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I dont really understand this advice, in fact its bad. High E2 will increase Prolactin ALL ON ITS OWN even without the presence of a 19nor like Tren. Prolactin/Progestin aggravated gyno is ALWAYS worse in the presence of too much estrogen. I am not saying its caused by estrogen because its not. But saying the letro is not going to help is foolish. When on Tren/Test (or anything aromatizing) you still want to keep your E2 under control, right? Many minds have hypothesized its actually the elevated estrogen in the presence of the elevated prolactin or progesterone that allows Tren based prolactin gyno to really rear its ugly head. Common knowledge I have seen says keeping estrogen low reduces the chances of a prolactin/prog based flare usp. Basically any change in E2 can change prolactin metabolism. E2 goes up = prolactin goes up and vice versa, its way more complex than most realize (and I barely grasp the interplay well). Prolactin itself doesnt do much, but it really increases estrogen's effect making estrogen much more active at lower levels. So high E2 + Prolactin elevated is never good. I agree caber or prami is a must (I believe caber is better as it has fewer sides). However, I still think an AI to keep estrogen low on this mix is also wise.
You can get gyno 3 ways. First off, from estrogen. Second, from progesterone alone, or progesterone making estrogenic gyno worse. And finally, from prolactin. Tamox can be used to treat gyno from either Deca or Tren, whether it be from estrogen or progesterone. BUT Tamox CANNOT treat prolactin induced gyno. But can treat estrogenic gyno or progestenic gyno (if that exists). For pure prolactin based gyno you need the caber or prami. The problem is, real world, there is always interplay between all these hormones and you never can be 100% sure what exactly is the issue when your on multiple compounds. I think the concept that Nolva makes prolactin based gyno worse is a myth though and based on some confusion from data from studies showing it upregulates prog receptor in certain OTHER tissue (uterus).
Kaladryn: I am on the dreaded Tren/Test/Drol combo right now. I have a slight lump under my left nipple which flares up pretty much anytime I use anything 19nor or higher test (no matter how much caber/AI I am on). The right nipple has never had a thing, only the left. Its strange. It quickly shrinks down once I'm off or on TRT levels. It's not large and not visibly noticeable but its there and its not going anywhere. I hit it real hard with high dose Letro/Nolva and rotated in some Torem once. It shrunk it up pretty good but once I'm back on anything, it "plumps" up again.
Anyway, my question is as to this "nolva making it worse" issue. I know you dont have time to lay it all out but in a nutshell could you explain what the hypothesized mechanism here is? Why would tomax make it worse? It competes for E2 receptor sites directly in the breast/glandular tissue itself but does not "directly" bind with Progesterone receptor like the E2 receptor.
I suspect the theory is that Nolva (Tamoxifen) upregulates the PgR (progesterone receptor) and can exacerbate existing gynecomastia conditions cause by elevated prolactin. So the logic would follow that in that situation, it's best to use an aromatase inhibitor + caber if you are 100% certain the gyno is from prolactin and not E2 because the Tomax can make it worse. Seems to make sense. I think often people get E2 based gyno when they add Tren in because the elevated prolactin will make the circulating estrogen so much more potent/active. A higher AI dose may be needed. Then when they get gyno, they assume it must be from the Tren (prolactin) when it very may well be E2 based. It's hard telling and I myself never really know what the fuck is causing what when on multiple things (especially test/tren/drol). Is this in line with your understanding of why Nolva could be said to make it worse? Still not sure I buy it but there is a pubmed on this precise mechanism BUT not in breast tissue.
Here is a counter point to that above logic which I think is based on some confusion. In some tissues, such as the uterus, upregulation of the progesterone receptor would be seen and expected as its highly estrogen sensitive. People see this an assume its global (all tissue). However, in other tissues, such as the breast (glands) of healthy people, Tamoxifen is an antagonist (blocks the ER). The progesterone receptor is synthesized in response to estrogen. So when the ER is blocked (in breast tissue), the progesterone receptor will also down regulate (not up regulate)!
Therefore, Tamoxifen should help reduce gyno even when using Tren or Deca, not make it worse. Its good when ots E2 or Prog based and should not hurt if its direct prolactin based but you still need Caber also.
Tamoxifen will down regulate the progesterone receptor in breast tissue. Some say Tamox will up regulate the progesterone receptor and cause or lead to gyno (as I stated above). However, this is not accurate and the assumption Tamox CANT be used with Deca or Tren is false. It should NOT up-regulate progesterone receptor sensitivity in breast tissue itself. IMO, the gold standard for ALL TYPES OF GYNO is still a SERM/AI in combination and if on Tren, throw in the Caber. You are covering every possible angle then.
Opinions please! I'm way over my head here. Where is Stewie!
More info on this here which seems to corroborate the confusion which birthed this BroScience.
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