3J
Musclechemistry Member
article credit: Jimithing
Part 1:
I see alot of reference to ai's, their applications, which one is "best", and how often they should be taken inn addition to proper dosage. I have personally had experience with all 2 main ai's, in addition to doing a good bit of research on them as well. I have decided to compile my experience as well as the data I have collected to try to help people understand the difference between them, when they should be used, and how they should be used. Hopefully this write up proves helpful to someone!
So first off what is an AI? An ai is an aromatase inhibitor. Aromatase in the enzyme responsible for the conversion of testosterone to estrogen in the body. AI's do just what they sound like they do, they inhibit the aronmatase enzyme. There are 2 primary means by which they go about doing this and thus 2 predominant types of ai's, type 1 & type 2.
Type 1 ai's, such as aromasin (or exemestane) are often referred to as suicide ai's. The reason being is that they actually render the aromatase enzyme useless. Type 2 ai's, such as arimidex (anastrozole) and femara (letrozole) actually attach to the aromatase enzyme, not allowing testosterone to attach and thus be converted to estrogen. When understanding ai's this is somewhat of an important distinction in that type 2 ai's do not reduce the amount of aromatase enzyme available, they simply render the available aromatase unusable. Type 1 ai's on the other hand, actually reduce the overall amount of aromatase present, thus reducing the conversion of testosterone to estrogen.
SO when should we use an ai? This is a fairly simple question in my mind although like many things when it comes to aas the answer to this question has become blurred. Often people recommend an ai to treat gyno or possibly for use in PCT. In my mind neither of these applications are where we should focus when it comes to ai use. The primary use for an ai in our circles should be to manage our estrogen levels when on a cycle of aromatizing steroids. Thats it, pure and simple.
You see estrogen is not all bad, so in order to get the benefits estrogen has to offer (immune system function, cholesterol management, igf levels) we require some estrogen be present. That being said as we are all aware estrogen, especially in males, can be quite detrimental at higher levels. Our goal when on cycle IMO, should be to keep estrogen within clinically normal levels even though we are on cycle. This affords us the benefits of estrogen without the detrimental effects in causes in males. An ai is the perfect tool for doing so.
So which ai should we use? Well this is not as simple a question as it may seem but it is still relatively easy to figure out once you know the difference in ai strength and how we each respond to aromatizing steroids. First of all there is a bit of a misconception as to the strength on the 3 main ai's we use. Quite often people incorrectly assume that the order of ai strength from strongest to weakest is as follows: Letro, Stane, and Dex. This is not correct. The correct order , strongest to weakest is in fact letro, dex and then stane. You see initially all the sdata available on stane was in studies conducted on woemn and women react quite differently than men when it comes to ai's. These studies indicated that stane was an extremely potent ai, much stronger than dex. The proble is people were comparing the results of stane in females to results of dex in males. Not an accurate means of comparison. When you compare the use of all 3 ai's in men dex is stronger thn stane for sure.'So now the thing we need to lok at is how do you personally respond to aromatizing steroids? You see we all have various levels of aromatse enzyme present. Many factors such as gentics as well as body composition effect the amount of aromatase enzyme present. 2 people taking the same cycle may have very different levels of estrogen due to the difference in aromatase enzyme present. This makes choosing which ai to use an individual one and it may in fact take some trial and error until you find which ai works best for you.
In part 2 I will touch on the dosing of all 3 ai's. How often you should take them and just how much might be a prudent amount to start of with. Obviously this depends a lot on the cycle you are running but we can definitely come up with some solid recommendations as far as dosing frequency as well as starting dosages for a "normal"cycle and adjustments in dosage amount can be made from there. Part 2 will get into these factors when it comes to ai use.
Part 2:
So having covered the 2 primary types of ai, how they work, and the potency of each lets get into the dosage frequency and some general dosing guidelines for some fairly common cycle dosages.
Letro and Dex should/can be very effectively taken EOD or ED. Either wy seems to work just fine and I would recommend starting at dosing them EOD and if the need to increase your ai dose should arise the very simple solution to doing so would just be to up them to daiy dosing.
Stane is a bit of a different animal. It has a significantly shorter half life and should be taken at a minimum every day. In some cases it is necessary to take it 2x/day. I use the same general guideline i mentioned above with letro and dex. I start my stane dosing as a single daily dose and if I need to increase my dosage amount I simply up it to 2x/day dosing, am & pm.
