switching from Mast P) for the next 6 weeks. After that, I'll drop TE down to 125 mg/ week while keeping NPP and Mast E at the same dosage. Weeks 8-10: 125 TE, 300 NPP, 150 Mast E. Weeks 10-12: 200 NPP, 200 Mast E. Clomid 25 mg/day and Naltrexone 25 mg/day will continue through PCT.

After the end of week 12 (starting PCT), I'll be running Ashwagandha extract, selegiline 5 mg/day, 5-HTP 100 mg x 3/day, pregnenolone 50 mg/day, vitamin D 200,000 iu/week, vitamine K2 5 mg/week, vitamin A 100,000 iu/week, 3000 mcg B12 injection twice weekly.

Everything I have read and understand leads me to think that you will have low test, high e2 and excessive aromatase throughout pct, unless there is a detail in your plan I missed amidst the onslaught of recent replies.

How will I have low test? Clomid alone puts me at almost 1000 ng/dl total testosterone. As the TE clears Cloimd (and Naltrexone) will pick up the slack. That I'm not shutdown right now means that I don't have to wait for natty test production to start, it's already running, albeit gingerly. Once the exogenous T goes away it will pick up very quickly.

As far as E2 I don't really care what it is. If I have any E2 sides I'll bump Masteron up. As TT falls so will E2.

I'm not looking at this cycle from the perspective of a bodybuilder, with all of the scientifically-baseless broscience claims, I'm looking at it from the perspective of a pharmacologist integrating the endocrine system as a whole.
 
I'm here, listening...you know, like the government does, just watching and listening.

:)

Keep going, interesting discussion!
 
As far as E2 I don't really care what it is. If I have any E2 sides I'll bump Masteron up. As TT falls so will E2.

I'm not looking at this cycle from the perspective of a bodybuilder, with all of the scientifically-baseless broscience claims, I'm looking at it from the perspective of a pharmacologist integrating the endocrine system as a whole.

uhm.

hate to point this out, but it's possible to have high E2 and low TT. pretty common at the end of cycles for guys who fail to manage E2 on cycle.

but you're a super-scientist, so I'm sure you knew that.
 
No. I specifically stated in other posts that 19-nors can damage Leydig cells. The method is malondialdehyde generation causing free-radical oxidation. 19-nors also increase the risk of testicular cancer.

Oh okay, so when I said that you can quite easily ruin your testes permanently by taking this type of drug combination, and you refuted it by equating it with seeing ghosts, you were just being a dickhead? Got it.
 
No, but I have an autoimmune disease and that's all I'll say about it.

okay.

I'm not expecting you to divulge your personal medical information online, but I think it's pretty clear that you have extenuating circumstances that a lot of folks don't have when running cycles. your results are likely much, much different than most people that don't have a pre-existing medi cal condition.


and, if it's an autoimmune issue of sorts, I suspect you have more bloodwork than you are claiming to.....



.
 
uhm.

hate to point this out, but it's possible to have high E2 and low TT. pretty common at the end of cycles for guys who fail to manage E2 on cycle.

but you're a super-scientist, so I'm sure you knew that.

And so what if I have high E2 and low TT? The Clomid and Masteron will take care of the E2 and the Masteron will replace the TT. People forget that DHT is what makes testosterone "feel good" Guys with 5-AR deficiency have high TT and low or no DHT, average E2, and feel like absolute garbage. DHT is what makes testosterone so great.

One can have low TT and high DHT and feel just fine. DHT is the king androgen.
 
okay.

I'm not expecting you to divulge your personal medical information online, but I think it's pretty clear that you have extenuating circumstances that a lot of folks don't have when running cycles. your results are likely much, much different than most people that don't have a pre-existing medi cal condition.

I'll grant that's a possibility.


and, if it's an autoimmune issue of sorts, I suspect you have more bloodwork than you are claiming to.....
.

I had bloodwork done related to this condition. None of it would be useful information for any BBers.
 
And so what if I have high E2 and low TT? The Clomid and Masteron will take care of the E2 and the Masteron will replace the TT. People forget that DHT is what makes testosterone "feel good" Guys with 5-AR deficiency have high TT and low or no DHT, average E2, and feel like absolute garbage. DHT is what makes testosterone so great.

One can have low TT and high DHT and feel just fine. DHT is the king androgen.

uh, okay.

so if masteron replaces TT, then your HPTA is not recovering.
 
