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Making Estrogen Work For You.

Nimrod25

New member
There are both positive and negative side effects when testosterone converts to estrogen. That is why using androgenic gear is more effective on bulking cycles. The main goal is to limit the conversion of estrogen from testosterone so that the negative side effects of excessive estrogen are minimized. The most common method to regulate estrogen levels are two drugs, Arimidex, and Femara. They both inhibit the enzyme that converts testosterone to estrogen.

It is a know fact that high androgens are very effective for mass, and also have the highest aromatization rates.
Aromatse inhibitors are very effective when on high androgen cycles, but when trying to put on size estrogen is needed, therefore inhibiting it too much is counter-productive.
Another drug that is sometimes called an "estrogen blocker", is nothing more than an androgen. That drug is called proviron.

Proviron works to limit estrogen in the same way that all non-aromatizing androgens limit testosterone conversion to estrogen.
The conversion process happens when the testosterone molecule attaches to the aromatase receptor and there an enzyme breaks the chemical down to produce estrogen. If you have another androgen that will bind to that receptor, that won't convert to estrogen, you are blocking the aromatase receptors and therefore cutting back on the conversion process.

Taking proviron on cycle is not a good idea at all, because it will also bind to androgen receptors in the muscles and therefore take up receptor space where stronger androgens could be creating growth. Two other drugs worth mentioning are clomid and nolvadex. Both of these drugs bind to the estrogen receptor site, and block estrogen from binding to these sites.

The main problem with these drugs is estrogen rebound. Once the drugs are discontinued all the estrogen that was not broken down by the liver will begin atttaching to estrogen receptors. This can be avoided by continuing drug use a number of weeks post cycle.

It should also be mentioned that all anti-estrogens have an effect on IGF-1 levels, which are also very important when trying to build muscle. The following chart shows this effect.

Femara - increases IGF-1 by 24%
Arimidex - decreases IGF-1 by 18%
Nolvadex - decreases IGF-1 by 23.5%
Faslodex - decreases IGF-1 by 70%

My advice would be to use anti-estrogens only when necessary, especially proviron and nolvadex. Drugs like arimidex and femara are your best bets, but always start out with low doses and gradually increase until you have received the desired effect.
By limiting estrogen only to the point of avoding side-effects you can secure greater gains in mass and strength.
 
good info. Femara is also cheaper than armidex per tab... What dose do you think is good? Would half a tab a day be comparable to half an armidex a day?
 
Well Femara comes in 2.5mg tabs, which I think is more than enough. I would start with 1/2 tab and increase dose as necessary.
 
How hard is femera to get? I've never seen it on a sources list b4! Also then what you are saying is that proviron would be better after the cycle, right? Also would taking proviron post cycle effect HPTA recovery?
 
You need a script for Femara, it's not very well known, so sources don't have it on their lists.
Also, Proviron doesn't compete for AR in muscles, so there's no reason not to use it.
And don't worry too much about Arimidex lowering your IGF-1 level slightly, it is overcompansated by boost of it by Testosteron you use in cycle.
 
panerai said:
What about Cytadren, how does it effect IGF-1 level?

Cytadren was not mentioned directly in the study, but it is believed to increase IGF-1 to an amount similar to femara.
I did not mention cytadren, because it is not a newbie drug due to the possiblity of desmolase inhibition and cortisol rebound.

Torch said:
So its not a good idea to take proviron during cycle?

If two drugs are both competing for the AR, that is fine as long as both drugs are effective anabolics. Proviron is not.


Never Enough said:
How hard is femera to get? I've never seen it on a sources list b4! Also then what you are saying is that proviron would be better after the cycle, right? Also would taking proviron post cycle effect HPTA recovery?

Femara is cheaper than arimidex, but not widely available. Like most anti-e's it is prescription only, but legal for personal use.
Also, I do not see any need for proviron, unless no other anti-gyno agents are available.
 
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panerai said:

Also, Proviron doesn't compete for AR in muscles, so there's no reason not to use it.

While most of the drug does not reach the AR in muscle tissue because it is enzymatically converted to the diol, the small amount that does has strong binding to the AR.
 
I was wondering why estrogen settles in my stomach area. I'm starting to get love handles. I heard it was estrogen build up and not fat.
 
monstar said:
I was wondering why estrogen settles in my stomach area. I'm starting to get love handles. I heard it was estrogen build up and not fat.

