anti-e's and anti-aromatisers?

hey guys
i have researched like a mad man the past year. i have read many things concerning anti-e's and anti-aromatisers. i am confused about one thing though. what is the deal with them hindering gains during a cycle? is this really true? if so, please explain the logic behind it. i just don't understand how they could hinder gains if all they do is block out estrogen or stop aromatising. is it because they block certain receptors that the roids would normally attach to? i don't know. anyway, thanks in advance.
flex

You must weigh the options....sides vs. gains...If you are prone to gyno, then there is no option....

Nolvadex is a competitive inhabitor of estrogen, meaning it fights for the recepter sites...whereas Armidex/Liquidex is a non-competitive inhabitor of estrogen....it plain shuts it down....peroid!

Using Clomid and nolvadex on a cycle will greatly reduce water retention, this is looked upon as a gain per-sey.....water equals extra strength, this leads to more intensity, creating greater muscle mass. It has been proven it also reduces IGF-1 production....this is a must for growth....

How much gains are lost will depend on the cycle, dosages, amount of anti-estro's....etc. BUT, my personal thoughts are this....

Ranger's Word's:

" I'd rather sacrafice 10 pounds of water weight, than add 5 pounds of titties..."

Heh heh heh....That's pretty much it, in a round about way Bro....*wink*

Ranger

Spoken like a true "RANGER"!!!! :cool:

thanks for clearing that up.
what about proviron though. that is an anti-aromatiser, right? does this hinder gains also? and water weight sucks anyway if you are trying to get cut, right? therefore, i would imagine that for a cutting cycle, using nolva or clomid or whatever wouldn't matter. in fact, it would probably benefit, right? (less water retention=more cut muscles)? the only downside that you mentioned that did strike me as a true con, was the proven fact that they lower the igf-1 production. that just plain out sucks!! does proviron do this too?? thanks.
flex

bump
and one more thing, does proviron act more like arimidex or nolvadex??

not sure about the arimidex relationship but it is more than a receptor blocker which is what nolva is, it effects the estrogen more so than the receptors.
ss

so if proviron and arimidex don't mess with receptors, then do they really hinder gains? or does it not matter? i mean, is it the estrogen that causes the water retention, which is looked upon as gains? also, do these 2 mess with igf-1 production? thanks.
flex

proviron acts like arimidex(anastrozole) but to alot lesser degree ,they both act as an aromatase inhibitor ,proviron will get you horny as a mother fu**er and won't effect your igf-1 but isn't as good as arimidex and i've seen that arimidex will effect your igf-1 level's by around 15-30 percent but you won't have to worry about estrogen plus AS increse igf-1 level's so most people don't worry about the igf-1 decresing effects.but there's a product called femara (letrozole) which act's the same way and is as good as arimidex but which actually increase's igf-1 by 24%. and is also cheaper than arimidex but not as cheap as liquidex. so i prefer fermara myself.

bigchewy

arimdex will not hinder any gains except water related, proviron is a wholly diff mechanism - nolva is the only one that will slightly inhibit gains - clomid during cycle is useless, there is no way to keep test up during exogeneous supplementation.

Quote:

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Originally posted by flexshack
so if proviron and arimidex don't mess with receptors, then do they really hinder gains? or does it not matter? i mean, is it the estrogen that causes the water retention, which is looked upon as gains? also, do these 2 mess with igf-1 production? thanks.
flex

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YES

I saw a study that Arimidex decreases your IGF-1 pretty drastically. There is another anti-estrogen can't remember the name but it does not mess with IGF-1 production, but its rare and very expensive.

adaptek look at my reply above.

I disagree bro, clomid during a cycle is not useless. Clomid acts as an anti estrogen albeit a weak one but if that is all you got then it is better than nothing. As for keeping test up while "supplementing" you are right for that clomid is useless.

Quote:

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Originally posted by CYCLEON
arimdex will not hinder any gains except water related, proviron is a wholly diff mechanism - nolva is the only one that will slightly inhibit gains - clomid during cycle is useless, there is no way to keep test up during exogeneous supplementation.

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Point taken, Kiser but there is no reason anyone should take clomid during - at least they should be taking nolva instead, save clomid till after. arimdex is best during of course but if its a concern get nolva at the least - forget about using the clomid during. thats my opinion anyway. :D

Quote:

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Originally posted by bigchewy
adaptek look at my reply above.