Oh okay, so when I said that you can quite easily ruin your testes permanently by taking this type of drug combination, and you refuted it by equating it with seeing ghosts, you were just being a dickhead? Got it.

You can't "quite easily" ruin your testes permanently. The doses used in animal studies are huge. There are no human studies on this.
 
You want to know my IgG, IgM, EBV antibodies, thyroid autoantibodies, NK, CD8, CD19, and whether I'm positive for CMV?

Is this useful data for you?

uhm, you have an organ transplant? or Epstein Barr?

I know people with both....
 
Sure it is. Masteron is barely suppressive, and running Naltrexone inhibits androgen negative feedback.

c'mon. DHT (masteron) binds stronger to the AR then testosterone does. you're running a higher dose that your normal dose of T production..... no way that you're HPTA is recovered.

sure, the clomid and naltrexone might help, but do you have any proof?

no, no you don't.
 
Not even close. Why did I spend $200,000 on school if not to have a body of a greek god?

Lol...

whatever dude.


I apologize to everybody here that that saw me get sucked into the BS with this troll.....





have fun, Achilles!




.
 
You do not need "prolactin control" on a Deca/NPP cycle

I'm assuming it's active right now, since all signs point to having pulsatile LH (testicle size, weight, and firmness) and FSH (large volume of thick ejaculate). When I come off cycle, I'll be staying on Clomid at 25 mg/day and Naltrexone at 25 mg/day, and may run Mast E at 200 mg/week as well, depending on how I feel.



I don't set my cycles in stone, I make an outline and then deviate if I feel it's beneficial or necessary. Right now the plan is to continue to run 875 mg/week of TE with 600 mg/week of NPP and probably 300 mg/week of Mast E (switching from Mast P) for the next 6 weeks. After that, I'll drop TE down to 125 mg/ week while keeping NPP and Mast E at the same dosage. Weeks 8-10: 125 TE, 300 NPP, 150 Mast E. Weeks 10-12: 200 NPP, 200 Mast E. Clomid 25 mg/day and Naltrexone 25 mg/day will continue through PCT.

After the end of week 12 (starting PCT), I'll be running Ashwagandha extract, selegiline 5 mg/day, 5-HTP 100 mg x 3/day, pregnenolone 50 mg/day, vitamin D 200,000 iu/week, vitamine K2 5 mg/week, vitamin A 100,000 iu/week, 3000 mcg B12 injection twice weekly.



How will I have low test? Clomid alone puts me at almost 1000 ng/dl total testosterone. As the TE clears Cloimd (and Naltrexone) will pick up the slack. That I'm not shutdown right now means that I don't have to wait for natty test production to start, it's already running, albeit gingerly. Once the exogenous T goes away it will pick up very quickly.

As far as E2 I don't really care what it is. If I have any E2 sides I'll bump Masteron up. As TT falls so will E2.

I'm not looking at this cycle from the perspective of a bodybuilder, with all of the scientifically-baseless broscience claims, I'm looking at it from the perspective of a pharmacologist integrating the endocrine system as a whole.

Ah, the flaws are apparent in plain writing now.

So, just tapering off the clomid and naltrexone then? The rest of your pct except pregnenolone (bad idea) is irrelevant to me, unless your ashwagandha extract is pure withanolide A and B prepared for IM injection.

Thinking like a pharmacologist is as bad as thinking like a bodybuilder when you need to be thinking like an endocrinologist.
 
Same as MAOIs ---> TCAs ---> SSRIs. Of these drugs, the MAOIs are the most efficious in the treatment of depression, followed by TCAs, and then SSRIs being the least effective.

Well this logic is kinda misleading. SSRI's have much lower side effect profile and MAOIs are still used but only later, when other treatements fail. So ... SSRI are definetly more advanced, less crude. This is like comparing sarms to aas I guess, if sarms actually were all that they were hyped up to be.

I haven't used MAOIs and I hope I wont need to. I've tried most ssri's and I have little love for them.
 
We all come from different professions, so let's keep it civil guys. I'm a producer/director, so this is far from my expertise, but I am in it for the chance to learn something new.

Spurfy, I understand you are frustrated but it's kinda silly isn't it? It's like I would go to a movie lovers forum or something and start having professional discussions with it's members. I have stopped discussing and stop being frustrated by amateurs a long time ago. Everybody thinks they know how to tell a story, everybody thinks they know a lot more then they do. Sure, we make it look easy, that's the whole point. Not going to go further into this, but you get the point. If you are a professional in one field, you know exactly what I'm talking about.

