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pct . . . serm inverse to Ai

billhough

New member
Just want some feedback, going to run epistane, trying to decide if I should run my serm inverse to an AI, suggestions?
 
I have looked at several different pcts where people run a serm such as nolva inverse to an Ai such as ATD, for example

week 1: Nolva 40 mg
week 2: Nolva 40 mg
week 3: Nolva 20 mg, ATD 25 mg ED
week 4: Nolva 20 mg, ATD 50 mg ED
week 5: ATD 75 mg ED
week 6: ATD 50 mg ED
week 7: ATD 50 mg ED
week 8: ATD 25 mg ED

I have also seen pcts where there is an abrupt stoppage at 75 mg, just want to get some feedback of what people think of this?
 
I always taper down my AI but its a matter of preference. The main thing is not to introduce the AI until the 4th or 5th day.
 
Just want to get some different opinions, not trying to offend anybody. When you say that you don't introduce the AI until the 4th or 5th day, I assume you mean of PTC?
 
I honestly don't know what that means, can you elaborate so I can learn? :)

running a SERM inverse to an AI means that during your four(or however many) weeks of your PCT, you are going to decrease the dosage of your SERM as you normally would, as for your AI, you would start at a low dose and 'ramp' up the dosage over the span of your PCT.

for example: (x/x/x/x=your dosage week by week: assume we are using nolva for our serm and 6 OXO for our AI)
SERM: 40/30/20/10
AI:300/400/500/600

pretty simple concept really. IMO though, i dont think an AI should be used right after the cycle like in my example, i think an AI should be run the following four weeks after your four weeks of using a serm. i also think the AI should be tapered down each week. my reasoning (some agree and some dont) is i would think this is the best way to avoid estrogen rebound, as some have experienced a few weeks after finishing up their epi PCT, as an example.

so i think it should look more like this:
weeks 1-4=SERM: 40/30/20/10...
weeks 5-8=AI:...500/400/300/200
 
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Does anybody think it is best to start both the AI and serm at teh same time, tapering both down in order to allow the estrogen production to increase while the Serm is still in full effect?
 
Does anybody think it is best to start both the AI and serm at teh same time, tapering both down in order to allow the estrogen production to increase while the Serm is still in full effect?

Uh, what? Dude in pct the serm blocks estro from the breast tissue. Your body is struggling to reach a natural Homeostasis, If your estro is high your body will raise test production to try to mach it. If you kill All estrogen in your body.......well you see were I'm going with this. Drop the ATD mofo!:cheers:
 
running a SERM inverse to an AI means that during your four(or however many) weeks of your PCT, you are going to decrease the dosage of your SERM as you normally would, as for your AI, you would start at a low dose and 'ramp' up the dosage over the span of your PCT.

pretty simple concept really. IMO though, i dont think an AI should be used right after the cycle like in my example, i think an AI should be run the following four weeks after your four weeks of using a serm. i also think the AI should be tapered down each week. my reasoning (some agree and some dont) is i would think this is the best way to avoid estrogen rebound, as some have experienced a few weeks after finishing up their epi PCT, as an example.

ah, ok. Yeah I'm familiar with the concept, just didn't know the terminology for that particular method. gonna shoot you a PCT PM sometime today...
 
running a SERM inverse to an AI means that during your four(or however many) weeks of your PCT, you are going to decrease the dosage of your SERM as you normally would, as for your AI, you would start at a low dose and 'ramp' up the dosage over the span of your PCT.

for example: (x/x/x/x=your dosage week by week: assume we are using nolva for our serm and 6 OXO for our AI)
SERM: 40/30/20/10
AI:300/400/500/600

pretty simple concept really. IMO though, i dont think an AI should be used right after the cycle like in my example, i think an AI should be run the following four weeks after your four weeks of using a serm. i also think the AI should be tapered down each week. my reasoning (some agree and some dont) is i would think this is the best way to avoid estrogen rebound, as some have experienced a few weeks after finishing up their epi PCT, as an example.

so i think it should look more like this:
weeks 1-4=SERM: 40/30/20/10...
weeks 5-8=AI:...500/400/300/200

I subscribe to this theory as well ...
 
I subscribe to this theory as well ...

i assume you mean the later of my two examples, right?
how do you feel about the dosage for the 6 oxo, to high, low, right on? also just carious as to which AI is your preference with this method, (assuming its the typical epi cycle) 6 oxo or a different AI?
 
I subscribe to this theory as well ...

Me too. The latter portion that is. Especially after a non aromatizing compound like Epi.


Hate4TheWeak said:
Uh, what? Dude in pct the serm blocks estro from the breast tissue. Your body is struggling to reach a natural Homeostasis, If your estro is high your body will raise test production to try to mach it. If you kill All estrogen in your body.......well you see were I'm going with this. Drop the ATD mofo!

Not quite. If estro is high you will start to produce less test. Estro is made FROM test in males through aromatase. If estro is low, you will start to produce more test so you have the substrate with which to make more estro.

Problem with AI's in PCT is you already have low estro from the getgo with compounds that shut down your natty test production and, unless they can aromatise, will subsequently cause estro to plummet.

