Aromasin for PCT

Researchstop · Apr 21, 2009

Sure you could. But since Nolva lowers your GH and IGF it's not a good idea.

VitoBrata · Apr 21, 2009

Researchstop said:
Sure you could. But since Nolva lowers your GH and IGF it's not a good idea.

Questions for you.

1- Is Nolva the only Anti E that has this effect?

2- On a scale of 1-10 where would you rate Clomids effectiveness as an anti Estrogen?

3- Is Aromasin not considered as useful on PCT on a stand alone basis as Clomid?

4- If Letrozole is more potent as an anti E than Arimidex why not use it at a lower dosage?

5- What would you outline as the ideal PCT when HCG is not to be employed?

Thanks

Slayerxx · Apr 21, 2009

a

Aromasin is an excellent PCT choice and what I have found an excellent drug to take if you decide to stop AAS all together if being on many years.
Aromasin lowers estrogen blood levels by 80%. Raises test by 60% lowers bad cholesterol and raises good cholesterol along with raising IGF-1 levels...find another anti-e that does this..it may lower estrogen a bit too much, but IMO its a great drug

617ricky · Apr 21, 2009

Slayerxx said:
it may lower estrogen a bit too much, but IMO its a great drug

This is what I hear alot.. Now a low dose would be considered 12.5mg, but I'm thinking of starting it at 6.25mg.. At this dosage it's not gonna lower it too crazy, right?

Conciliator · Apr 21, 2009

Macro said:
tamoxifen's action is actually estrogenic, the heightened release of GnRH is via estrogenic priming. so if you are producing LH or taking hcg, it will amplify those effects. if you are not... well there is no evidence that it stimulates LH release as clomiphene does.

Estrogen priming? You do realize we're talking about males, right? Men don't have a preovulatory period or spikes in LH. Reference works like Grossman's Clinical Endocrinology explain that in contrast to the positive feedback that estrogen has in the pituitary of females, "In males, the situation is more straightforward... Oestrogens in the male reduce pituitary responsiveness to GnRH." That's also what you'll find in the most recent research looking at the suppressive effects of testosterone and estrogen in the pituitary and hypothalamus of men. Accordingly, an increase in the LH response to GnRH would appear to be from ER antagonism.

However, if you have any research showing that estrogen "primes" the pituitary in human males, I'd love to see it.

Macro said:
the primary issue with tamoxifen is in cases were there is either high level progesterone synthesis suppression or progesterone from removal of offending compound, its upregulation of PgR expression can cause a lot of different issues. upregulated PgR in the absence and overabundance of progesterone are both problematic and likely why tamoxifen has been linked to numerous cases of post cycle gyno.

The progesterone receptor is synthesized in response to estrogen, so in tissues where tamoxifen exerts a weak estrogenic effect upregulation of the progesterone receptor would be expected. That includes the endometrium, which is a tissue that's highly sensitive to estrogen. It's no surprise that several studies have found that tamoxifen upregulates the progesterone receptor in the endometrium. But what about in mammary glands, where tamoxifen is an estrogen receptor antagonist? When tamoxifen is administered to treat breast cancer, there is not upregulation, but a downregulation of both the estrogen and progesterone receptors (at least for a good while until the cancers become resistant).

If you have any research showing that tamoxifen upregulates the progesterone receptor in the breast (which is what the worry seems to be about), I'd love to see it.

Conciliator · Apr 21, 2009

terryd5150 said:
Nolvadex isn't an anti-estrogen. It is a SERM (Selective Estrogen Receptor Modulator).

Do yourself a favor and search for "antiestrogen tamoxifen" (with quotes) on pubmed. Note the hundreds of academic papers that refer to tamoxifen as an antiestrogen.

That doesn't mean it's not a SERM. It means it has at least some effect as an estrogen antagonist. It's frequently referred to as an "antiestrogen" because that's what it's primarily used for.

Researchstop · Apr 21, 2009

VitoBrata said:
Questions for you.

1- Is Nolva the only Anti E that has this effect?

2- On a scale of 1-10 where would you rate Clomids effectiveness as an anti Estrogen?

3- Is Aromasin not considered as useful on PCT on a stand alone basis as Clomid?

4- If Letrozole is more potent as an anti E than Arimidex why not use it at a lower dosage?