I am however greateful to have somebody from the medical field here talking to us. And I think I understand the noise in communication that's occurring. But either way, this is not eroids, so let's stop it with the insults :)

Back to the topic at hand... I really don't agree with the whole mast vs Ai's topic. I just don't get it, why would you allow e2 to sky rocket if you can prevent it from doing that in the first place? What am I missing? Ai's aren't really toxic or anything, why not take them? Serm's have more sides then Ai's; for me notably a loss in libido, which translates to a lowering in self esteem and lot's of other stuff. And clomid, ugh, don't get me started on that chit. I get small zits, I get emotional as fuak, in a bad way... If I can just take an Ai and not experience any of those sides, then hurray. I don't mind viron though, but do mind loosing hair and getting acne. So again, I revert to Ai's...
 
Back to the topic at hand... I really don't agree with the whole mast vs Ai's topic. I just don't get it, why would you allow e2 to sky rocket if you can prevent it from doing that in the first place? What am I missing? Ai's aren't really toxic or anything, why not take them? Serm's have more sides then Ai's; for me notably a loss in libido, which translates to a lowering in self esteem and lot's of other stuff. And clomid, ugh, don't get me started on that chit. I get small zits, I get emotional as fuak, in a bad way... If I can just take an Ai and not experience any of those sides, then hurray. I don't mind viron though, but do mind loosing hair and getting acne. So again, I revert to Ai's...

1. E2 is highly anabolic itself. High levels of E2 directly equate to higher levels of nitrogen retention and protein synthesis.

2. I've yet to meet anyone who experiences negative side effects on Torem. I chose Cloimid for this experiement because I did not want a SERM that prevents or treats gyno. I wanted to see how well the Mast performed in this regard.

3. E2 is anti-inflammatory -- dose dependently

4. E2 directly repairs joints by increasing type I, III, and III collagen synthesis -- dose dependently

5. E2 is a potent modulator of IGF-1

Bodybuilders in the 1970's had only two drugs to control E2: Proviron and Masteron. These drugs prevented the negative effects of E2 (by interfering with ER-a binding) while allowing for the positive effects of ER-b activation. I've never seen a pic from the 1970's of a BBer with gyno, even mild gyno -- and I've looked.

I understand being wary of having too-high E2 levels, but high E2 levels are irrelevant if ER-a binding and downstream cascade is suppressed. I'm not sure why this proven scientific fact is so angrily disputed on here, especially among guys who have never even tried using DHT as their source of E2 control.

I get that this flies in the face of what has been parroted on bodybuilding forums for the past decades, but just because something gets repeated over and over doesn't make it true. I am really the only person here who consistently posts citations to science journal articles to back up my arguments, and instead of appreciation for sharing knowledge, I get angrily rebuked without any proof other than speculation or anecdote.

I never claimed scientific proof for running SERMs on cycle other than one study, and my data for this is largely anecdotal. And for those saying, "SERMs lower IGF-1 = NO GAINZ!" I would offer that the IGF-1 reductions are very modest even at high doses, no more than 20%, and that both T and E2 potently elevate IGF-1 and would more than overcome the slight reduction that might occur from the modest use of SERMs.

Finally, to those who have criticized my method of explanation: You have to realize how difficult it is to explain some of these concepts to people who lack even a basic understanding of molecular biology. People who don't even understanding the basic of action potentials, inhibitory and excitatory neurons, downstream cascade signalling, and the difference between agonists, partial agonists, antagonists, mixed agonists/antagonists, inverse agonists, receptor subtypes, and receptor-mediated nuclear gene expression. These are basic topics that any 1st year pharmacology grad student knows. Which is not to say I'm saying people here are stupid, they just generally lack the fundamental knowledge to even understand some of the concepts I'm trying to explain. Some get angry and defensive, some are open-minded and willing to learn.

So yeah, I'm not very nice sometimes, but you have to understand that my time is money. When I give detailed explanations, I'm offering graduate-level knowledge for free. If people would at least give that a cursory consideration and show even an iota of appreciation, I wouldn't be so rude.

The only reason I post on this forum -- and this is the ONLY forum I post on -- is to try to stimulate discussion on new concepts and to educate people on bodybuilding pharmacology. If I can get one person to consider a new viewpoint then I've succeeded and my time has not been wasted.
 
