femera, armi and others...

[neurosys]

after doing some reading i have found many people love armidex and even further reading i have found femera to be a superior product above armi.

my question is why would anyone not use femera over other anti-e's? easy to take, dont have to take it every day, cheap and so forth.

from what i read, it stops the estro all together...sounds good to me...so why doesnt everyone use it?

neuro

 

[Desibaba]

after doing some reading i have found many people love armidex and even further reading i have found femera to be a superior product above armi.

my question is why would anyone not use femera over other anti-e's? easy to take, dont have to take it every day, cheap and so forth.

from what i read, it stops the estro all together...sounds good to me...so why doesnt everyone use it?

neuro

Costs more $ and hasnt received the same coverage as anastrozole has so most people think arimidex is the best.Its still relatively new as far as most people are concerned.Nolvadex and arimidex are the most popular.

 

[einstein1905]

Letro does the same thing as adex, but only does it with slightly more effeiciency. Neither of them, "stop estrogen altogether". You want estrogen, and lots of it. It's a very anabolic hormone. We take anti e's to merely control the levels. As for doesing, you can take adex EOD too, if you want. Since adex is slightly less efficient than letro, it makes it a better choice so as to fine tune the dosing.

 

[Bob Smith]

The difference in conversion between ari and femara is minimal. Maybe a 2-3% point difference. Big deal when youre talking ~95%. Also, ari has been shown to lower IGF-1 levels while femara increases. Both are great products, but I think femara is a better choice, if only by a small margin.

 

[einstein1905]

The difference in conversion between ari and femara is minimal. Maybe a 2-3% point difference. Big deal when youre talking ~95%. Also, ari has been shown to lower IGF-1 levels while femara increases. Both are great products, but I think femara is a better choice, if only by a small margin.

I know the study you're referring to, but adex actually increases IGF-1 levels just as letro does.
They work by identical mechanisms, and the only difference is the slight difference in binding affinity.

J Steroid Biochem Mol Biol. 2002 Apr;80(4-5):411-8. Related Articles, Links


Short-term effects of anastrozole treatment on insulin-like growth factor system in postmenopausal advanced breast cancer patients.

Ferrari L, Martinetti A, Zilembo N, Pozzi P, Buzzoni R, La Torre I, Gattinoni L, Catena L, Vitali M, Celio L, Seregni E, Bombardieri E, Bajetta E.

Nuclear Medicine, Istituto Nazionale per lo Studio e la Cura dei Tumori of Milan, Via G. Venezian, 1, 20133 Milan, Italy.

Insulin-like growth factors (IGFs) play a fundamental role in cancer development by acting in both an endocrinal and paracrinal manner, and hormone breast cancer treatments affect the IGF system by modifying circulating growth factor levels. We evaluated total IGF-1, IGF-2, IGF binding protein (IGFBP)-1 and IGFBP-3 in the blood of 34 postmenopausal advanced breast cancer patients (median age 63 years, range 41-85) treated with anastrozole, a non-steroidal structure aromatase inhibitor (NSS-AI). The plasma samples were obtained at baseline, and after 2, 4, 8 and 12 weeks of treatment. The IGFs were quantitated by means of sensitive radioimmunoassays (RIAs). IGF-1 significantly increased during anastrozole treatment (baseline versus 12 weeks, P=0.031), IGF-2 showed a trend towards an increase, and IGFBP-1 constantly but not significantly decreased; IGFBP-3 did not seem to be affected at all. The anastrozole-induced changes in IGFs and IGFBP-1 appeared to be different in the patients receiving a clinical benefit from those observed in non-responders. We have previously shown that letrozole (a different type of NSS-AI) modifies blood IGF-1 levels, and the results of this study of the biological effects of anastrozole on the components of the IGF system confirm our previous observations.

 

[neurosys]

consider me stupid, but with the higher igf levels your cycle would be more productive so the only major difference i see would be cost. if it's no factor then which ever product raises the ifg level higher then the better the product.

now, if a person was to jump their cycle using igh-1 how would this affect armi or femera?

sorry, getting into the scientific aspect of it, but i'm just curious.

neuro

 

[Desibaba]

Hmm.In his monthly column in MD Dave Palumbo said that arimidex is better than nolvadex because nolvadex lowers IGF-1.I didnt know arimidex did that too?