There are a large number of estrogen receptors in that area, which is why BF can increase on high androgen cycles without the use of an anti-estrogen, aside from just eating an extreme number of calories. Estrogen fat deposits are very stubborn. Try hitting a cutting cycle, increase cardio, adjust diet, and add in some topical yohimbine.
 
Nimrod25 said:
The main problem with these drugs is estrogen rebound. Once the drugs are discontinued all the estrogen that was not broken down by the liver will begin atttaching to estrogen receptors.

This is exactly why people use proviron to combat the onset of gyno when on high androgen cycles (or if you're simply prone to it). Proviron has no rebound and effectively prevents the creation of estrogen rather than merely treating the symptoms the way Nolvadex does.

To me it makes sense to keep both on hand to combat gyno. Proviron can also be used to enhance sex drive if you're using too much progesterone AS in your cycle.

I might be all wrong, of course, but I've read about these products in quite a few places. Some guys are adamant about running both during certain phases of their cycles.
 
I see your point, but I would not use proviron if I could get arimidex or femara, they are both superior. Also, proviron was not proven to eliminate PR related libido problems.
 
I can't remember where, but I've see Letrozole (Femara) 2.5mg tabs were around $140 for 30. Do a search, and I'm sure you can find it. Some places you need a script, others you don't.
 
Nimrod25 said:
I see your point, but I would not use proviron if I could get arimidex or femara, they are both superior. Also, proviron was not proven to eliminate PR related libido problems.

Kinda like saying you'd skip the Chevy if a Mercedes were handy. Quite a price difference between Arimidex and the proviron/nolvadex combo. I realize anything is cheaper than gyno surgery, but ...
 
Nimrod25 said:


While most of the drug does not reach the AR in muscle tissue because it is enzymatically converted to the diol, the small amount that does has strong binding to the AR.

That's right, it does converts to diol, so it's deactivated. As for strong affinity to the AR...it doesn't make any difference. Will using Masteron with Test limit your gains? No way! You simply won't gain from Masteron, but still will gain same if not more from Test. Same with Tren...
If you are using 2g of Test instead of 500mg, you will get considerably greater gains, so what competition for AR are we talking about, here?
 
As for Cytadren, here we go:

Influence of tamoxifen, aminoglutethimide and goserelin on human plasma IGF-I levels in breast cancer patients.

J Steroid Biochem Mol Biol 1992 Mar;41(3-8):541-3 (ISSN: 0960-0760)

Lien EA; Johannessen DC; Aakvaag A; Lonning PE [Find other articles with these Authors]
Medical Department, Haukeland University Hospital, Bergen, Norway.

Plasma insulin-like growth factor-I (IGF-I) was measured in breast cancer patients before and during treatment with tamoxifen, goserelin or aminoglutethimide. 24 out of 27 postmenopausal women treated with tamoxifen 20 or 30 mg daily experienced a decrease in plasma IGF-I levels (mean levels before treatment 14.8 nM, during treatment 10.2 nM, P less than 0.001). In 8 out of 12 premenopausal breast cancer patients there was a reduction in plasma IGF-I during treatment with goserelin (mean levels before treatment 23.3 nM, during treatment 19.4 nM, P = 0.052). Contrary, 15 out of 17 postmenopausal women treated with the aromatase inhibitor aminoglutethimide had an increase in plasma IGF-I level (mean level before treatment 17.0 nM, during treatment 21.1 nM, P less than 0.01). These preliminary results indicate that different forms of endocrine treatment of breast cancer may influence plasma IGF-I levels in different directions.
--------------------------------------------------------------------------------

So, Cytadren increases IGF-1 level by 23%, which is practically the same as Femara, and it's much less expensive.
Liquidex still is the best choice.
 
panerai said:


So, Cytadren increases IGF-1 level by 23%, which is practically the same as Femara, and it's much less expensive.
Liquidex still is the best choice.

Ok I see that, but the risk of sides with cytadren are much greater than that of any other aromatse inhibitor.
 
quote:
--------------------------------------------------------------------------------
Originally posted by panerai


So, Cytadren increases IGF-1 level by 23%, which is practically the same as Femara, and it's much less expensive.
Liquidex still is the best choice.
--------------------------------------------------------------------------------



"Ok I see that, but the risk of sides with cytadren are much greater than that of any other aromatse inhibitor."