5- What would you outline as the ideal PCT when HCG is not to be employed?

Thanks

1. That I have seen. Yes.
2. It's weak and should not be used an anti-e in the traditional sense.
3. Aromasin should be used in conjunction with Clomid. They serve two different purposes even though some aspect of the two are similar.
4. You SHOULD use Letro over Arimidex. I don't recommend using Arimidex.
5. Depends on the cycle. I think I've answer that question in relation specific cycles several times. Note: for most cycles, there is no "ideal" PCT without HCG.

terryd5150 · Apr 21, 2009

Conciliator said:
It's frequently referred to as an "antiestrogen" because that's what it's primarily used for.

Bro, I don't need to do any research. Having "anti-estogen"-like effects, and being an actual anti-estrogen are not the same thing.

Nolvadex itself IS an estrogen. It will not reduce your estrogen levels.

Conciliator · Apr 21, 2009

terryd5150 said:
Bro, I don't need to do any research. Having "anti-estogen"-like effects, and being an actual anti-estrogen are not the same thing.

No, you definitely do need to do some research. Make that query on pubmed. You need to learn that when something is an estrogen receptor antagonist, it is acting as an "anti-estrogen."

terryd5150 said:
Nolvadex itself IS an estrogen.

It depends on the tissue. Tamoxifen is a mixed agonist/antagonist. In breast tissue, tamoxifen is an antagonist. It does not exert an estrogenic effect, but acts as an anti-estrogen (which is why people refer to it as such). In other tissues it exerts a weak estrogenic effect. That's why it's called a "selective" modulator of the estrogen receptor. It's selective, depending on the tissue.

terryd5150 said:
It will not reduce your estrogen levels.

Well you've got a problem on your hands then. Fulvestrant doesn't reduce estrogen levels either. It competitively binds to the estrogen receptor as an ER antagonist. It is not selective. And you know what it's called? A "pure anti-estrogen". (That's in contrast to tamoxifen, which is sometimes called a "partial", "mixed", or "selective" anti-estrogen.)

You really need to learn that anti-estrogens include compounds that not only prevent the synthesis of estrogen, but also response to estrogen (as competitive antagonists).

Macro · Apr 22, 2009

Conciliator said:
However, if you have any research showing that estrogen "primes" the pituitary in human males, I'd love to see it.
.

1: Mol Endocrinol. 2008 Oct;22(10):2250-9. Epub 2008 Aug 13. Links

Erratum in:
Mol Endocrinol. 2009 Mar;23(3):423.
Converse regulatory functions of estrogen receptor-alpha and -beta subtypes expressed in hypothalamic gonadotropin-releasing hormone neurons.Hu L, Gustofson RL, Feng H, Leung PK, Mores N, Krsmanovic LZ, Catt KJ.
Endocrinology and Reproduction Research Branch, PDEGEN, National Institue of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892-4510, USA.

Estradiol (E(2)) acts as a potent feedback molecule between the ovary and hypothalamic GnRH neurons, and exerts both positive and negative regulatory actions on GnRH synthesis and secretion. However, the extent to which these actions are mediated by estrogen receptors (ERs) expressed in GnRH neurons has been controversial. In this study, Single-cell RT-PCR revealed the expression of both ERalpha and ERbeta isoforms in cultured fetal and adult rat hypothalamic GnRH neurons. Both ERalpha and ERbeta or individual ERs were expressed in 94% of cultured fetal GnRH neurons. In adult female rats at diestrus, 68% of GnRH neurons expressed ERs, followed by 54% in estrus and 19% in proestrus. Expression of individual ERs was found in 24% of adult male GnRH neurons. ERalpha exerted marked G(i)-mediated inhibitory effects on spontaneous action potential (AP) firing, cAMP production, and pulsatile GnRH secretion, indicating its capacity for negative regulation of GnRH neuronal function. In contrast, increased E(2) concentration and ERbeta agonists increase the rate of AP firing, GnRH secretion, and cAMP production, consistent with ERbeta-dependent positive regulation of GnRH secretion. Consonant with the coupling of ERalpha to pertussis toxin-sensitive G(i/o) proteins, E(2) also activates G protein-activated inwardly rectifying potassium channels, decreasing membrane excitability and slowing the firing of spontaneous APs in hypothalamic GnRH neurons. These findings demonstrate that the dual actions of E(2) on GnRH neuronal membrane excitability, cAMP production, and GnRH secretion are mediated by the dose-dependent activation of ERalpha and ERbeta expressed in hypothalamic GnRH neurons.

for more on eralpha erbeta potentials
http://www.pnas.org/content/96/7/3999.full?ck=nck

though there is also the differential effect on gonadal tissue

note- this merely lays out differentials, other factors like igf-1 suppression may be as relevant to priming/release potentials.

but if you are looking for silver bullet study... not really one out there.

