guardianactual
MuscleChemistry Registered Member
The following text talks about how to proplery implement both AI's and serms during your PCT, for optimal effect.
</br>
</br> I will start off strong by saying right up front that we should not wait 3 weeks to begin using an AI with our serm. Rather, it should be implemented right from the start of PCT, in conjunction with the Clomid. There are a few reasons for this, but first I would like to provide you with a brief understanding of Clomid and how it works in the body. First off, Clomid is a synthetic estrogen derivative which possesses inhernet estrogenic activity. This inherent estrogenic activity has a direct, negative effect on natural testosterone production at the level of the HPTA. This is due to Clomid's ability to act as both an agonist & antagonist at the estrogen receptor, with Clomid sensitizing the pituitary cells to the effect of GnRH through its estrogenic activity, rather than anti-estrogenic activity. The estrogenic effect of Clomid at the level of the pituitary presents a unique problem, as other serms, such as Nolvadex, do not have this effect. Because of this, Clomid needs to be handled a bit differently, as far as how we incorporate it into a cycle with AI's. We will not be addressing the proper use of Nolvadex in this post, as it is outside the scope of this short article. (Clomid increases SHBG thus lowering Free test)
</br>
</br> When neglecting to use an AI with Clomid, the high level of circulating estrogens produced as a result of Clomid administration will have an inhibitory effect on natural testosterone production. Fortunately, this inhibitory effect is mostly overcome by Clomid's dual and potent anti-estrogenic activity, but it is still a relevant issue none the less. Much more importantly, when Clomid is administered in the absence of an AI, it is impossible to achieve an optimal response in terms of endogenous testosterone production. Why? In a word...estrogen. Every time testosterone levels increase, so to do estrogen levels increase, via increased aromatization.. The problem with this is that estrogen is one of the most potent inhibitors of natural testosterone production, which is why aromatizable steroids suppress the HPTA so severely. In addition, this is also why anti-estrogens do such an excellent job as at elevating testosterone levels. Whether estrogen levels are elevated by using a bunch of aromatizable steroids...or by using PCT drugs, estrogen will still have a suppressive effect on testosterone production. This limits the effectiveness of serms like Clomid and Nolvadex when used in the absence of an AI...because as soon as testosterone levels start to rise, the body responds by increasing the rate of aromatization, which leads to increased estrogen, which in turn causes the body to say..."Hey, testicles...stop producing so much testosterone because estrogen levels are getting too high".
</br>
</br> However, we can counteract this effect by using an AI with our serm right from the start. By waiting 3 weeks to begin AI therapy, we allow systematic estrogen levels to increase...and once this has happened, there is nothing we can do to fix the situation, other than to accept it and wait for the newly formed estrogen to live out its full life. Not only does this prevent maximal testosterone production from occuring during the first 3 weeks, but it will continue to cause problems in the coming weeks, as the suppressive influence of the estrogen will remain until it is no longer active in the system. By using an AI right from the start, estrogen levels will be kept low the entire time, eliminating their suppressive influence. So, with estrogen now taken out of the picture, how high will testosterone level rise? They will continue to increase until our androgen level gets too high for the body's liking..."and just how high is this?", you might ask. According to multiple university studies, total testosterone levels increased over 250% within 4 weeks of use, while free testosterone levels were increased over 600%!!!! Yp to this point, none of the serms were able to match those numbers. The AI out-performed the serms by a measurable margin.
</br>
</br> So, what is the conclusion? The conclusion is that we should begin using an AI along with a serm, at the outset of PCT. Remember, estrogen is the enemy of HPTA recovery, so we must minimize its production during PCT if we hope to acheive a maximum increase in testosterone levels. Below you will find a properly structured PCT.
</br>
</br> Before listing the PCT program, I want to take a brief moment to address PCT length relative to cycle length. When running short 30 day oral-only cycles, the length of PCT does not need to exceed the length of the cycle itself...or thereabouts . It just isn't necessary, as the suppressive effects of a 30 day oral-only cycle are generally signifcantly easier to recover from than a heavy, 16 week injectable cycle, for example. A more concentrated, less time consuming PCT would better serve the BBr under these circumstances. Anecdotal evidence testifies this this, as well.
</br>
</br> As for dosage for Exemastane you can do this: Exemastane 12.5-25mg EOD Remember Exemastane can rapidly destroy estrogen, and our bodies need some estrogen to function.
