I honestly don't know what that means, can you elaborate so I can learn?![]()
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?
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.
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 ...
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!
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?
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.
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?
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.
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).
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?