Having outlined the dosing frequency of each ai based on the compounds half lives lets take a look at some starting doses. I suppose we should base the initial dosing on a simple test only cycle at a dosage of 500mgs of test per week. Based on thaat I would dose the respective ai's as follows:
Dex: .25-.5mg EOD
Stane: 12.5-25mg/day
Letro: .125-.25mg EOD
These are simply some general dossing guidelines. As I stated I would start at the above mentioned doses and should the need arise to increase dosing quite often the simplest approach is to increase your dosing frequency. For example start your dex at .25 EOD, if your mid cyce bloods show your e2 evels are high simply up your doing by taking .25mg dex ED instead of EOD. This is the easiest way IMO to increase your dosing and to maintain stable blood levels of ai.
So in Part 2 we have covered dosing frequency and given some guidelines for dosing amounts. PArt 3 will focus on which ai may be besst for you and why. I will also focus on ai interactions with other compounds and if those interactions are of any signficance when it comes to our ai dosing (for example you may have heard nolva can reduce adex's effectiveness, but does it really?) Stay tuned tomorrow for the third and final part of this ai Write up!
Part 3:
Ok so having covered the 2 types of ai's, how they differ in mechanism of action, the relative potency of the 3 main ai's, dosing frequency and some general dosage starting points or guidelines where does that leave us? Well now that we know all this how do we choose which ai is best suited for our purpose? Let me start by saying all 3 ai's have their place and once you determine which one works best for you it will definitely improve the safety of your cycle and even your overall cycle experience.
So first lets compare type 1 to type 2 ai's. Type 1 ai's such as exemestane directly regulate how much aromatase enzyme is available to convert test to estrogen. By controlling the amount of aromatase exemestane directly controls your levels of estrogen. Type 2 ai's like dex or letro do not effect the amount of aromatase enzyme at all. What they do is attach to a certain amount of aromatase enzyme, preventing the testosterone molecule from attaching to the aromatase that is occupied by the type 2 ai. Ok so big deal? Whats the difference? Well there is a difference although I feel it is slightly overblown. You see when using a type 2 ai like adex for example when you cease using it all the aromatase enzyme that was bound to the ai becomes available and active to aromatize test to estrogen. This can create a situation referred to as an estrogen spike. While this sounds very bad it really isnt all that significant if we look at when we stop the use of our ai (right before starting pct) and what we start taking immediately after cessation of our ai use. By immediately starting a serm based pct we are effectively blocking the e2 receptor in many of the most important site which prevents e2 from exerting its deleterious effects. Also this spike in estrogen may fore the body to quickly react or compensate and potentially even help our hpta to restart. This, however, is not significant either way. I feel the estrogen rebound thing has been blown way out of proportion.
So now that we have determined that although type 1 and type 2 ai's lower estrogen via different mechanisms of action both ways are very effective and if their is any advantage to a suicide ai like stane it is a small one when it comes to the area of estrogen rebound.
Now quite often people will look at various studies to compare the respective ai's and their effect on other overall general health markers or hormone levels. For example it is often said that letrozole has a very bad impact on your lipid profile (cholesterol) and it lowers igf significantly. I would like to convey something here and I cannot emphasize this enough. Basing your decision of which ai to use based on the ai's supposed effects on things like I just mentioned is a very imprudent thing to do IMO and I will explain why.
You see estrogen is responsible for many effects in the body, some good, some bad. It regulates our cholesterol levels (the more estrogen the lower our cholesterol), it also has a direct bearing or effect on serum igf levels. I pick these 2 things specifically because they are most often the markers spoken of when someone is talking about how good or bad an ai is for you. Here is the thing some are missing. These effects IMO are not so much related to the ai itself, but the ai's ultimate effect on estrogen levels that impact the cholesterol and igf levels.
For example as we already discussed letrozole is the most potent ai, it also happens to be the ai with the reputation for being bad on your cholesterol levels as well as lowering your igf levels. Coincidence? No way. Now lets look at the opposite end of the spectrum. Quite often it is said that Exemestane has minimal impact on cholesterol levels as well as no adverse effect on igf levels. Well of course it doesnt because it happens to be the weakest of the 3 ai's available to us for our use. You see people have erroneously related the effects on things like cholestrol and igf to the compound they are talking when the fact is the effects directly correlate to the levels of estrogen.