</br>
</br>
</br>
</br> Exemastane excerpt: "In males exemestane was found to increase total testosterone by ~60% after 10 days @ 25mg/day, however the same study found that while it increased total testosterone by 60% free testosterone was increased by over 100 percent! that's right, it DOUBLES bio-available testosterone (natty of course). "
</br>
</br> More here http://www.musclechemistry.com/uplo...ane-its-benefits-beyond-estrogen-control.html
</br>
</br> Exemastane & Nolva Aromasin (Exemestane) is one of those weird compounds that nobody really knows what to do with. What we generally hear about it makes it very uninteresting…It’s a third generation Aromatase Inhibitor (AI) just like Arimidex (Anastrozole) and Femera (Letrozole). Both of those two drugs are very efficient at stopping the conversion of androgens into estrogen, and since we have them, why bother with Aromasin? It’s a little harder to get than the other two commonly used aromatase inhibitors, because it’s not in high demand, and there’s never been a readily apparent advantage to using it. And I mean…lets face it: It’s awkward-sounding. Aromasin doesn’t have much of a ring to it, and exemestane is even worse. Arimidex has a bunch of cool abbreviations ("A-dex" or just ‘dex) and even Letrozole is just "Letro" to most people. Where’s the cool nickname for Aromasin/exemestane? A-Sin? E-Stane? It just doesn’t work. It’s the black sheep of AIs. And why do we even need it when we have Letrozole, which is by far the most efficient AI for stopping aromatization (the process by which your body converts testosterone into estrogen)? Letro can reduce estrogen levels by 98% or greater; clinically a dose as low as 100mcgs has been shown to provide maximumaromatase inhibition (2)!
</br>
</br> So why would we need any other AIs? Well, first of all, estrogen is necessary for healthy joints (3) as well as a healthy immune system (4). So getting rid of 98% of the estrogen in your body for an extended period of time may not be the best of ideas. This may be useful on an extreme cutting cycle, leading up to a bodybuilding contest, or if you are particularly prone to gyno, but certainly can’t be used safely for extended periods of time without compromising your joints and immune system.
</br>
</br> That leaves us with Arimidex, which isn’t as potent as Letrozole, but at .5mgs/day will still get rid of around half (50%) of the estrogen in your body. Problem solved, right? Use Arimidex on your typical cycles, and if you are very prone to gyno or are getting ready for a contest, use Letro. But what about Post Cycle Therapy (PCT)?
</br>
</br> I think at this point most people are sold on the use of Nolvadex (Tamoxifen Citrate) instead of Clomid for post cycle therapy (PCT), since both compete estrogen at the receptor site, both increase serum test levels, and both drugs may also alter blood lipid profiles favorably (6). But since 20mgs of Tamoxifen is equal to 150mgs of clomid for purposes of testosterone elevation, FSH and LH, but Tamoxifen doesn’t decrease the LH response to LHRH (6) I think most people agree to Nolvadex’s superiority for PCT. Aromasin with Nolvadex I’ve always been in favor of using Nolvadex during PCT, along with an AI, because reducing estrogen levels has been positively correlated with an increase in testosterone (7) so in my mind, it’s be beneficial to increase testosterone by as many mechanisms as possible while trying to recover your endogenous testosterone levels after a cycle. SO which AI do we use? Letro or A-dex? Well, why don’t we just keep using whichever one we used during the cycle, and add in some Nolvadex? Unfortunately, Nolvadex will significantly reduce the blood plasma levels of both Letrozole as well as Arimidex (8). So if we choose to use one of them with our Nolvadex on PCT, we’re throwing away a bit of money as the Nolvadex will be reducing their effectiveness. This, of course, is where Aromasin comes in, at 20-25mgs/day.
</br>
</br> Aromasin, at that dose, will raise your testosterone levels by about 60%, and also help out your free to bound testosterone ratio by lowering levels of Sex Hormone Binding Globulin (SHBG), by about 20% (12)…SHBG is that nasty enzyme that binds to testosterone andrenders it useless for building muscle. But what about using it along with Nolvadex for PCT?
</br>
</br> Difference Between Type-I and Type-II Aromatase Inhibitors To understand why Aromasin may be useful in conjunction with Nolvadex while both Letro and A-dex suffer reduced effectiveness, we’ll need to first understand the differences between a Type-I and Type-II Aromatase Inhibitor. Type I inhibitors (like Aromasin) are actually steroidal compounds, while type II inhibitors (like Letro and A-dex) are non-steroidal drugs. Hence, androgenic side effects are very possible with Type-I AIs, and they should probably be avoided by women. Of course, there are some similarities between the two types of AIs…both type I & type II AIs mimic normal substrates (essentially androgens), allowing them to compete with the substrate for access to the binding site on the aromatase enzyme. After this binding, the next step is where things differ greatly for the two different types of AI’s. In the case of a type-I AI, the noncompetitive inhibitor will bind, and the enzyme initiates a sequence of hydroxylation; this hydroxylation produces an unbreakable covalent bond between the inhibitor and the enzyme protein. Now, enzyme activity is permanently blocked; even if all unattached inhibitor is removed. Aromatase enzyme activity can only be restored by new enzyme synthesis. Now, on the other hand, competitive inhibitors, called type II AI’s, reversibly bind to the active enzyme site, and one of two things can happen:
</br>
</br> 1.) either no enzyme activity is triggered or 2.) the enzyme is somehow triggered without effect.
