pct! use SERM or AI

[grimmeyctrain]

ok im bout to come off test pro and 'var. I know that tam is a good antagonist for receptor sites, but how and why is that superior to arimidex , which is an aromatase inhibitor, which is better during pct and why? please help

[Swifto]

ok im bout to come off test pro and 'var. I know that tam is a good antagonist for receptor sites, but how and why is that superior to arimidex, which is an aromatase inhibitor, which is better during pct and why? please help

Arimidex .

It will LOWER estrogen whilst raising LH/FSH/T.

Nolva wont and cant lower estrogen.

[fLgAtOr]

Arimidex .

It will LOWER estrogen whilst raising LH/FSH/T.

Nolva wont and cant lower estrogen.

Why only one?

[stocky121]

run at least a serm and an ai during pct

[fLgAtOr]

run at least a serm and an ai during pct

Thats what i thought too...

I stop the AI first and then the SERM.

[Swifto]

ok im bout to come off test pro and 'var. I know that tam is a good antagonist for receptor sites, but how and why is that superior to arimidex , which is an aromatase inhibitor, which is better during pct and why? please help

"Which is better", means Arimidex OR Nolva. I choose Arimidex. Which I stated in my post above.

The more I read about SERM's during PCT and when "on", the less I want to use them.

Some claim an estrogen rebound is possible with a SERM and lots of estrogen present, which can happen when using higher doses, androgens that aromotase heavily, any enviroment where estrogen can possibly build up. It seems logical when all Nolva does is "block" estrogen, let it build up, stop blocking it, then can estrogenic side become evident...Possibly.

Also vision problems seem to associate themselves with both Clomid and Nolva, more common with Clomid, however. Same be said about AI's...?

[fLgAtOr]

"Which is better", means Arimidex OR Nolva. I choose Arimidex. Which I stated in my post above.

The more I read about SERM's during PCT and when "on", the less I want to use them.

Some claim an estrogen rebound is possible with a SERM and lots of estrogen present, which can happen when using higher doses, androgens that aromotase heavily, any enviroment where estrogen can possibly build up. It seems logical when all Nolva does is "block" estrogen, let it build up, stop blocking it, then can estrogenic side become evident...Possibly.

Also vision problems seem to associate themselves with both Clomid and Nolva, more common with Clomid, however. Same be said about AI's...?

I wasn't challending you bro...Just asking "why" to continue a good conversation.

Where would the estro rebound come from when using a SERM? Is it the high estro environment that is then not "blocked" when Nolva's removed?

I would think that there would be a bigger chance of an actual estro rebound when using an AI (moreso letro). The same reason why you can boost your natty test by using these products would be the same reason for the rebound. Suppress estro sooo much that once you remove the compound, your body is still trying to increase estro levels by increasing test and aromatase.

I'm not a fan of Nolva while ON either...60mgs of Nolva for gyno symptoms??? Whatever, I guess it still works for some becuase people still do it. Old school, IMO. But I still think it has its place in PCT along with other compounds.

[Swifto]

I wasn't challending you bro...Just asking "why" to continue a good conversation.

Where would the estro rebound come from when using a SERM? Is it the high estro environment that is then not "blocked" when Nolva's removed?

I would think that there would be a bigger chance of an actual estro rebound when using an AI (moreso letro). The same reason why you can boost your natty test by using these products would be the same reason for the rebound. Suppress estro sooo much that once you remove the compound, your body is still trying to increase estro levels by increasing test and aromatase.

I'm not a fan of Nolva while ON either...60mgs of Nolva for gyno symptoms??? Whatever, I guess it still works for some becuase people still do it. Old school, IMO. But I still think it has its place in PCT along with other compounds.

Exactly what I'm thinking. I'm going to look into this a bit more and post my findings.

I think as PCT protocols progress and new ideas come about, SERM's wont serve a purpose. Why use them to increase LH/FSH/T, when AI's do the same and lower estrogen not block it. From a cost point of view, it already seems inferior IMHO.

[vitor]

An serm is a synthetic estrogen that binds to the E-recepter in tissues like the breast and hypotalamus(which are of most intrest), while it binds to the E-recepter, it doesnt have estrogenic activity there. And it will make it difficult(not impossible) for estrogen to pass thrue in these tissues, and cause problems like gyno and inhibition of the hypotalamus. But the estrogen levels will yust keep building up(if you use compunds that aromatase).
Ive been reading some materiall lately that elevated estrogen levels might limit the number of androgen recepters in each cell(so aas gets less open recepters to bind too), and it will defently have a negative effect on your mood and could cause plenty of other problems.