What i my point for going into this? Well I am trying to point out that it is not prudent to select your ai based on the things we just discussed (cholesterol /igf/etc) as its actually the e2 levels that are effecting these things!
So how do you choose? Well we are respond differently when it come to the aromatization of testosterone to estrogen. The are genetic factors and predispositions which impact this as well as factors such as body com********** You see one of the primary storage area for the aromatase enzyme itself is in adipose tissue so the higher your bodyfat the liklihood is that the higher your levels of aromatase and the more potent the ai you may require to do the same job someone at a lower bodyfat can do with a weaker ai.
It all comes down to cycle dosages of aromatizing steroids and your individual response to aromatization of test to estrogen. How do you know which ai to use then? Well trial and error my friends! It may be prudent when starting out to take the middle of the road. Simply start off with adex dosed at .25-.5mg EOD (base don a 500mg/week test cycle). This is where blood work becomes so essential. It is IMPERATIVE, especially initially that you rely on blood work to make changes in your ai dosage or even changes in which ai you are using. The ultimate goal is to keep e2 levels within clinically normal range even when on cycle. Its impossible to accomplish this goal without the assistance of mid cycle blood work.
So again perhaps start with dex, get your mid cycle bloods. If need be you can try to adjust your dex dosage. If for whatever reason you cannot effectively or efficiently dial your e2 levels in using adex you may need to go with the more powerful ai, letro, starting at the introductory dose I mentioned and again using blood work to adjust from there or perhaps you may not be able to get e2 low enough taking reasonable measurable doses of dex and the need may arise to drop to stane, again at the recommended starting dose.
The "start with dex"methodology I outlined is simply my suggestion for someone new just starting out, using an ai for the first time. Your other option may be to experiment over several cycles, trying different ais'work to dial it and see how it goes for you.
I hope this write up has covered the basics of the ai, how they work, what the differences are, how frequently they should be dosed, what dosage you should use (or at least start with) and how to select which ai may be best to start off trying. I also wanted to over HOW to make proper dosage adjustment utilizing blood work and not how you "feel" in addition to presenting a logical way to determine which ai may be best for you as an individual.
I would def like to open the thread for discussion at this time!
Thanks for Reading!
Jimi
Part 1:
I see alot of reference to ai's, their applications, which one is "best", and how often they should be taken inn addition to proper dosage. I have personally had experience with all 2 main ai's, in addition to doing a good bit of research on them as well. I have decided to compile my experience as well as the data I have collected to try to help people understand the difference between them, when they should be used, and how they should be used. Hopefully this write up proves helpful to someone!
So first off what is an AI? An ai is an aromatase inhibitor. Aromatase in the enzyme responsible for the conversion of testosterone to estrogen in the body. AI's do just what they sound like they do, they inhibit the aronmatase enzyme. There are 2 primary means by which they go about doing this and thus 2 predominant types of ai's, type 1 & type 2.
Type 1 ai's, such as aromasin (or exemestane) are often referred to as suicide ai's. The reason being is that they actually render the aromatase enzyme useless. Type 2 ai's, such as arimidex (anastrozole) and femara (letrozole) actually attach to the aromatase enzyme, not allowing testosterone to attach and thus be converted to estrogen. When understanding ai's this is somewhat of an important distinction in that type 2 ai's do not reduce the amount of aromatase enzyme available, they simply render the available aromatase unusable. Type 1 ai's on the other hand, actually reduce the overall amount of aromatase present, thus reducing the conversion of testosterone to estrogen.
SO when should we use an ai? This is a fairly simple question in my mind although like many things when it comes to aas the answer to this question has become blurred. Often people recommend an ai to treat gyno or possibly for use in PCT. In my mind neither of these applications are where we should focus when it comes to ai use. The primary use for an ai in our circles should be to manage our estrogen levels when on a cycle of aromatizing steroids. Thats it, pure and simple.
You see estrogen is not all bad, so in order to get the benefits estrogen has to offer (immune system function, cholesterol management, igf levels) we require some estrogen be present. That being said as we are all aware estrogen, especially in males, can be quite detrimental at higher levels. Our goal when on cycle IMO, should be to keep estrogen within clinically normal levels even though we are on cycle. This affords us the benefits of estrogen without the detrimental effects in causes in males. An ai is the perfect tool for doing so.
