You and your AI

[Kohen_Gadol]

I don't post much and I do not intend to post much but while I am killing some time tonight waiting for someone, I decided to scan this board and the amount of brotological nonsense I see posted on here is just overwhelming.

Look, if you are a man, you want to use a steroidal AI over a triazole AI if you can help it. I realize that the triazole based stuff (letrozole, anastrazole, vorozole) have better IC-50 values than just about all the steroidal based/mechanical AI's like formestane, exemestane, atamenstane with ATD being about as close as its going to get. I also realize that the steroidal AI's probably mean most people are going to need to take something 2-3X per day unlike a triazole which can probably be taken every other or third day.

Lets forget the drug vs supp aspect for a moment, OK?

The biggest reason why men should stick to steroidal based AI's is there is good evidence that they actually bind to and destroy aromatase (that is to say they reduce the amount of the enzyme floating around) while the triazole based AI's tend to have the OPPOSITE effect (despite being more "potent" if that is the word I am looking for).

If you are going to rebound from an AI its gonna be from letrozole or anastrazole and not a steroidal like ATD, androst-4-ene-3,6,17-trione or the 5a (or exemestane or atamestane).

I would never use or go near an illegal "anything" ever again and I'm not an MD and I will not suggest anyone use anything illegal but without a doubt, if I were going to use and needed a PCT agent it would for sure be a steroidal AI and not a triazole AI if I had a choice (and I realize I might not) and for sure its not going to be a SERM (which is just like delaying the inevitable).

One more time - there is good evidence that steroidal AI's actually inactivate aromatase through a protease mechanism thus decreasing both aromatase activity and sheer amount of it (wicked cool!) while triazole type AI's inactivate aromatase (better than steroidal AI's for sure) but tend to increase sheer enzyme amount.

Yeah, letro and anastro are wicked potent. But if you are likely to rebound and not everyone is, its gonna be off a triazole and not a steroidal AI.

I know the brotologists will attack me here and say I am clueless and they have all this experience and I am just some stupid, ex-con juice dealer who has no clue and then they'll attack my character or whatever.

I am correct about this. If you do your homework, you'll conclude that indeed I am spot on 100% here.

For my money, nothing beats ATD and 6-bromo and 5a-trione. Nothing that is available as a supplement anyhow...nothing..."yet"


BK

[BlackCoffee]

great post.

[TrainingACU]

Got any specific products in mind, OP?

[UNCfan1]

I love your posts, I wish you would post more.

[quank]

Subbed!!

[thauncle]

interesting post i agree to an extent.so when is your 5a-trione product coming out I'm interested in this.

[kerplunk]

I learned something

[jeremyleinen]

So, I'm not sure I understand... Are you saying that ATD, 6bromo, or Formex would be better suited for PCT than a SERM?

[taze13]

Had to read it a few times to process it lol. Good stuff though.

[thauncle]

So, I'm not sure I understand... Are you saying that ATD, 6bromo, or Formex would be better suited for PCT than a SERM?

I believe he is.this should be a very interesting discuss.

[jeremyleinen]

I believe he is.this should be a very interesting discuss.

I'm hoping he'll be back around to confirm. If this is the case, this should turn into a pretty hotly debated topic.

[Problem]

You didn't type anything new.

I still think SERMs are needed.

What if you used a compound that doesn't aromatize?

[cal62887]

Nice post, B

[samson08]

So would you say forget the Nolva and get a bottle of Hyperdrol X2 for PCT? (On something that does not aromatize or is an anti estrogen i.e. Epistane?)

[factotum]

Interesting.

Granted the anecdotal reports of estrogen rebound and gyno come primarily from those who have used the steroidal AIs; so why is this? Could it be that since they are OTC and easily acquirable more people (mis)use them? And those going grey market may pay greater diligence to dosing protocols hence the far fewer reports of gyno? Of course the whole self diagnosis of gyno is another issue in itself. And then there's the use of AIs for gyno treatment, of which 'triazole' AIs seem to elicit better effects, presumably because they are more "potent" inhibitors. Or perhaps the prolonged half-life conveys some additional benefits and offsets some drawbacks.

But more interestingly, let's talk about why you don't like a SERM for PCT.

[jeremyleinen]

But more interestingly, let's talk about why you don't like a SERM for PCT.

I would very much like to see this discussion.

[Teledin]

subbed

[thauncle]

Interesting.

Granted the anecdotal reports of estrogen rebound and gyno come primarily from those who have used the steroidal AIs; so why is this? Could it be that since they are OTC and easily acquirable more people (mis)use them? And those going grey market may pay greater diligence to dosing protocols hence the far fewer reports of gyno? Of course the whole self diagnosis of gyno is another issue in itself. And then there's the use of AIs for gyno treatment, of which 'triazole' AIs seem to elicit better effects, presumably because they are more "potent" inhibitors. Or perhaps the prolonged half-life conveys some additional benefits and offsets some drawbacks.

But more interestingly, let's talk about why you don't like a SERM for PCT.

solid questions fact.

I guess kb must be very confident in the new product they are releasing if he created a thread such as this.

[DR_P]

I don't post much and I do not intend to post much but while I am killing some time tonight waiting for someone, I decided to scan this board and the amount of brotological nonsense I see posted on here is just overwhelming.