</br>
</br> The type II inhibitor can now actually disassociate from the binding site, eventually allowing renewed competition between the inhibitor and the substrate for binding to the site. This means that the effectiveness of competitive aromatase inhibitors depends on the relative concentrations and affinities of both the inhibitor and the substrate, while this is not so for noncompetitive inhibitors. Aromasin is a type-I inhibitor, meaning that once it has done its job, and deactivated the aromatase enzyme, we don’t need it anymore. Letrozole and Arimidex actually need to remain present to continue their effects. This is possibly why Nolvadex does notalter the pharmacokinetics of Aromasin (11).
</br>
</br> Before we close the book on Aromasin, it’s worth noting that you can (and should) still use one of the non-steroidal AIs during your cycle to reduce estrogen, if necessary. When you are ready for PCT, you can then switch over to Aromasin and still experience the full effects of an AI, since there is no cross-over tolerance experienced between steroidal and non-steroidal AIs (9). Since Aromasin is about 65% efficient at suppressing estrogen (10), it’s certainly a very powerful agent, especially considering you won’t experience reduced effectiveness because of your concurrent use of Nolvadex or from any sort of tolerance developed by using other AIs on your cycle(9). There is also a decent amount of preclinical data suggesting that Aromasin has a beneficial effect on bone mineral metabolism that is not seen with non-steroidal agents, and it may also have beneficial effects on lipid metabolism that are not found in the non-steroidal Letro and A-dex (9).
</br>
</br> Finally, as we’re going to be using Nolvadex for PCT anyway, and we ought to be using an AI with it for maximum recovery…I think Aromasin- considering it’s compatibility with Nolvadex and beneficial effects on bone mineral content and lipid profile, has finally stopped being the black sheep of AIs and found a home in our cycles.
</br>
</br> I will start off strong by saying right up front that we should not wait 3 weeks to begin using an AI with our serm. Rather, it should be implemented right from the start of PCT, in conjunction with the Clomid. There are a few reasons for this, but first I would like to provide you with a brief understanding of Clomid and how it works in the body. First off, Clomid is a synthetic estrogen derivative which possesses inhernet estrogenic activity. This inherent estrogenic activity has a direct, negative effect on natural testosterone production at the level of the HPTA. This is due to Clomid's ability to act as both an agonist & antagonist at the estrogen receptor, with Clomid sensitizing the pituitary cells to the effect of GnRH through its estrogenic activity, rather than anti-estrogenic activity. The estrogenic effect of Clomid at the level of the pituitary presents a unique problem, as other serms, such as Nolvadex, do not have this effect. Because of this, Clomid needs to be handled a bit differently, as far as how we incorporate it into a cycle with AI's. We will not be addressing the proper use of Nolvadex in this post, as it is outside the scope of this short article. (Clomid increases SHBG thus lowering Free test)
</br>
</br> When neglecting to use an AI with Clomid, the high level of circulating estrogens produced as a result of Clomid administration will have an inhibitory effect on natural testosterone production. Fortunately, this inhibitory effect is mostly overcome by Clomid's dual and potent anti-estrogenic activity, but it is still a relevant issue none the less. Much more importantly, when Clomid is administered in the absence of an AI, it is impossible to achieve an optimal response in terms of endogenous testosterone production. Why? In a word...estrogen. Every time testosterone levels increase, so to do estrogen levels increase, via increased aromatization.. The problem with this is that estrogen is one of the most potent inhibitors of natural testosterone production, which is why aromatizable steroids suppress the HPTA so severely. In addition, this is also why anti-estrogens do such an excellent job as at elevating testosterone levels. Whether estrogen levels are elevated by using a bunch of aromatizable steroids...or by using PCT drugs, estrogen will still have a suppressive effect on testosterone production. This limits the effectiveness of serms like Clomid and Nolvadex when used in the absence of an AI...because as soon as testosterone levels start to rise, the body responds by increasing the rate of aromatization, which leads to increased estrogen, which in turn causes the body to say..."Hey, testicles...stop producing so much testosterone because estrogen levels are getting too high".