What sides are you talking about? Aromatase inhibition occurs at around 150-250mg/day, while desmolase inhibition doesn't happen until one gets into the gram range.

Cytadren is a useful drug that has a bad reputation.
 
cockdezl said:
quote:

What sides are you talking about? Aromatase inhibition occurs at around 150-250mg/day, while desmolase inhibition doesn't happen until one gets into the gram range.

Cytadren is a useful drug that has a bad reputation.

That is all well and good for guys that know what they are doing.
This post was intended to clear up misconceptions among newbies. I think you will agree that cytadren is not a beginners drug.
 
Actually, Cytadren is good for newbies, because they use usually around 500mg/week of aromatics(Test, or Test+ dbol). In this range, 250mg/day of Cytadren is perfect amount to not only prevent gyno but also to prevent most of the water retention.
Of course, they need to do a little research to know what they are dealing with and how to use it properly, but it applies also to any drugs and if they are using steroids, they should be ready to investigate everything, including anti-estrogens, no big deal, being newbie is not an excuse.
A little different story is for someone who uses 1500mg/week of Test, on a top of 50-100mg of dbol and may be some EQ, or whatever.
Anyway, from my personal experience: I've used 1200mg/week of Test with 60mg/day of dbol, starting with 500mg/day of Cytadren, tapering it down 125mg/every 3 week, to 250mg/week but discontinuing dbol at that point. No signs of gyno, of course, and water retention wasn't too bad, easy to tolerate.
-----------------------------------------

As for Proviron, I don't think, it's a bad choice. First of all, it doesn't effect gains negatively, that's outdated info. Second, it's very good(especially, considering the price!) aromatise inhibitor. Third, it keeps user hard and dry, better then other aromatise inhibitors(for diff reason, but still, it does). Fourth, as a man, you will feel good...very good, all the time, hehe...
And, fifth...again, price is very nice!
 
_____________________________________________
Taking proviron on cycle is not a good idea at all, because it will also bind to androgen receptors in the muscles and therefore take up receptor space where stronger androgens could be creating growth.
_____________________________________________

In theory maybe, assuming one is taking enough of the stronger androgen to saturate androgen receptors. If not, proviron shouldn't hurt gains at all.

(Is this just a theory or is their clinical evidence backing this?)
 
Nimrod, can you explain why Femara can increase IGF-1 levels since its an anti-estrogen?

Is taking nolva at 10mg ed too high a dosage?
 
yiyangzhi said:
Nimrod, can you explain why Femara can increase IGF-1 levels since its an anti-estrogen?

Is taking nolva at 10mg ed too high a dosage?

I have attached the study about femara.
I would not use nolvadex unless needed.
Get some arimidex or liquidex

Femara(letrozole) - potent aromatise inhibitor, easily available, slightly less expensive then Arimidex, but cost a little more then Liquidex.

The aromatase inhibitor letrozole in advanced breast cancer: effects on serum insulin-like growth factor (IGF)-I and IGF-binding protein-3 levels.
J Steroid Biochem Mol Biol 1997 Nov-Dec;63(4-6):261-7 (ISSN: 0960-0760)
Bajetta E; Ferrari L; Celio L; Mariani L; Miceli R; Di Leo A; Zilembo N; Buzzoni R; Spagnoli I; Martinetti A; Bichisao E; Seregni E [Find other articles with these Authors]
Medical Oncology B Division, Istituto Nazionale per lo Studio e la Cura dei Tumori, Milan, Italy.
Serum insulin-like growth factor (IGF)-I and IGF-binding protein-3 levels were measured in two groups of postmenopausal women with advanced breast cancer, who received the aromatase inhibitor letrozole 0.5 or 2.5 mg p.o. once daily. Blood samples were obtained from 15 patients in each dose group at baseline, and one and three months after starting therapy. Circulating IGF-I and IGFBP-3 concentrations were determined by means of radioimmunoassay. In both dosage groups a statistically significant increase in the IGF-I levels was observed during three months of letrozole treatment (P=0.003). In addition, the multiple testing procedure yielded in the whole patient population a significant result in the comparison between mean IGF-I values after three months of therapy and those observed at baseline (P=0.004), the estimated average increase being of 24%. No significant result was obtained in the analysis for the dose effect (P=0.077) and for the time x dose interaction (P=0.208). Circulating IGFBP-3 levels did not appear to be affected by letrozole treatment in either of the dose groups. This is the first report concerning the short-term effects of letrozole on components of the IGF system in breast cancer patients; further investigations are warranted in order to confirm these preliminary data.
 