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Fuck man, sorry about that, your shit is pretty accurate. fermara is the name. I need some, whats the cost.. where do you get it?

Its not a controlled substance is it? I am sure my pharmacies here should have it.

Thanks

I think this thread started by Nimrod25 a few months back answers part of your question:

Making Estrogen Work For You

Aromatase 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 avoiding side-effects you can secure greater gains in mass and strength.

This was an article about the powerful Femara as an aromatase inhibitor:

Femara Effective In Postmenopausal Women With Advanced Breast Cancer

EAST HANOVER, NJ -- February 5, 1998 -- Clinical data published in this month’s Journal of Clinical Oncology show Novartis Pharmaceuticals Corp.’s Femara(TM) (letrozole tablets, USP) 2.5 mg once-a-day therapy to be an effective treatment of advanced breast cancer in postmenopausal women with disease progression following antiestrogen therapy.

The study was an international double-blind trial of 551 advanced breast cancer patients. These patients were randomised to one of three treatment arms: 0.5 mg Femara, 2.5 mg Femara or 160 mg of megestrol acetate (MA). The study showed that 2.5 mg Femara once daily to be effective and generally well-tolerated in postmenopausal women with disease progression following antiestrogen therapy (for example, tamoxifen).


"In the advanced disease setting when antiestrogen therapy fails, it is vital to have additional treatment options," said David Parkinson, MD, vice president of clinical research at Novartis Pharmaceuticals. "These data demonstrate that Femara may be an effective option to help shrink tumours or slow the progression of the disease in postmenopausal women for whom antiestrogen therapy has failed."


In the study, an objective (complete or partial) response to treatment was demonstrated in approximately 24% of those receiving Femara 2.5 mg and in approximately 16% of those receiving megestrol acetate. The study also showed that the median duration of response had not been reached with Femara 2.5 mg; the median duration of response for megestrol acetate had been reached at 18 months.


This trial showed that Femara was generally well tolerated. The most common adverse effects with 2.5 mg Femara were musculoskeletal pain, nausea, headache, arthralgia (joint pain), fatigue, vomiting, and dyspnea (breathing difficulty).


Typically in treating breast cancer, hormone therapies such as antiestrogens and aromatase inhibitors may be used to block actions of hormones, such as estrogen, that stimulate the growth of hormone-dependent cancer cells. Antiestrogens, such as tamoxifen, block estrogen from stimulating cancer cells by binding to estrogen receptors in the cancer cells.


Rather than blocking estrogen from reaching the estrogen receptor sites in cancer cells, aromatase inhibitors reduce the amount of estrogen circulating in the body. As an aromatase inhibitor Femara binds to the enzyme aromatase and inhibits it from converting a precursor hormone -- androstenedione -- to estrogen in tissues, such as fat, liver and muscle.


Women whose disease cannot be controlled by antiestrogen therapy may be switched to other hormone therapies, including aromatase inhibitors. In postmenopausal women, the aromatase pathway is the primary source of estrogen production. According to a recent report, nearly 120,000 U.S. women are living with advanced breast cancer. Of these women, the majority are postmenopausal (over the age of 50).

Also, two studies done recently has shown that femara is more effective as an anti-estrogen than arimidex or nolvadex.

Geisler J, Anker G, Dowsett M, Lonning PE.
Letrozole suppresses plasma estrogen levels in postmenopausal breast cancer patients more completely than anastrozole. Presented at the 36th Annual Meeting of the American Society of Clinical Oncology (ASCO), May 20-23, 2000, New Orleans, Louisiana. Abstract 394.

Mouridsen H, Gershanovich M, Sun Y, et al.
Superior efficacy of letrozole (Femara ®) versus tamoxifen as first-line therapy for postmenopausal women with advanced breast cancer: results of a phase III study of the international Letrozole Breast Cancer Group. J Clin Oncol. 2001; 19(10):2596-2606.

Heads up bros, Femara can well overthrow arimidex as king of the anti-estrogens.

A lot of good stuff mentioned. One that wasn't is that higher estrogen rates will increase IGF-1 activity. This is one reason why women respond 30% better to hGH. If you cut out estrogen you limit the IGF-1, IGF-2 binding proteins from working at their best.