</br>
</br> However, we can counteract this effect by using an AI with our serm right from the start. By waiting 3 weeks to begin AI therapy, we allow systematic estrogen levels to increase...and once this has happened, there is nothing we can do to fix the situation, other than to accept it and wait for the newly formed estrogen to live out its full life. Not only does this prevent maximal testosterone production from occuring during the first 3 weeks, but it will continue to cause problems in the coming weeks, as the suppressive influence of the estrogen will remain until it is no longer active in the system. By using an AI right from the start, estrogen levels will be kept low the entire time, eliminating their suppressive influence. So, with estrogen now taken out of the picture, how high will testosterone level rise? They will continue to increase until our androgen level gets too high for the body's liking..."and just how high is this?", you might ask. According to multiple university studies, total testosterone levels increased over 250% within 4 weeks of use, while free testosterone levels were increased over 600%!!!! Yp to this point, none of the serms were able to match those numbers. The AI out-performed the serms by a measurable margin.
</br>
</br> So, what is the conclusion? The conclusion is that we should begin using an AI along with a serm, at the outset of PCT. Remember, estrogen is the enemy of HPTA recovery, so we must minimize its production during PCT if we hope to acheive a maximum increase in testosterone levels. Below you will find a properly structured PCT.
</br>
</br> Before listing the PCT program, I want to take a brief moment to address PCT length relative to cycle length. When running short 30 day oral-only cycles, the length of PCT does not need to exceed the length of the cycle itself...or thereabouts . It just isn't necessary, as the suppressive effects of a 30 day oral-only cycle are generally signifcantly easier to recover from than a heavy, 16 week injectable cycle, for example. A more concentrated, less time consuming PCT would better serve the BBr under these circumstances. Anecdotal evidence testifies this this, as well.
</br>
</br> As for dosage for Exemastane you can do this: Exemastane 12.5-25mg EOD Remember Exemastane can rapidly destroy estrogen, and our bodies need some estrogen to function.
</br>
</br>
</br>
</br> Exemastane excerpt: "In males exemestane was found to increase total testosterone by ~60% after 10 days @ 25mg/day, however the same study found that while it increased total testosterone by 60% free testosterone was increased by over 100 percent! that's right, it DOUBLES bio-available testosterone (natty of course). "
</br>
</br> More here http://www.musclechemistry.com/uplo...ane-its-benefits-beyond-estrogen-control.html
</br>
</br> Exemastane & Nolva Aromasin (Exemestane) is one of those weird compounds that nobody really knows what to do with. What we generally hear about it makes it very uninteresting…It’s a third generation Aromatase Inhibitor (AI) just like Arimidex (Anastrozole) and Femera (Letrozole). Both of those two drugs are very efficient at stopping the conversion of androgens into estrogen, and since we have them, why bother with Aromasin? It’s a little harder to get than the other two commonly used aromatase inhibitors, because it’s not in high demand, and there’s never been a readily apparent advantage to using it. And I mean…lets face it: It’s awkward-sounding. Aromasin doesn’t have much of a ring to it, and exemestane is even worse. Arimidex has a bunch of cool abbreviations ("A-dex" or just ‘dex) and even Letrozole is just "Letro" to most people. Where’s the cool nickname for Aromasin/exemestane? A-Sin? E-Stane? It just doesn’t work. It’s the black sheep of AIs. And why do we even need it when we have Letrozole, which is by far the most efficient AI for stopping aromatization (the process by which your body converts testosterone into estrogen)? Letro can reduce estrogen levels by 98% or greater; clinically a dose as low as 100mcgs has been shown to provide maximumaromatase inhibition (2)!
</br>
</br> So why would we need any other AIs? Well, first of all, estrogen is necessary for healthy joints (3) as well as a healthy immune system (4). So getting rid of 98% of the estrogen in your body for an extended period of time may not be the best of ideas. This may be useful on an extreme cutting cycle, leading up to a bodybuilding contest, or if you are particularly prone to gyno, but certainly can’t be used safely for extended periods of time without compromising your joints and immune system.
</br>
</br> That leaves us with Arimidex, which isn’t as potent as Letrozole, but at .5mgs/day will still get rid of around half (50%) of the estrogen in your body. Problem solved, right? Use Arimidex on your typical cycles, and if you are very prone to gyno or are getting ready for a contest, use Letro. But what about Post Cycle Therapy (PCT)?