I understand being wary of having too-high E2 levels, but high E2 levels are irrelevant if ER-a binding and downstream cascade is suppressed. I'm not sure why this proven scientific fact is so angrily disputed on here, especially among guys who have never even tried using DHT as their source of E2 control.

This has been discussed yes and the general argument against this, is that serms do not bind to all relevant ER's. They are very tissues selective, so in those tissues that they don't elicit strong action, the high serum estradiol will have a much bigger effect. I have stated this argument on page 1, but you shrugged me away, saying "I know everything" ...

You miss a lot of stuff like this and often times use your knowledge in a biased way, just to prove something, no matter if the statements you have stated are used/interpreted highly subjectively. Just for the gain of winning an argument. For instance the SRRI anecdote, or the rejection of all roid users experiences, bc they all have gear that can't be trusted.

It is this preferential and biased rhetoric, that is jolting all of us into an oppositional stance. You don't see it, I don't blame you, rhetoric is not your profession. Most doctors, researches, schollars of empirical sciences have this problem.

Look, but I'm sure we'll find common language eventually :)

It's still a good discussion, it could do withouth the ego's and misinterpretations, but it is what it is.
 
Franc columbo
Right peck... Dude had gyno

I agree with a lot of what youre saying... This is your first cycle with 19 nors. Its great its working for you... But ive run masteron w trest and needed an ai. Its great that you havent had any sides but youre limiting you're results on your limited experience w 19 nors.

Id like to see you try trest ace without an ai and I dont care how much mast or proviron you run that shyts gonna get ya.Invalid Link RemovedInvalid Link RemovedInvalid Link Removed
 
Well this logic is kinda misleading. SSRI's have much lower side effect profile

This is debatable -- 26% of SSRI users rate their side-effects as "very bothersome" or "extremely bothersome" (Invalid Link Removed), and the majority of side effects attributed to TCAs were actually present prior to the initiation of drug therapy (Invalid Link Removed).

and MAOIs are still used but only later, when other treatements fail.

MAOIs are still the most effective drug treatment for depression that we have, in some studies showing 70% or more rates of remission, as opposed to SSRIs which technically fare no better than placebo. Reversible MAOIs have no dietary restrictions and are just as safe as SSRIs.

So ... SSRI are definetly more advanced, less crude.

More advanced how? They are less effective at treating depression than TCAs or MAOIs -- given the review of all evidence, they're no better than placebo -- and the true incidence of severe side effects is greater than 1 in 4 persons.

I haven't used MAOIs and I hope I wont need to. I've tried most ssri's and I have little love for them.

Emsam is a MAOI and scores the highest self-reported improvement rating of any anti-depressant on Drugs.com (Invalid Link Removed).

My whole point in all this is that Masteron is essentially just as effective as SERMs or AIs in treating breast cancer and has less side effects (AIs in particular are horrific when used to treat BC) than either drug, but Masteron isn't used now as a treatment.

Why?

Because newer drugs came along with new patents that were very profitable for the companies that developed them, while poor old Masteron, which had no patent protection and which exorbitant prices could not be charged, has languished in obscurity.

Aromasin's retail cost is around $1000 for a 1 month supply.
Arimidex is about $600 for a 1 month supply.
Femara (letrozole) is about $750 for a 1 month supply.
 
Id like to see you try trest ace without an ai and I dont care how much mast or proviron you run that shyts gonna get ya.

I lactated bad on NPP and Trest. No amount of AI (any AI, letro included) was controlling it. Trest gave me gyno that I got later rid off with ralox. Then I tried Trest/Ralox/adex and got gyno symptoms with lactating again. Suspecting that on trest, AI's and-or serms do NOTHING, I kept AI low, 0.5mg adex eod -and started 0.25mg caber eod. Now it worked without trouble. Prolactin were the issue. I understand that I'm sensitive to 19 nors. Others may get away using serms -and or AI's (maybe even DHT).
 
This has been discussed yes and the general argument against this, is that serms do not bind to all relevant ER's. They are very tissues selective, so in those tissues that they don't elicit strong action, the high serum estradiol will have a much bigger effect. I have stated this argument on page 1, but you shrugged me away, saying "I know everything" ...

I'm not talking about SERMs in this respect, as I stated in my post that you replied to, I'm talking about DHT.
 
