aromatase inhibitor facts must read!!! aromasin (exemestane) vs arimidex letrozole

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Ok there is a lot of newbies and even some who dont really know what is best and the effects it has on you in way of aromatase inhibitors (pcts and the like) so I am staying up late to help you guys out a bit. I hope this helps its an accumalative of many different facts all put together for you here.



Products /aromatase inhibition/risudual aromatase%


formestance(4-androstenoldion) /91.6/8.1%

aromasin(exemestance)/97.9/2.1%

cytradren (aminoglutethimide)/90.6/9.4%

arimidex
(amastrozole)/96.7/3.1%

femera(letrozole)/98.7/1.3%

Produc/effect/percentage

formestance(4-androstenoldion) /increases IGF-1/26%

femera(letrozole)/increases IGF-1/24%

aromasin(exemestance)/increases IGF-1/28%

arimidex
(amastrozole)/decreases IGF-1/18%

nolvadex(tamoxifen citrate)/decreases IGF-1/23.5%

faslodex(fulvestrant)/decreases IGF-1/70%

cytradren (aminoglutethimide)/increases IGF-1/27%


I prefer formestane there are many facts about this that i will post later but above should help in you to decide whats best for you and what effects it will have.

obviously if IGF levels decrease so does packing on weight and the amount of lean tissue lost during a calorie restricted periods as well.
Aromatase inhibitors decrease the amount of estrogen/estradiol and etrogen receptor antagonists to keep out of the specific pituitary receptors.
the use of certain inhibitors can affect the IGF-1 production and receptors our tisues posses.

Hope this helps bro's.


works from:
dose-related endocrine effects and pharma of oral and intramuscular 4 hydroxyandrostenedione in post menapausal breast cancer patients, cancer research, 49(5) 1306-1312 1989

muscular development issue july 2004 pgs 328-332

effects of igf-1 and inhibitors on the human body to steroid use and relation, j.steroid biochem mol biol. 1998 nov-dec 63(4-6) 261-7
 
That's some really good info bro!
I had no idea about some of those, damn bio chemistry can be so picky sometimes.
 
From those numbers it looks like femera(letrozole) or aromasin(exemestance) are the top two. femera(letrozole) being cheaper would be the best buy then.
 
any idea as to what the mechanism is by which these compounds increase igf? I thought it would perhaps be the reduced levels or circulating estradiol,,,but this cannot be since arimidex somehow lowers igf levels.

This upsets me because i would have hoped it was lowered levels of estradiol triggering increases in igf since i take both femera and nolvadex, and since the femera lowers circulating estro, it would negate the igf lowering effects of the nolvadex, but the arimdex example seems to suggest this is not the case, unless arimidex somehow lowers igf by a completely unrelated mechanism...
 
Maby this good info should be put under the MuscleChemistry Encyclopedia forum in some format. I know I'll be useing it for later referance.
 
I do know this that there are 2 types of inhibitors type 1 is a steroidal inactivator, such as extremestane and formestane are actually androgen analouges.
Now type 2 is anastrozole,letrozole, and vorozole and aminoglutethimide. Both act in a very different fashion as well and same fashion eliminating or lowering the amount of estrogen/estridiol in the system. however some help to prevent the binding of the estrogen to fat/satellite cells in the body, the major drawback being that some of these are chemically structured to just that prevent, which aldso limits the body tissue to regenerate while its binded and being blocked of estrogen, to enhance or produce IGF-1.


The shitty part is that they will work for the right stuff as intended estrogen blocking, but however can decrease muscle tissue browth while resting due tyo the lack of IGF-1 in the body, cure NONE! simply as suggested taking an/a non araomtizing agent at evening or bed time.

testrogen and estriodiol actually trigger GH release from the pituatary gland. inhibitors decrease the amount of estrogen/estradiol and the estrogen receptor anatagonists to keep estrogen out oif that specific pituatay gland that poroduces the GH from the estrogen. some can and some do and other do not it depends on the type and the number of IGF receptors our body tissues posses i would assume given the basic chemical nature and anatomy and biological values..
so this is just my opinion but it appears to be somewhat helpful, I would think so due to the fact out there.

but what do i know..im just the oaty oats rep.
 
damn! nolvadex decreases IGF-1!!!!!!! =( man i don't even want to take that Post cycle anymore! how depressing!
 
but you need it! switch to one thats better than nolva, use letrozole, or arimi or something
 
i'll have to find some letrozole.. increase in IGF-1! hrmm guess i'll have to start hunting for a source..
 
I was taking 2.5mgs a day and 30mgs of nolva a day. after i found this out i started taking 2.5 mgs letr a day and clomid at 50mgs a day and it works well. but honestly i dont know.
 