So I agree with Swifto, an AI is far better on an off cycle. Post-cycle an aromaste inhibitor will increase testosterone levels far more effective than an serm ever could. Nolva and Clomid is a bit outdated, but I guess it could increase the overall effect(like stimulating LH production etc) when combined with and AI, atleast when you use some of the weaker once.

When using letro though, there would be no need for an Serm imho.

[hosam4ever]

the only AI available for me is proviron here so will estrogen rebound will have less chance while using proviron over nolva ?

[Swifto]

the only AI available for me is proviron here so will estrogen rebound will have less chance while using proviron over nolva ?

Proviron didnt do much for estrogenic related sides for me. My nipple (right) swoled slightly and I felt a tiny lump. It binds to the aromotase enzyme, yes. But it wasnt an effective compound and combating aromotase, for me anyhow. I wouldnt use it again either, other to increase labido, reduce SHBG and use it only if I was using compounds that aromotase slowly or none at all.

Another AI will take Proviron's place for my next cycle...I'm thinking Aromasin .

[hungry4fitness]

Personally I have used Letro during my cycles at .5mg and then nolva and clomid for my pct and it has worked great so far for me, but everyone is different.

[toobigforyou]

Personally I have used Letro during my cycles at .5mg and then nolva and clomid for my pct and it has worked great so far for me, but everyone is different.

This, too has been my protocal. I decided to go with letro rather than arimidex because i'm more prone to gyno. Letro has worked great while on cycle @ .75mg eod, then for PCT, nolva & clomid.

[fLgAtOr]

So since this thread has been officially hijacked:

For those that don't like SERMS (ahem Swifto)...What about the estrogen rebound from AI's? Like I said above (esp with Letro) removing the thing thats deactivating or binding to the aromatase enzyme wouldn't neccessarily stop the extra test production right then and there, right? (Assuming your body is still producing extra test to increase estro levels.) It sounds more like estro would shoot up and then in turn lower test again. And tapering sounds a little touchy without some sort of back up (like nolva).

[Swifto]

So since this thread has been officially hijacked:

For those that don't like SERMS (ahem Swifto)...What about the estrogen rebound from AI's? Like I said above (esp with Letro) removing the thing thats deactivating or binding to the aromatase enzyme wouldn't neccessarily stop the extra test production right then and there, right? (Assuming your body is still producing extra test to increase estro levels.) It sounds more like estro would shoot up and then in turn lower test again. And tapering sounds a little touchy without some sort of back up (like nolva).

We can combat an estrogenic rebound if we taper the AI. If your concerned about an estrogen rebound. Taper the dosage down gradually.

If your that worried about a rebound use an SI (Suicidal Inhibitor).

[lifterjaydawg]

great pct info

[cfiler]

I like both. I haven't run a AI by itself, but I would expect it to be fine.

[fLgAtOr]

If your that worried about a rebound use an SI (Suicidal Inhibitor).

Liek Aromasin ? I think I read on another board that Aromatase activity stayed lowered even after it was stopped...Pretty iinteresting.

[fLgAtOr]

Booya!

Clin Breast Cancer 2000 Sep;1 Suppl 1:S68-73

Comparison of in vitro exemestane activity versus other anti-aromatase agents.

Soudon J.

Anastrozole, letrozole , and exemestane are the most selective and potent oral antiaromatase agents currently available. However, in vitro and in vivo studies comparing these agents are lacking. Anastrozole and letrozole are reversible, competitive nonsteroidal type II inhibitors, whereas exemestane is an irreversible steroidal type I inactivator. The study was conducted to determine the impact of this characteristic on in vitro residual aromatase activity and protein levels after incubation of JEG-3 cells with aminoglutethimide (a type II inhibitor), anastrozole, exemestane, or letrozole. Aromatase activity was measured after various incubation times with each antiaromatase agent at a concentration 10 times higher than IC50 (concentration giving 50% inhibition). Only exemestane induced a residual inhibition of aromatase activity after its removal, without any change in the aromatase protein level. Aromatase activity increased after preincubation of JEG-3 cells with either aminoglutethimide or anastrozole without any change in the aromatase protein level. The aromatase protein level increased rapidly when cells were incubated with letrozole and aromatase activity inhibition disappeared immediately after removal of the drug. The breakthrough effects in aromatase activity or protein levels observed after treatment with reversible inhibitors may be a factor in therapeutic failure with these agents. These results suggest a possible advantage for exemestane because it is the only clinically available oral irreversible aromatase inactivator.



Now would anyone like to explain to me what significance aromatase protein levels have?