</br>
</br> I think at this point most people are sold on the use of Nolvadex (Tamoxifen Citrate) instead of Clomid for post cycle therapy (PCT), since both compete estrogen at the receptor site, both increase serum test levels, and both drugs may also alter blood lipid profiles favorably (6). But since 20mgs of Tamoxifen is equal to 150mgs of clomid for purposes of testosterone elevation, FSH and LH, but Tamoxifen doesn’t decrease the LH response to LHRH (6) I think most people agree to Nolvadex’s superiority for PCT. Aromasin with Nolvadex I’ve always been in favor of using Nolvadex during PCT, along with an AI, because reducing estrogen levels has been positively correlated with an increase in testosterone (7) so in my mind, it’s be beneficial to increase testosterone by as many mechanisms as possible while trying to recover your endogenous testosterone levels after a cycle. SO which AI do we use? Letro or A-dex? Well, why don’t we just keep using whichever one we used during the cycle, and add in some Nolvadex? Unfortunately, Nolvadex will significantly reduce the blood plasma levels of both Letrozole as well as Arimidex (8). So if we choose to use one of them with our Nolvadex on PCT, we’re throwing away a bit of money as the Nolvadex will be reducing their effectiveness. This, of course, is where Aromasin comes in, at 20-25mgs/day.
</br>
</br> Aromasin, at that dose, will raise your testosterone levels by about 60%, and also help out your free to bound testosterone ratio by lowering levels of Sex Hormone Binding Globulin (SHBG), by about 20% (12)…SHBG is that nasty enzyme that binds to testosterone andrenders it useless for building muscle. But what about using it along with Nolvadex for PCT?
</br>
</br> Difference Between Type-I and Type-II Aromatase Inhibitors To understand why Aromasin may be useful in conjunction with Nolvadex while both Letro and A-dex suffer reduced effectiveness, we’ll need to first understand the differences between a Type-I and Type-II Aromatase Inhibitor. Type I inhibitors (like Aromasin) are actually steroidal compounds, while type II inhibitors (like Letro and A-dex) are non-steroidal drugs. Hence, androgenic side effects are very possible with Type-I AIs, and they should probably be avoided by women. Of course, there are some similarities between the two types of AIs…both type I & type II AIs mimic normal substrates (essentially androgens), allowing them to compete with the substrate for access to the binding site on the aromatase enzyme. After this binding, the next step is where things differ greatly for the two different types of AI’s. In the case of a type-I AI, the noncompetitive inhibitor will bind, and the enzyme initiates a sequence of hydroxylation; this hydroxylation produces an unbreakable covalent bond between the inhibitor and the enzyme protein. Now, enzyme activity is permanently blocked; even if all unattached inhibitor is removed. Aromatase enzyme activity can only be restored by new enzyme synthesis. Now, on the other hand, competitive inhibitors, called type II AI’s, reversibly bind to the active enzyme site, and one of two things can happen:
</br>
</br> 1.) either no enzyme activity is triggered or 2.) the enzyme is somehow triggered without effect.
</br>
</br> The type II inhibitor can now actually disassociate from the binding site, eventually allowing renewed competition between the inhibitor and the substrate for binding to the site. This means that the effectiveness of competitive aromatase inhibitors depends on the relative concentrations and affinities of both the inhibitor and the substrate, while this is not so for noncompetitive inhibitors. Aromasin is a type-I inhibitor, meaning that once it has done its job, and deactivated the aromatase enzyme, we don’t need it anymore. Letrozole and Arimidex actually need to remain present to continue their effects. This is possibly why Nolvadex does notalter the pharmacokinetics of Aromasin (11).
</br>
</br> Before we close the book on Aromasin, it’s worth noting that you can (and should) still use one of the non-steroidal AIs during your cycle to reduce estrogen, if necessary. When you are ready for PCT, you can then switch over to Aromasin and still experience the full effects of an AI, since there is no cross-over tolerance experienced between steroidal and non-steroidal AIs (9). Since Aromasin is about 65% efficient at suppressing estrogen (10), it’s certainly a very powerful agent, especially considering you won’t experience reduced effectiveness because of your concurrent use of Nolvadex or from any sort of tolerance developed by using other AIs on your cycle(9). There is also a decent amount of preclinical data suggesting that Aromasin has a beneficial effect on bone mineral metabolism that is not seen with non-steroidal agents, and it may also have beneficial effects on lipid metabolism that are not found in the non-steroidal Letro and A-dex (9).
</br>
</br> Finally, as we’re going to be using Nolvadex for PCT anyway, and we ought to be using an AI with it for maximum recovery…I think Aromasin- considering it’s compatibility with Nolvadex and beneficial effects on bone mineral content and lipid profile, has finally stopped being the black sheep of AIs and found a home in our cycles.