I thought letra completely screwed up your lipid profile.....Looks like formestane is the player of the week until congress puts it on the bench permanently.
 
Here is another good article on the same subject...

The Best Anti-E

theres been a lot of talk on other boards about this lately, and a lot of bad information thrown out as well. i wanted to share the good info.

somone keeps posting how letrozole is the strongest and doesnt negatively affect cholesterol. this is not true. letrozole is NOT the strongest and it DOES negative affect cholesterol/lipid profile in a bad way.

aromasin(exemestane) is the best. this is why

both arimidex/ldex/anastrozole and femara/letrozole hurt your cholesterol. the way these 2 anti e's work is they inhibit the aromatase enzyme. by inhibiting the enzyme which converts testosterone to estrogen, you reduce or even come close to eliminating estrogen production. we need some estrogen to be healthy. the major drawback to this is without estrogen, your lipid profile gets fucked.

exemestane works differently. it does not stop the body from producing estrogen. rather, it makes it so the estrogen is unable to bind to receptors by deactivating the binding enzyme. if the estrogen cannot bind, you simply will not get bloated or get gyno. the estrogen is crippled due to exemestane. however, since the estrogen is still floating around, it will not negatively affect your lipid/cholesterol profile.

anastrozole doesnt cause a rebound effect, and neither does exemestane, but letrozole does. this means after you stop the letrozole, your estrogen rebounds and goes pretty high for a while, eventually it normalizes. you can avoid this by tapering your letro dose down before stopping it, but that is a pain in the ass. higher than normal can mess many things up post cycle when you stop. since the hpta has a feedback loop is primarily controlled by estrogen, high estrogen will tell your hpta to produce less testosterone, because it thinks the high estrogen is caused by too much testosterone. this is fact. now post cycle, dont we want to raise our test levels, not lower them? of course! so rebounds are bad. if you use letro taper the dose off to zero over a couple weeks.

fyi- nolvadex(tamoxifen) is a SERM(Selective Estrogen Receptor Modulator). this means on certain tissue it can act antagonisticaly or agonistically. in the case of lipid profiles, it acts agonistically. so, running tamoxifen with your anti e's will IMPROVE your cholesterol profile even if not on cycle or using any gear or other anti e's. its just plain good for cholesterol.

one thing to keep in mind though when runing tamoxifen with letro. letro reduces blood levels of tamoxifen by over 50%. a study showed 2.5mg letro ed made nolva levels drop to 40% of what they were before adding letro. this does not mean you cant use tamoxifen with letro, it just means you need to use more, about double. 20mg of nolva will act like 8mg if running letro. so make sure you are aware of this because you will need to buy more nolva to compensate. this does not happen when mixing tamoxifen with anastrozole or exemestane, it only hppens with letro.

also, many people and myself experince a reduction of libido on letro. this doesnt happen w/ ldex or exmestane as far as i know, and in my own experience, and ive run all 3 quite a bit.

the best combo IS exemestane and tamoxifen together. your cholesterol will be as good as can be considering your on a cycle of steroids. the dose of aromasin will vary depending on the users needs and how much aromatizing gear is being taken. usually 10-25mg ed works well. run 10mg ed nolva to improve your cholesterol.

second best combo i feel is anastrozole(ldex) and tamoxifen. ldex dose ranges from usually .15mg ed to 1mg ed. run 10mg nolva ed to improve cholesterol.

thierd best is letro and nolvadex. letro doses usually range from 1-2.5mg ed. run 20mg ed nolva to improve cholesterol w/ letro.

you do not need to run nolva with any of these 3, i do recomend it though as it will improve cholesterol compared to using the anti e's alone without nolva.

so in order of strength, on a dose per dose basis(not mg per mg) aromasin is def the strognest, next is letro, and then ldex.

ive been running aromasin now for about 4 months, i wont switch back to ldex or letro. it works much better and its much healthier for cholesterol profiles.

i think we all need to stop only worrying about side effects that we can see visually. cholesterol KILLS many people around the world everyday(well not directly kills but leads to it). steroids are hrting us badly in this sense. steroids do mess our cholesterol up pretty badly, and we will pay for it later in life. now not many of us are going to stop using gear because of that, but we should at least take the proper other drugs to help minimize.

aromasin is only a little bit more expensive than ldex or letro, and its actually about the same price as many places sell ldex or letro for. but its more powerful and healthier. people spend money all the time on steroids which dont have as many side effects as some of the harsher, cheaper steroids. a few extra bucks for the proper anti e's is def money well spent.
 
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