A SERM on the other hand will not directly effect estro but will stimulate the HPTA and, once test & estro begin to rise, ensure that any excess estrogen conversion isn't binding with the breast tissue.
 
i assume you mean the later of my two examples, right?
how do you feel about the dosage for the 6 oxo, to high, low, right on? also just carious as to which AI is your preference with this method, (assuming its the typical epi cycle) 6 oxo or a different AI?

With the second portion and I run 6-oxo at 4/3/2/1 so that's 400/300/200/100 if you run for 4 weeks or 300/200/100 @ 3 weeks ...
 
A SERM on the other hand will not directly effect estro but will stimulate the HPTA and, once test & estro begin to rise, ensure that any excess estrogen conversion isn't binding with the breast tissue.[/QUOTE]


My question, and by no means am I questioning anybody in general, just looking for clarification, is, once the test and estro begin to rise, and the serm is phased out what mechanism ensures that excess estrogen conversion isn't binding with breast tissue? The AI?
 
A SERM on the other hand will not directly effect estro but will stimulate the HPTA and, once test & estro begin to rise, ensure that any excess estrogen conversion isn't binding with the breast tissue.


My question, and by no means am I questioning anybody in general, just looking for clarification, is, once the test and estro begin to rise, and the serm is phased out what mechanism ensures that excess estrogen conversion isn't binding with breast tissue? The AI?[/QUOTE]

In theory yes. Introducing the AI and ramping it up as you ramp down the SERM should prevent the conversion of test to estrogen. The problem is that when you ramp up and then suddenly stop the AI there is no estrogen control and that is typically when you might see a rebound as the body tries to balance out estrogen and test levels.
 
A SERM on the other hand will not directly effect estro but will stimulate the HPTA and, once test & estro begin to rise, ensure that any excess estrogen conversion isn't binding with the breast tissue.


My question, and by no means am I questioning anybody in general, just looking for clarification, is, once the test and estro begin to rise, and the serm is phased out what mechanism ensures that excess estrogen conversion isn't binding with breast tissue? The AI?[/QUOTE]

serms have very long half lives so even after phasing out the serm it will still be circulating in your body for at least a week or more. once the serm is completely removed from your body, there wont be anything that actually prevents estrogen from binding to breast tissue, but the AI is now going to be phased in which regulates the amount of circulating estrogen. so estorgen may bind to breast tissue but hopefully, with the use of the AI, your estrogen will be in a normal or slightly below normal range so the small amount that dose bind to breast tissue wont cause gyno.
 
My question, and by no means am I questioning anybody in general, just looking for clarification, is, once the test and estro begin to rise, and the serm is phased out what mechanism ensures that excess estrogen conversion isn't binding with breast tissue? The AI?

serms have very long half lives so even after phasing out the serm it will still be circulating in your body for at least a week or more. once the serm is completely removed from your body, there wont be anything that actually prevents estrogen from binding to breast tissue, but the AI is now going to be phased in which regulates the amount of circulating estrogen. so estorgen may bind to breast tissue but hopefully, with the use of the AI, your estrogen will be in a normal or slightly below normal range so the small amount that dose bind to breast tissue wont cause gyno.[/QUOTE]

AI's can also hypersenstize ER's so it is best to taper them off to prevent this from happening. With hypersensitive ER's even a small amount of estrogen can cause a larger effect (rebound gyno).
 
Me too. The latter portion that is. Especially after a non aromatizing compound like Epi.




Not quite. If estro is high you will start to produce less test. Estro is made FROM test in males through aromatase. If estro is low, you will start to produce more test so you have the substrate with which to make more estro.

Problem with AI's in PCT is you already have low estro from the getgo with compounds that shut down your natty test production and, unless they can aromatise, will subsequently cause estro to plummet.

A SERM on the other hand will not directly effect estro but will stimulate the HPTA and, once test & estro begin to rise, ensure that any excess estrogen conversion isn't binding with the breast tissue.

Thanks bro, someone else had to straighten my ass out on that too. I swear someone told me that on here though! Anyways repps...:wave:
 
AI's can also hypersenstize ER's so it is best to taper them off to prevent this from happening. With hypersensitive ER's even a small amount of estrogen can cause a larger effect (rebound gyno).

good point. serms up regulate the estrogen receptors as well.
 
My question, and by no means am I questioning anybody in general, just looking for clarification, is, once the test and estro begin to rise, and the serm is phased out what mechanism ensures that excess estrogen conversion isn't binding with breast tissue? The AI?

In theory yes. Introducing the AI and ramping it up as you ramp down the SERM should prevent the conversion of test to estrogen. The problem is that when you ramp up and then suddenly stop the AI there is no estrogen control and that is typically when you might see a rebound as the body tries to balance out estrogen and test levels.[/QUOTE]

Last question! You mentioned above that introducing the AI and ramping it up, is the ramping up necessary?, or, in theory is it as effective just to introduce the AI (say 400 mg of 6 oxo) after the nolva has been phased out or must it first be ramped up?

Thanks for all the input
 
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