So which ai should we use? Well this is not as simple a question as it may seem but it is still relatively easy to figure out once you know the difference in ai strength and how we each respond to aromatizing steroids. First of all there is a bit of a misconception as to the strength on the 3 main ai's we use. Quite often people incorrectly assume that the order of ai strength from strongest to weakest is as follows: Letro, Stane, and Dex. This is not correct. The correct order , strongest to weakest is in fact letro, dex and then stane. You see initially all the sdata available on stane was in studies conducted on woemn and women react quite differently than men when it comes to ai's. These studies indicated that stane was an extremely potent ai, much stronger than dex. The proble is people were comparing the results of stane in females to results of dex in males. Not an accurate means of comparison. When you compare the use of all 3 ai's in men dex is stronger thn stane for sure.'So now the thing we need to lok at is how do you personally respond to aromatizing steroids? You see we all have various levels of aromatse enzyme present. Many factors such as gentics as well as body composition effect the amount of aromatase enzyme present. 2 people taking the same cycle may have very different levels of estrogen due to the difference in aromatase enzyme present. This makes choosing which ai to use an individual one and it may in fact take some trial and error until you find which ai works best for you.
In part 2 I will touch on the dosing of all 3 ai's. How often you should take them and just how much might be a prudent amount to start of with. Obviously this depends a lot on the cycle you are running but we can definitely come up with some solid recommendations as far as dosing frequency as well as starting dosages for a "normal"cycle and adjustments in dosage amount can be made from there. Part 2 will get into these factors when it comes to ai use.
Part 2:
So having covered the 2 primary types of ai, how they work, and the potency of each lets get into the dosage frequency and some general dosing guidelines for some fairly common cycle dosages.
Letro and Dex should/can be very effectively taken EOD or ED. Either wy seems to work just fine and I would recommend starting at dosing them EOD and if the need to increase your ai dose should arise the very simple solution to doing so would just be to up them to daiy dosing.
Stane is a bit of a different animal. It has a significantly shorter half life and should be taken at a minimum every day. In some cases it is necessary to take it 2x/day. I use the same general guideline i mentioned above with letro and dex. I start my stane dosing as a single daily dose and if I need to increase my dosage amount I simply up it to 2x/day dosing, am & pm.
Having outlined the dosing frequency of each ai based on the compounds half lives lets take a look at some starting doses. I suppose we should base the initial dosing on a simple test only cycle at a dosage of 500mgs of test per week. Based on thaat I would dose the respective ai's as follows:
Dex: .25-.5mg EOD
Stane: 12.5-25mg/day
Letro: .125-.25mg EOD
These are simply some general dossing guidelines. As I stated I would start at the above mentioned doses and should the need arise to increase dosing quite often the simplest approach is to increase your dosing frequency. For example start your dex at .25 EOD, if your mid cyce bloods show your e2 evels are high simply up your doing by taking .25mg dex ED instead of EOD. This is the easiest way IMO to increase your dosing and to maintain stable blood levels of ai.
So in Part 2 we have covered dosing frequency and given some guidelines for dosing amounts. PArt 3 will focus on which ai may be besst for you and why. I will also focus on ai interactions with other compounds and if those interactions are of any signficance when it comes to our ai dosing (for example you may have heard nolva can reduce adex's effectiveness, but does it really?) Stay tuned tomorrow for the third and final part of this ai Write up!
Part 3:
Ok so having covered the 2 types of ai's, how they differ in mechanism of action, the relative potency of the 3 main ai's, dosing frequency and some general dosage starting points or guidelines where does that leave us? Well now that we know all this how do we choose which ai is best suited for our purpose? Let me start by saying all 3 ai's have their place and once you determine which one works best for you it will definitely improve the safety of your cycle and even your overall cycle experience.
So first lets compare type 1 to type 2 ai's. Type 1 ai's such as exemestane directly regulate how much aromatase enzyme is available to convert test to estrogen. By controlling the amount of aromatase exemestane directly controls your levels of estrogen. Type 2 ai's like dex or letro do not effect the amount of aromatase enzyme at all. What they do is attach to a certain amount of aromatase enzyme, preventing the testosterone molecule from attaching to the aromatase that is occupied by the type 2 ai. Ok so big deal? Whats the difference? Well there is a difference although I feel it is slightly overblown. You see when using a type 2 ai like adex for example when you cease using it all the aromatase enzyme that was bound to the ai becomes available and active to aromatize test to estrogen. This can create a situation referred to as an estrogen spike. While this sounds very bad it really isnt all that significant if we look at when we stop the use of our ai (right before starting pct) and what we start taking immediately after cessation of our ai use. By immediately starting a serm based pct we are effectively blocking the e2 receptor in many of the most important site which prevents e2 from exerting its deleterious effects. Also this spike in estrogen may fore the body to quickly react or compensate and potentially even help our hpta to restart. This, however, is not significant either way. I feel the estrogen rebound thing has been blown way out of proportion.