Nimrod,

I always use 25mg/day of proviron all through my cycle and until i start clomid therapy - never had any gyno symptoms and have gotten solid gains. I would like to know more about loss of effectiveness of AS when on proviron as all I've come up with so far is really anedotal evidence. Your logic make sense but if you have any references i'd love to see them.


Great posts by the way - i think i actually felt my brain stretch.!
 
I personally do not like proviron, but I am done bashing it because i think panerai wants to ring my neck. The theory on proviron is just that, a theory. I have no evidence to prove it, and there are alot of good arguments here against me. I have talked with numerous vets from other boards about this subject and have gotten mixed reactions. I am far from done looking into this topic, so ill let u know.
 
panerai said:
Oh my god...I'm speechless...
We just having freindly discussion, don't make me into a bad guy. :)

Not the bad guy at all, I love contradicting opinions, because it gets me thinking. Especially when coming from a man of your knowledge and stature. To be perfectly honest, I love reading your responses.
 
something to ponder.. high levels of IGF may(this and other growth factors have been implicated) = aggravation and GROWTH of hard glandular tissue (true gyno)
 
macrophage69alpha said:
something to ponder.. high levels of IGF may(this and other growth factors have been implicated) = aggravation and GROWTH of hard glandular tissue (true gyno)

ponder indeed........hmm........what do you think Nim and Panerai?
 
Nimrod25 said:


No, it is an effective anti-gyno agent, but not my first choice.

It is the BEST choice for progesterone-based AAS cycles
because of its libido-boosting abilities.

And what on earth is Fasloden????(70%IGF-1 increase!!!!!
OK.....)

Fonz
 
Nimrod25 said:
I see your point, but I would not use proviron if I could get arimidex or femara, they are both superior. Also, proviron was not proven to eliminate PR related libido problems.

It might not have been clinically proven in a laboratory situation, but I've used it, and as far as I'm concerned it's the best thing available for any kind of libido poroblems, fast, effective, and cheap. Arimidex, Femara, Nolvadex, even Clomid are bets during a cycle, but when you're comming off, Proviron has a very beneficial effect not only if you have libido problems from long cycles, but also to to avoid the estrogen rebound you can get from using nolvadex etc. It definitely has it's uses, I'm a big fan of Proviron. I always wonder when I hear studies about the effectiveness of products, moistly they are paid for by someone wit a vested interest in the outcome, and often they contradict real world experience, so I take it all with a grain of salt....the Proviron debate has been going on forever and it will probably keep going like the energizer bunny lol!:)
 
I thought the "competition at the AR" concept was
disproven???
Bill Roberts has said many times that different roids
CANNOT cancel each other out.(such as stacking deca/tren)
Llewellyn is a proponent of proviron as well,if I'm not mistaken.
 
Taking proviron on cycle is not a good idea at all, because it will also bind to androgen receptors in the muscles and therefore take up receptor space where stronger androgens could be creating growth.

"All androgens are "full agonists"... if they are bound to the receptor they are all just as good as each other. It is like turning on a light switch: the receptor is activated, or not. It changes to the conformation that makes it bind to DNA and increase mRNA synthesis and therefore protein synthesis: or it does not.

There is never an issue of reducing effect of anabolic steroids by adding more anabolic steroids of a different kind. "
-Bill Roberts
 
Also,the way I understood it,receptors don't "soak" up
the available androgen but are turned on depending on
the plasma androgen level.
Roberts said something like:1000mg of test saturates like 90%,
2000mg saturates 95% and so on.You can never quite reach
100% though.
 
"the percent of receptors occupied is independent of the number of receptors. It is dependent only on the binding constant between the receptors and the steroid, and the concentration of free steroid.
That wouldn't be the case if there were many receptors relative to how many molecules of steroid -- in that case, having more receptors could appreciably deplete the concentration of free steroid -- but in this case the number of molecules of steroid outnumbers the number of receptors by, I don't recall, millions or billions to one, so the concentration of free steroid doesn't change at all significantly as a result of number of receptors changing, so the percent occupancy remains the same. "
-bill roberts
 
While your stats for decreases in igf-1 levels may be accurate for normal humans, those taking large doses of steroids will already have increased igf-1 levels and the decreases in igf-1 from any anti aromatase will be insignificant.

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