Macro · Apr 22, 2009

Conciliator said:
It depends on the tissue. Tamoxifen is a mixed agonist/antagonist. In breast tissue, tamoxifen is an antagonist. It does not exert an estrogenic effect, but acts as an anti-estrogen (which is why people refer to it as such). In other tissues it exerts a weak estrogenic effect. That's why it's called a "selective" modulator of the estrogen receptor. It's selective, depending on the tissue.

this is not entirely accurate. it is somewhat tissue specific, in the context of the "norm" of ER isoform expression as well as presenting promoter sites and unliganded binding of other active hormones. those tissue specific are generalizations and there are many exogenous and endogenous factors that can alter that response. Note- breast tissue in females is NOT the same as breast tissue in males, because of androgenic and differential progestenic regulation of tissue presentation and growth.

Conciliator · Apr 22, 2009

Conciliator said:
However, if you have any research showing that estrogen "primes" the pituitary in human males, I'd love to see it.

Macro said:
1: Mol Endocrinol. 2008 Oct;22(10):2250-9. Epub 2008 Aug 13. Links

Umm, that's not looking at the pituitary. That paper doesn't talk about leutinzing hormone even once, let alone LH responsiveness to GnRH. Do you have anything showing that estrogen "primes" the pituitary in any male species?

Conciliator said:
but if you are looking for silver bullet study... not really one out there.

Silver bullet study? How about even a rat study? Anything at all that supports your claim that there's "estrogenic priming" in the male pituitary? Anything that would suggest the most recent human reasarch is somehow incorrect or misleading?

Also, any comment on the claim that tamoxifen upregulates PgR expression in the breast? That "danger" has sure been tossed around a lot lately.

Conciliator · Apr 22, 2009

Macro said:
this is not entirely accurate.

It's accurate enough (and general enough) that it's stated almost ubiquitously in the literature, notwithstanding isolated or specific differences in the modulation of co-regulator binding.

Macro said:
Note- breast tissue in females is NOT the same as breast tissue in males, because of androgenic and differential progestenic regulation of tissue presentation and growth

It's different, but tamoxifen still acts as an antagonist in the male breast as well. As I'm sure you're aware numerous studies have shown that tamoxifen is effective in treating male gynecomastia.

02052007 · Apr 22, 2009

Researchstop said:
Note: for most cycles, there is no "ideal" PCT without HCG.

What type of cycle would be okay without HCG in the PCT protocol?

Macro · Apr 22, 2009

Conciliator said:
It's accurate enough (and general enough) that it's stated almost ubiquitously in the literature, notwithstanding isolated or specific differences in the modulation of co-regulator binding.
It's different, but tamoxifen still acts as an antagonist in the male breast as well. As I'm sure you're aware numerous studies have shown that tamoxifen is effective in treating male gynecomastia.

actually, its only effective with central mass. and then only in shrinkage, not apoptosis beyond. Though would not mind seeing a study with tamoxifen and calorie restriction to see if that improves response (maintainance and certainly calorie surplus, creates an environment of hormonal influence not well suited to regression and apoptosis.

and the studies are not exactly numerous. again, because differing tissue types have differing expression of ER subtypes, tamoxifen does not act like an ER agonist in all of them. PLUS, under the influence of other hormones and/or suppression of endogenous hormones (progesterone in particular) or other signalling factors, even in tissue in which its normally an antagonist it can have either superceded activity (PRL transactivation of eralpha) or shift toward weak/even strong agonism.

Macro · Apr 22, 2009

btw- its generally accepted practice to call tamoxifen and other serms "anti-estrogens", though IMO its misnomer. but again not at all, outside of clinical practice or discourse.