 

[einstein1905]

Hmm.In his monthly column in MD Dave Palumbo said that arimidex is better than nolvadex because nolvadex lowers IGF-1.I didnt know arimidex did that too?

Arimidex doesn't lower IGF-1 levels. There was just an isolated study that showed this....all the rest show increases in IGF-1. I don't agree with comparisons like "arimidex vs nolva". IMO they are inseparable....they are to be used together.


As for the other question. A cycle of IGF-1 will be completely unaffected by arimidex or nolva....they merely have impacts on the synthesis of IGF-1, not on already formed IGF-1.

 

[Desibaba]

Arimidex doesn't lower IGF-1 levels. There was just an isolated study that showed this....all the rest show increases in IGF-1. I don't agree with comparisons like "arimidex vs nolva". IMO they are inseparable....they are to be used together.


As for the other question. A cycle of IGF-1 will be completely inaffected by arimidex or nolva....they merely have impacts on the synthesis of IGF-1, not on already formed IGF-1.

If you dont mind me asking have you been to medical school or learnt all this just as a hobby? You seem to have quite an impressive knowledge of pharmaceutical substances which are used in bodybuilding.

 

[jboldman]

i like exemestane better than both although it is very expensive. I believe that a major drawback to femara is the estrogen rebound that occurs after cessation.

jb

 

[Bob Smith]

Hmm.In his monthly column in MD Dave Palumbo said that arimidex is better than nolvadex because nolvadex lowers IGF-1.I didnt know arimidex did that too?

I wouldnt listen to anything Palumbo says.

 

[VDC]

Leave it JB to bring up the cutting edge,,,This the kind of thread I like and need,,,Keep going I'm learning,,,What is Exemenstane???How does it work???How is it used???What dose schedule do you use???VDC

 

[einstein1905]

If you dont mind me asking have you been to medical school or learnt all this just as a hobby? You seem to have quite an impressive knowledge of pharmaceutical substances which are used in bodybuilding.

I'm an MD/PhD student now, but the kinds of stuff talked about on the boards aren't covered in med school.....all of this information is available to anyone with an internet connection.....it just takes a lot of reading.
pubmed or sciencedirect are great sites to search journals....don't just read the abstracts though....that's what too many others do.

 

[einstein1905]

Leave it JB to bring up the cutting edge,,,This the kind of thread I like and need,,,Keep going I'm learning,,,What is Exemenstane???How does it work???How is it used???What dose schedule do you use???VDC

exemestane is very similar to letro or adex except that when it binds aromatase, it's permanent. So, each molecule of exemestane that binds an aromatase enzyme renders it incapable of ever again converting estrogen (the life of enzymes is very short anyway), but this is in contrast to the class II AIs, adex and letro, which are in a constant state of binding and release from aromatase, which leaves openings for test or andro to bind aromatase and be converted. therefore, exemestane (aromasin) is more efficient.




In regards to the above, letro doesn't cause any significant estrogen rebound ( no more than adex or exemestane) as long as it's used for the proper duratio of time (i.e. long enough so that the high levels of aromatizable substrate have left the body).

 

[jboldman]

Clin Breast Cancer. 2000 Sep;1 Suppl 1:S68-73.

Comparison of in vitro exemestane activity versus other antiaromatase agents.

Soudon J.

