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Post Cycle Therapy PCT and Post Cycle Therapy are used in bodybuilders after a bodybuilding steroid or prohromone cycle. Here you will find alternatives on different types of Post Cycle Therapy




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  #11  
Old 07-12-2004, 04:29 PM
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^bump
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  #12  
Old 07-12-2004, 10:00 PM
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nice....definately bump worthy
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  #13  
Old 10-03-2004, 11:50 AM
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Bro I'm not trying to dispute you but I've read conflicting views about whether aromatase inhibitors are a good idea during PCT. Do you think this statement below is accurate?

Origional link used: http://anabolicminds.com/forum/show...swales+protocol

I like Arimidex during the cycle (in fact, consider use of an AI while taking aromatisables a necessity) but it ABSOLUTELY should not be used post cycle (even though it has been shown to increase LH production) because the risk of driving estrogen too low, and therefore further damaging an already compromised Lipid Profile, is too great (this also drives libido back into the ground—and we don’t want that, do we?).
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  #14  
Old 10-03-2004, 04:14 PM
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Originally Posted by Zoldian
Bro I'm not trying to dispute you but I've read conflicting views about whether aromatase inhibitors are a good idea during PCT. Do you think this statement below is accurate?

Origional link used: http://anabolicminds.com/forum/show...swales+protocol

I like Arimidex during the cycle (in fact, consider use of an AI while taking aromatisables a necessity) but it ABSOLUTELY should not be used post cycle (even though it has been shown to increase LH production) because the risk of driving estrogen too low, and therefore further damaging an already compromised Lipid Profile, is too great (this also drives libido back into the ground—and we don’t want that, do we?).
Don't even need to click on the link to know it's SWALE's. Him and I happen to disagree on this aspect. My case on this is

Anastrozole supresses estrogen conversion at about 85% with a full clinical dose in a subject with normal levels of estrogen. We are males with supraphysiological levels of estrogen existing in the body post cycle, utilizing a 1/4 of the clinical dose(.25mg). At least thats the dose I recommend. You do need some estrogen to help with correlation to the AR(which is why I don't like letro) but estrogen is the main inhibitor of recovering HPTA. It needs to be controlled in order to prevent SHBG to accumilate and prolong F. Test reaching base line.

Anastrozole doesn't effect my lipids to a great extent. This of course being individualistic but if concerns are warranted(which they should be if a person isn't getting blood work to thwart that concern) then both the SERMs(primarily nolva for selectivity to bone and liver ERs) aid in alleviating the lipid effect. You can aslo take it a step further and add 20mg of policosinol.
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  #15  
Old 10-04-2004, 04:23 PM
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Quote:
Originally Posted by .......
Anastrozole supresses estrogen conversion at about 85% with a full clinical dose in a subject with normal levels of estrogen. We are males with supraphysiological levels of estrogen existing in the body post cycle, utilizing a 1/4 of the clinical dose(.25mg). At least thats the dose I recommend. You do need some estrogen to help with correlation to the AR(which is why I don't like letro) but estrogen is the main inhibitor of recovering HPTA. It needs to be controlled in order to prevent SHBG to accumilate and prolong F. Test reaching base line.

Anastrozole doesn't effect my lipids to a great extent. This of course being individualistic but if concerns are warranted(which they should be if a person isn't getting blood work to thwart that concern) then both the SERMs(primarily nolva for selectivity to bone and liver ERs) aid in alleviating the lipid effect. You can aslo take it a step further and add 20mg of policosinol.
Thanks for the reply Bro...I am sold. That is what I was thinknig that Swales post was maybe based on clinical doses of anastrozole. What ae thoughts on his advice to administer small doses of HCG throughout cycle?
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  #16  
Old 10-04-2004, 07:54 PM
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I am a strong advocateof HCG use during the cycle. I didnt inlcude it in my PCT as I feel it's part of the cycle and not the PCT. I like 500iu's every Mon/Tues, but 500 E4D is a good protocol as well
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  #17  
Old 11-13-2004, 10:01 AM
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Hi .......,

This is a great post with so much info. I been to quite a few forums, but this board seems to have all the answers.

As you seem to have in depth knowledge of Serm's, I was wondering if you would be able to help with a couple of questions.

1.You mention that Nolva is selective/expressed in breast, bone, and liver. And that clomid is selective to suprapituitary.

Not sure if I misread some of the post but I thought that clomid also had the same effect as nolva in the tissues you mentioned?? Specifically I am interested in the bone side of things. As i have heard it mentioned that clomid is an agonist in bone tissue.

2. Assuming that clomid is an agonist in bone tissue, when literature refers to clomid being an agonist, is this implying the compound (clomid) is illiciting an effect on the bone tissue that is stronger than naturally produced estrogen.....or that clomid imparts the same effects as naturally produced estrogen would, whilst blocking estrogens effects in other tissues.

Any comments information much appreciated.

T
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  #18  
Old 11-14-2004, 05:54 PM
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Quote:
Originally Posted by Taoist
Hi .......,

This is a great post with so much info. I been to quite a few forums, but this board seems to have all the answers.

As you seem to have in depth knowledge of Serm's, I was wondering if you would be able to help with a couple of questions.

1.You mention that Nolva is selective/expressed in breast, bone, and liver. And that clomid is selective to suprapituitary.

Not sure if I misread some of the post but I thought that clomid also had the same effect as nolva in the tissues you mentioned?? Specifically I am interested in the bone side of things. As i have heard it mentioned that clomid is an agonist in bone tissue.

2. Assuming that clomid is an agonist in bone tissue, when literature refers to clomid being an agonist, is this implying the compound (clomid) is illiciting an effect on the bone tissue that is stronger than naturally produced estrogen.....or that clomid imparts the same effects as naturally produced estrogen would, whilst blocking estrogens effects in other tissues.

Any comments information much appreciated.

T
1. It does have agonistic effects in relation to nolva on the forementioned tissues(and vice versa), but in studies nolva seems to have selectivity towards those tissue types in a much more substantial capacity

2. Nolva, nor clomid offer an agonistic effect which surpasses natural estrogens ability to maintain bone density. OTherwise, nolva would be prescribed to block estrogen binding in order to strengthen bone denisity regardless of a subjects estrogen count.
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  #19  
Old 11-16-2004, 05:20 AM
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Thanks .......,

Thats clarified things for me!
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  #20  
Old 05-28-2005, 02:28 PM
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Can Aromasin be used in place of the l-dex?

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