You have almost 600 posts, and yet you throw a crazy ass cycle out there...whats up with that? You have bulkers, with cutters....nolva with 19 nors. You only really need 3 compounds at a time. Looks like you are try ing to start a bulk and end with a cut....what is going on.?
I see that priapis posted several studies attempting to support his claim that tamoxifen (nolva) upregulates the progesterone receptor (PgR) in breast tissue. The first
two studies he posted looked at cancerous breast tumors (i.e. not normal breast tissue). The next two studies he posted (
here and
here) looked at the effect in en***etrial tissue (the uterus).
First, let's address the latter, en***etrial tissue: I've talked about that
here. The gist is that it's no surprise tamoxifen upregulates the PgR in the uterus, where 1) there is high sensitivity to estrogen and *especially* where 2) tamoxifen is known to act as an estrogen receptor agonist (acting like estrogen, not blocking it). This is not the case in normal breast tissue. I argue that Eric Potratz is an idiot (and he is) for extrapolating from en***etrial tissue in women to healthy breast tissue in men, without even mentioning (or being aware of) the differential tissue effects. He's misleading people about the dangers of tamoxifen so he can sell a competing product.
Second, let's address the effects in breast cancer tissue: My position is that the effect on PgR expression is not uniform, though there is often a statistically significant increase. If we look at the full text of the first study that priapi posted, we see in table 2 that 24% the tamoxifen group had down-regulation of the PgR, 26% had no change, and 50% showed up-regulation. In contrast,
this study found what they described as "a modest decline" in PgR levels in all three histologies they tested with tamoxifen treatment, though it failed to achieve statistical significance (p values of .19, .82, and .15).
But most importantly, what do we see in normal, healthy breast tissue? Before I address that, note that
earlier in this thread priapis said that I have "an unsupported/undocumented opinion that contradicts science, based on an incorrect reading of some other guys article." He says that the studies above (in cancer tissue and en***etrial tissue) "and many more" show that my opinion is incorrect. He ends his post arguing that "the fact of upregulation in BREAST TISSUE is so well established..."
priapis couldn't be more wrong. He fails to understand that there is a significant difference between cancerous breast tumors and normal breast tissue.
This study looked at ER and PgR expression in
normal breast tissue (i.e. not cancer tissue) in tamoxifen treated women. They found that
tamoxifen "shows no stimulatory activity on either PgR levels, a well known oestrogen regulated protein... or the important parameter of cell proliferation (Figure 2)." "In conclusion, the data presented do not show any adverse effects of tamoxifen on normal breast tissue."
This finding was confirmed in the most extensive study that I've seen looking at the effects of tamoxifen in
normal breast tissue, which was published in 2003. This quote couldn't be any more relevant or explicit. Read it and reread it:Here are images showing the effect of different doses of tamoxifen on the level of estrogen receptors (ER, on the left) and progesterone receptors (PR, on the right) in
normal breast tissue:
These results in normal breast tissue are in perfect accordance with my statement that "There is no evidence showing that tamoxifen upregulates the progesterone receptor in the breast (which is what the worry is all about). It shows it does the opposite." priapis is demonstrating his ignorance when he says that this statement "contradicts science." In fact, it's based on the science (and the most relevant science at that).
I stand by my argument that "Nolvadex will not make progesterone related gyno worse. It will help prevent it." (Unless, of course, your breast tissue is a uterus or a cancer
)
Join Date: Dec 2009
Posts: 755
Rep Power: 8
Progesterone Gyno
Not mine, but a good read none the less.
I would like to cear up a few misconceptions about progesterone and gynecomastia.
Their is absolutely no steroid that aromatizes into progesterone. The reason for this is that progesteron does not have an aromatic A ring. So toss that myth out the window. Tren? Deca? Sorry but it just doesn't happen.
Now Tren and Deca bind pretty well to the PR. They are progestins in their own right without undergoing any structural changes, but their affinity is MUCH weaker than progesterone itself. Even more so when nandrolone is reduced by 5-alpha reductase into DHN. Their is a small chance of progestogenic activity that could aid in manifesting a mass in the mammry IF estrogen is present in supraphysiological amounts, without proper ratio to testosterone but I have never see a documented case of progestogenic gynecomastia. The reason for this is that the PR has two isoforms. The PR-A and PR-B. PR-B mediates stimulatory effects of progestins; PR-A which is bound with progestins or anti-progestins inhibits PR-B, and PR-A is ***inant,. The response to progesterone is determined by the relative expression of the two isoforms.
There is a direct relationship between the PR isoforms and steroid concentrations an this direct relationship suggests high progesterone concentrations, but this will induce the expression of PR-A, which represses transcription of PR-B, which in turn supresses PR function and progestin effect
With initial administration of nandrolone or it's dirivitives, I could see an expression of PR-B but a rapid rise in PR-A will ultimately supress the function of the PR. IMO, you would need a high ratio of the two before concerns, and this is a bit more of a possiblity with the begining of administration. In this time of vulnerability, rest assured in aromatase inhibitors as progesterone is an E2 agonist so the utilization of an AI will help. I personally don't think the concern is warranted though
Their are 4 combinations of hormones that cause gyno- Estrogen, Progesterone, Prolactin, and IGF. Nandrolone is a weak progestin, which agonizes the PRL, it also raises IGF. Progesterone induced gyno is not really of a concern given binding affinity to the PR and the mechanism of the two isoforms. The production of prolactin is a deffinate risk. Not only can it be an inductor for gyno along side estrogen, IGF, and pogesterone; this chance is increased as prolactn lowers testosterone. So you need to make sure to take proper precautions to not only keep estrogen in check, but prolactin as well.
Also, basically from what I've read on the matter, prolactin or progesterone will not cause gyno unless there is excess estrogen that has been aromatized in the body and already beginning the stages of gyno. It just adds on to the problem and brings with it lactation. Having said that, if you are on nonaromatizing compounds along with tren, you should not get gyno. If you are on winny (and anti-progestagenic) you will not get gyno. If you are on aromatizing compounds and you supplement with anti-e's and AI, you should not get gyno because your estrogen level will be in check therefore not causing excess estrogen for the progesterone to team up with. Its all starting to make a little more sense to me now. If any of you have any conflicting or additional information to this topic, please post it. I am in the process of adding the Tren E back in my cycle as soon as I feel comfortable that I have my gyno in check.
And i have another read of this kind...