Pharmacell, Paris, France; pharm2@jupiter.chu-stlouis.fr

Anastrozole, letrozole, and exemestane are the most selective and potent oral antiaromatase agents currently available. However, in vitro and in vivo studies comparing these agents are lacking. Anastrozole and letrozole are reversible, competitive nonsteroidal type II inhibitors, whereas exemestane is an irreversible steroidal type I inactivator. The study was conducted to determine the impact of this characteristic on in vitro residual aromatase activity and protein levels after incubation of JEG-3 cells with aminoglutethimide (a type II inhibitor), anastrozole, exemestane, or letrozole. Aromatase activity was measured after various incubation times with each antiaromatase agent at a concentration 10 times higher than IC50 (concentration giving 50% inhibition). Only exemestane induced a residual inhibition of aromatase activity after its removal, without any change in the aromatase protein level. Aromatase activity increased after preincubation of JEG-3 cells with either aminoglutethimide or anastrozole without any change in the aromatase protein level. The aromatase protein level increased rapidly when cells were incubated with letrozole and aromatase activity inhibition disappeared immediately after removal of the drug. The breakthrough effects in aromatase activity or protein levels observed after treatment with reversible inhibitors may be a factor in therapeutic failure with these agents. These results suggest a possible advantage for exemestane because it is the only clinically available oral irreversible aromatase inactivator.

 

[VDC]

Thanks Einstein and JB,,,JB starting early today,,,VDC

 

[einstein1905]

Clin Breast Cancer. 2000 Sep;1 Suppl 1:S68-73.

Comparison of in vitro exemestane activity versus other antiaromatase agents.

Soudon J.

Pharmacell, Paris, France; pharm2@jupiter.chu-stlouis.fr

Anastrozole, letrozole, and exemestane are the most selective and potent oral antiaromatase agents currently available. However, in vitro and in vivo studies comparing these agents are lacking. Anastrozole and letrozole are reversible, competitive nonsteroidal type II inhibitors, whereas exemestane is an irreversible steroidal type I inactivator. The study was conducted to determine the impact of this characteristic on in vitro residual aromatase activity and protein levels after incubation of JEG-3 cells with aminoglutethimide (a type II inhibitor), anastrozole, exemestane, or letrozole. Aromatase activity was measured after various incubation times with each antiaromatase agent at a concentration 10 times higher than IC50 (concentration giving 50% inhibition). Only exemestane induced a residual inhibition of aromatase activity after its removal, without any change in the aromatase protein level. Aromatase activity increased after preincubation of JEG-3 cells with either aminoglutethimide or anastrozole without any change in the aromatase protein level. The aromatase protein level increased rapidly when cells were incubated with letrozole and aromatase activity inhibition disappeared immediately after removal of the drug. The breakthrough effects in aromatase activity or protein levels observed after treatment with reversible inhibitors may be a factor in therapeutic failure with these agents. These results suggest a possible advantage for exemestane because it is the only clinically available oral irreversible aromatase inactivator.

The full text isn't available, but you need the actual numbers to draw any conclusions. "Aromatase activity increased rapidly".....to what level? You have to consider they were using class II AIs in amounts that cause 50% suppression, so "increased rapidly" could mean back up to only 80% suppression, which means still below baseline (i.e. still causing suppression). Also, these clinical studies that are like this one aren't really relevant to us. We are using AIs only when we are concurrently introducing very high levels of aromatizable substrate into our body. Keep in mind that anastrozole at 1mg suppresses E2 at roughly 80-85% in normal women (where there are normal physiological levels of aromatizable substrate)....we use a fraction of that dose (although a lean male has less inherent aromatase activity) and with at least 10x the level of aromatizable substrate. I use an AI all the way through pct, so my test levels are back to physiological levels when I cease its use....no estrogen "rebound" to speak of.

This abstract could just be saying that ceasing administration of class II AIs lessened E2 suppression, but in any even, the timing of administration of AIs in the context of our use of them alleviates any concern of this.

 

[jboldman]

it is difficult to make assumptions since we are a subset that is unlikely to be studied but the study could actually mean what it says just as easily. I think the best we can do is to look at all the evidence and make our best guess. My best guess is that exemestane has no rebound and letrozole does.

jb

 

[jboldman]

you have to be an early riser to keep up with you!

jb

Thanks Einstein and JB,,,JB starting early today,,,VDC

 

[VDC]

I'm still getting back into the swing off things,,,but I don't want to hijack this thread,,,To be honest being on fulltime and doing ari ed is working out just fine for me,,,but I like learning all the details,,,Sometimes a detail will fit into place and I can intuit an improvement to my cycle(like I did with HCG),,,and I'll be better equipped to help someone out,,,Good to see ya jb,,,VDC