So now that we have determined that although type 1 and type 2 ai's lower estrogen via different mechanisms of action both ways are very effective and if their is any advantage to a suicide ai like stane it is a small one when it comes to the area of estrogen rebound.
Now quite often people will look at various studies to compare the respective ai's and their effect on other overall general health markers or hormone levels. For example it is often said that letrozole has a very bad impact on your lipid profile (cholesterol) and it lowers igf significantly. I would like to convey something here and I cannot emphasize this enough. Basing your decision of which ai to use based on the ai's supposed effects on things like I just mentioned is a very imprudent thing to do IMO and I will explain why.
You see estrogen is responsible for many effects in the body, some good, some bad. It regulates our cholesterol levels (the more estrogen the lower our cholesterol), it also has a direct bearing or effect on serum igf levels. I pick these 2 things specifically because they are most often the markers spoken of when someone is talking about how good or bad an ai is for you. Here is the thing some are missing. These effects IMO are not so much related to the ai itself, but the ai's ultimate effect on estrogen levels that impact the cholesterol and igf levels.
For example as we already discussed letrozole is the most potent ai, it also happens to be the ai with the reputation for being bad on your cholesterol levels as well as lowering your igf levels. Coincidence? No way. Now lets look at the opposite end of the spectrum. Quite often it is said that Exemestane has minimal impact on cholesterol levels as well as no adverse effect on igf levels. Well of course it doesnt because it happens to be the weakest of the 3 ai's available to us for our use. You see people have erroneously related the effects on things like cholestrol and igf to the compound they are talking when the fact is the effects directly correlate to the levels of estrogen.
What i my point for going into this? Well I am trying to point out that it is not prudent to select your ai based on the things we just discussed (cholesterol /igf/etc) as its actually the e2 levels that are effecting these things!
So how do you choose? Well we are respond differently when it come to the aromatization of testosterone to estrogen. The are genetic factors and predispositions which impact this as well as factors such as body com********** You see one of the primary storage area for the aromatase enzyme itself is in adipose tissue so the higher your bodyfat the liklihood is that the higher your levels of aromatase and the more potent the ai you may require to do the same job someone at a lower bodyfat can do with a weaker ai.
It all comes down to cycle dosages of aromatizing steroids and your individual response to aromatization of test to estrogen. How do you know which ai to use then? Well trial and error my friends! It may be prudent when starting out to take the middle of the road. Simply start off with adex dosed at .25-.5mg EOD (base don a 500mg/week test cycle). This is where blood work becomes so essential. It is IMPERATIVE, especially initially that you rely on blood work to make changes in your ai dosage or even changes in which ai you are using. The ultimate goal is to keep e2 levels within clinically normal range even when on cycle. Its impossible to accomplish this goal without the assistance of mid cycle blood work.
So again perhaps start with dex, get your mid cycle bloods. If need be you can try to adjust your dex dosage. If for whatever reason you cannot effectively or efficiently dial your e2 levels in using adex you may need to go with the more powerful ai, letro, starting at the introductory dose I mentioned and again using blood work to adjust from there or perhaps you may not be able to get e2 low enough taking reasonable measurable doses of dex and the need may arise to drop to stane, again at the recommended starting dose.
The "start with dex"methodology I outlined is simply my suggestion for someone new just starting out, using an ai for the first time. Your other option may be to experiment over several cycles, trying different ais'work to dial it and see how it goes for you.
I hope this write up has covered the basics of the ai, how they work, what the differences are, how frequently they should be dosed, what dosage you should use (or at least start with) and how to select which ai may be best to start off trying. I also wanted to over HOW to make proper dosage adjustment utilizing blood work and not how you "feel" in addition to presenting a logical way to determine which ai may be best for you as an individual.
I would def like to open the thread for discussion at this time!
Thanks for Reading!
Jimi
