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i just started a tren and test cycle 800 of test 400 of tren both short esters.... will taking some nolva throughout the cycle stop gyno? does nolva stop gyno from tren?
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I would save the nolva until gyno starts. I personally would use an AI prevent bloat and reduce risk of gyno during the cycle.ADMIN/OWNER@Peak-Muscle -
i dnt know if its gyn symptons or not but my nipple like the achual lil nipple part you know when ur really cold and it turns hard it gets like that but looks a lil more swallen and sensitive maybe i was just over reacting, i dont have any problems with bloat... um if i were to use a ai which 1 and how would you use it?Comment
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If you are taking tren, you do not want to take nolva.
However, nolva for PCT is fine.increased risk for progesteronic sides, as nolvadex may increase progesterone receptors (Gynecol Oncol. 1999 Mar;72(3):331-6)
Pramipexole at .25mg should control prolactin, and Anastrozole(Arimidex) .25mg should control estrogen, protecting you from gyno induced by prolactin and/or estrogen.Comment
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Next time Joe run an AI. Prevention is better than treatment..
In regards to Tamoxiphene and 19nors... well I've never had any issues.
Read 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 endometrial tissue (the uterus).
First, let's address the latter, endometrial 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 endometrial 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 endometrial 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)"
Also..
"PROGESTERONE AND PROLACTIN INDUCED GYNECOMASTIA
Before delving into this subject, I’d like to say first and foremost, that in users of anabolic/androgenic steroids (AAS) the first step in combating the development of gynecomastia, or male breast enlargement, is to eliminate the causative agent: the anabolic steroid. Drug-induced gynecomastia almost invariably resolves on its own when a person quits taking the drugs responsible for it, if caught before permanent fibrosis develops. Unfortunately, most AAS users don’t want to employ this simple approach, for obvious reasons, so the foregoing will all be under the assumption that a person wants to prevent or treat gyno and still continue steroid use.
In the belief that certain anabolic steroids increase prolactin levels as well as act as agonists at the progesterone receptor, some have advocated the use of antiprolactin agents, like bromocriptine, or progesterone receptor blockers like RU-486 to treat AAS related gynecomastia, in lieu of more traditional drugs like tamoxifen.
In truth, the etiology of gynecomastia is unknown and a number of agents including estrogens, progestins, GH, IGF-1, and prolactin may be involved. However, most authorities believe that a decreased (T+DHT)/E ratio is central to the development of gyno, and that blocking the effects of estrogen, or increasing T + DHT levels, is central to ameliorating the problem.
Regarding prolactin, androgens decrease prolactin levels whereas estrogens increase prolactin. Non-aromatizing androgens have never been shown to elevate prolactin levels in humans, but testosterone has, due to its aromatization to estradiol (19). Prolactin secreting tumors, or prolactinomas, are often associated with gyno. But in these cases the prolactin is believed to induce gyno by suppressing testosterone production: “Prolactinomas that are sufficiently large to cause gynecomastia do so as a result of impairment of gonadotropin secretion and secondary hypogonadism”. (20). However, this is a moot issue in AAS users whose gonadotropin secretion is already blunted.
According to research cited in (20), prolactin may have a direct stimulatory effect on mammary tissue development, but only in the presence of high estrogen levels:
The presence of mild hyperprolactinaemia is therefore not uncommon in patients with estrogen excess. Significant primary hyperprolactinaemia, on the other hand, may directly stimulate epithelial cell proliferation in an estrogen-primed breast, causing epithelial cell proliferation and gynaecomastia.
So rather than focusing solely on lowering prolactin levels which may be elevated in users of aromatizing androgens, attacking estrogen should be the first line of action.
GH and IGF-1 are considered critical to the proliferation of mammary tissue. An excellent review of the role played by these hormones, as well as a general overview of gynecomastia can be found here:
Since elevated GH and IGF-1 are considered important to the anabolic effect of AAS, it would be impractical and counterproductive to attempt to prevent gynecomastia by blocking GH/IGF.
Progesterone acts in concert with estrogen to promote breast development, and at least part of any role played by synthetic progestins may be to stimulate IGF-1 production in the breast. But again, blocking the action of progesterone or synthetic progestins is not practical. Specific progesterone receptor antagonists like RU-486 block not only the progesterone receptor, but the androgen receptor as well, and have actually been associated with the development of gynecomastia (21). In any case, progesterone is thought to act on the breast to enhance the effects of estrogen (22) so once again, attacking estrogen is the easiest and most logical approach.
DHT gel (Andractim) or a generic knockoff might help as well. DHT is thought to act as an aromatase inhibitor (23) and perhaps compete directly with estrogen for binding at the estrogen receptor (24). DHT has been used in several case reports and controlled trials to successfully treat gynecomastia. So perhaps a viable strategy would be to combine DHT gel with tamoxifen. I would recommend tamoxifen rather than an aromatase inhibitor due to the simple fact that tamoxifen has been widely used in numerous controlled studies to succesfully treat gynecomastia, whereas the evidence to support the efficacy of aromatase inhibitors is scanty at best."Comment
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do you think countinuing nolva and add armidex would help? then maybe stop the nolva and countinue the adex?Comment
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It was Hooker aka Anthony Roberts who came up with the bullshit about nolvadex in the first place. So consider the source of(mis)information.ADMIN/OWNER@Peak-MuscleComment
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do you have gyno problems? if not dont worry about it until you do - way to many guys are adding things for gyno who do not even see gyno symptoms - many have nothing more than over active glands and thi8nk its gyno so they start taking all kind sof extra stuff they dont even needOriginally Posted by Doink the clown;
"Every gym has the tard who never gets bigger,never shuts up,and never goes away!"
"If you say you are not afraid to die either your lying or your a Ghurka,"
"Amatures built the Ark - professionals built the Titanic."Comment
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like i said im not sure my nipples just get hard and a lil tiny puffy and sensitive im going to cuba the last thing i want is to go jack with bitch tits lolComment
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can i do adex eod? throught my cycle or should i be doing it ed?Comment
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Originally Posted by Doink the clown;
"Every gym has the tard who never gets bigger,never shuts up,and never goes away!"
"If you say you are not afraid to die either your lying or your a Ghurka,"
"Amatures built the Ark - professionals built the Titanic."Comment
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