I lactated bad on NPP and Trest. No amount of AI (any AI, letro included) was controlling it. Trest gave me gyno that I got later rid off with ralox. Then I tried Trest/Ralox/adex and got gyno symptoms with lactating again. Suspecting that on trest, AI's and-or serms do NOTHING, I kept AI low, 0.5mg adex eod -and started 0.25mg caber eod. Now it worked without trouble. Prolactin were the issue. I understand that I'm sensitive to 19 nors. Others may get away using serms -and or AI's (maybe even DHT).

Prolactin gyno is directly caused by androgen (DHT) deficiency:

"Although prolactin (PRL) receptors are present in male breast tissue, hyperprolactinemia may lead to gynecomastia through effects on the hypothalamus, causing central hypogonadism'
Invalid Link Removed

This says that prolactin gyno is caused by androgen deficiency. Which does what? Increases ER-a signalling because there's not enough DHT to stop it...

You have to remember that 19-nors themselves bind ER-a same as E2 does, so an AI is useless in this regard because it's not E2 that's causing the gyno, it's the 19-nor mimicking E2. So yes, you can lower prolactin with DA-agonists, or you can prevent the rise in prolactin in the first place by treating with DHT. Prolactin follows ER-a activation, and it's likely that the way that 19-nors affect ER-a gene transcription they do so in a manner that upregulates PRL release. Still, at the root of all this is excessive ER-a signalling, which DHT stops.

DA-agonists are not treating the root cause, which is insufficient DHT levels to counter-balance ER-a signalling.

I have explained this at least 5 different times, with citations, and not one person here is seemingly able to grasp this concept. Why?

DHT keeps E2 in check, which is why some guys who run finasteride get gyno even from normal TT and normal E2 levels. Without adequate DHT, ER-a signalling surges, so even normal amounts of E2 can cause gyno in the absence of normal levels of DHT.
 
I lactated bad on NPP and Trest. No amount of AI (any AI, letro included) was controlling it. Trest gave me gyno that I got later rid off with ralox. Then I tried Trest/Ralox/adex and got gyno symptoms with lactating again. Suspecting that on trest, AI's and-or serms do NOTHING, I kept AI low, 0.5mg adex eod -and started 0.25mg caber eod. Now it worked without trouble. Prolactin were the issue. I understand that I'm sensitive to 19 nors. Others may get away using serms -and or AI's (maybe even DHT).
When I say ai I'm talking about caber or prami which arent technically ais I know. Traditional ais dont work w 19 nors. Did you try either of those to control sides w your 19nor runs HGP?

Edit: duh nevermind just saw you stated the caber worked
 
Prolactin gyno is directly caused by androgen (DHT) deficiency:

"Although prolactin (PRL) receptors are present in male breast tissue, hyperprolactinemia may lead to gynecomastia through effects on the hypothalamus, causing central hypogonadism'
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This says that prolactin gyno is caused by androgen deficiency. Which does what? Increases ER-a signalling because there's not enough DHT to stop it...

You have to remember that 19-nors themselves bind ER-a same as E2 does, so an AI is useless in this regard because it's not E2 that's causing the gyno, it's the 19-nor mimicking E2. So yes, you can lower prolactin with DA-agonists, or you can prevent the rise in prolactin in the first place by treating with DHT. Prolactin follows ER-a activation, and it's likely that the way that 19-nors affect ER-a gene transcription they do so in a manner that upregulates PRL release. Still, at the root of all this is excessive ER-a signalling, which DHT stops.

DA-agonists are not treating the root cause, which is insufficient DHT levels to counter-balance ER-a signalling.

I have explained this at least 5 different times, with citations, and not one person here is seemingly able to grasp this concept. Why?

DHT keeps E2 in check, which is why some guys who run finasteride get gyno even from normal TT and normal E2 levels. Without adequate DHT, ER-a signalling surges, so even normal amounts of E2 can cause gyno in the absence of normal levels of DHT.

Because you mostly lack the ability to be as clear, concise, or relevant to the topic at hand as you have been here. I already understood everything you’ve attempted poorly to explain in this thread, before it was ever posted. However, your apparent lack of ability to explain yourself in clear language makes it difficult for most here to grasp your reasoning one way or another on many statements. It brings your own understanding into question for anyone reading it, as you seem to contradict yourself, omit facts, and tout pure opinion as fact; such as the superiority of an maoi over an ssri. You seem like someone with absolutely no real world experience whatsoever playing copy paste. Which, likely you aren’t.
 
Frankly as I stated before I think the entire methodology behind your interaction with this forum is flawed and dangerous. You need less words, more data, clearer explanations, and you will help the people who read what you write.
 
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