Look, if you are a man, you want to use a steroidal AI over a triazole AI if you can help it. I realize that the triazole based stuff (letrozole, anastrazole, vorozole) have better IC-50 values than just about all the steroidal based/mechanical AI's like formestane, exemestane, atamenstane with ATD being about as close as its going to get. I also realize that the steroidal AI's probably mean most people are going to need to take something 2-3X per day unlike a triazole which can probably be taken every other or third day.

Lets forget the drug vs supp aspect for a moment, OK?

The biggest reason why men should stick to steroidal based AI's is there is good evidence that they actually bind to and destroy aromatase (that is to say they reduce the amount of the enzyme floating around) while the triazole based AI's tend to have the OPPOSITE effect (despite being more "potent" if that is the word I am looking for).

If you are going to rebound from an AI its gonna be from letrozole or anastrazole and not a steroidal like ATD, androst-4-ene-3,6,17-trione or the 5a (or exemestane or atamestane).

I would never use or go near an illegal "anything" ever again and I'm not an MD and I will not suggest anyone use anything illegal but without a doubt, if I were going to use and needed a PCT agent it would for sure be a steroidal AI and not a triazole AI if I had a choice (and I realize I might not) and for sure its not going to be a SERM (which is just like delaying the inevitable).

One more time - there is good evidence that steroidal AI's actually inactivate aromatase through a protease mechanism thus decreasing both aromatase activity and sheer amount of it (wicked cool!) while triazole type AI's inactivate aromatase (better than steroidal AI's for sure) but tend to increase sheer enzyme amount.

Yeah, letro and anastro are wicked potent. But if you are likely to rebound and not everyone is, its gonna be off a triazole and not a steroidal AI.

I know the brotologists will attack me here and say I am clueless and they have all this experience and I am just some stupid, ex-con juice dealer who has no clue and then they'll attack my character or whatever.

I am correct about this. If you do your homework, you'll conclude that indeed I am spot on 100% here.

For my money, nothing beats ATD and 6-bromo and 5a-trione. Nothing that is available as a supplement anyhow...nothing..."yet"


BK

This is pretty old news and has been discussed several years ago here at this board.
Nonetheless, it's correct. Non-steroidal AI's do indeed tend to upregulate aromatase while steroidal AIs don't.

However, the conclusions you draw are not necessarily correct.

As long as you are on letrozole or anastrozole, aromatase upregulation gets completely overridden by the anti-aromatase effect of the active substance. And how long do increased aromatase levels stay in your system after cessation of the drug? A few hours perhaps? What is the real-world relevance of this temporary upregulation?

SERMs are well known to increase estrogen levels and to even increase estrogen receptor sensitivity. Nonetheless, they represent an implicit 'gold standard' in PCT.

If your conclusions were correct, then boards would be full of reports about rebound gyno and rebound hypogonadism from people who have been using triazole AIs and / or SERMs.

Interestingly, however, the most noise about delayed gyno arouse just in relation to Superdrol + ATD (when this cycle / PCT combo got populare three years ago)

Just an example that some biochemical properties and their theoretical, expected effects do not always necessarily need to translate to real-world effects.

[UNCfan1]

Interesting.

Granted the anecdotal reports of estrogen rebound and gyno come primarily from those who have used the steroidal AIs; so why is this? Could it be that since they are OTC and easily acquirable more people (mis)use them? And those going grey market may pay greater diligence to dosing protocols hence the far fewer reports of gyno? Of course the whole self diagnosis of gyno is another issue in itself. And then there's the use of AIs for gyno treatment, of which 'triazole' AIs seem to elicit better effects, presumably because they are more "potent" inhibitors. Or perhaps the prolonged half-life conveys some additional benefits and offsets some drawbacks.

But more interestingly, let's talk about why you don't like a SERM for PCT.

I love your posts too! This could be a GREAT thread!

[thauncle]

This is pretty old news and has been discussed several years ago here at this board.
Nonetheless, it's correct. Non-steroidal AI's do indeed tend to upregulate aromatase while steroidal AIs don't.

However, the conclusions you draw are not necessarily correct.

As long as you are on letrozole or anastrozole, aromatase upregulation gets completely overridden by the anti-aromatase effect of the active substance. And how lobg do increased aromatase levels stay in your system after cessation of the drug? A few hours perhaps?

SERMs are well known to increase estrogen levels and to even increase estradiol levels. Nonetheless, they represent an implicit 'gold standard' in PCT.

If your conclusions were correct, then boards would be full of reports about delayed gyno or rebound gyno and reboundhypogonadism from people who have been using triazole AIs and / or SERMs.

Interestingly, the most noise about delayed gyno arouse after Superdrol + ATD.

Just an example that some biochemical properties and their theoretical, expected effects do not always necessarily need to translate to real-world effects.

very well said.too bad i'm on spread.I'd rep you with the lil reps i have left.you always give good responses.

[Billton]

You didn't type anything new.

I still think SERMs are needed.

What if you used a compound that doesn't aromatize?

By your logic a SERM is not useful for a non-aromatizing compound either. There is no need to block or reduce estrogen while on a non-aromatizing compound. The problem is once you're off. Your body starts to produce test, but your ER's are sensitive from the lack of estrogen over the past weeks. Your test aromatizes into estrogen and attaches to ER's. The over sensitive ER's cause estrogen related sides and shutdown of test production. If you took a SERM it would prevent the estrogen related sides by prevent estrogen from attaching to the receptor, while causing estrogen levels to build up. If you took an AI you would prevent the estrogen production in the first place.

[bryan101b]

comming from someone who doesn't like bro science, im suprised there isn't more data in your post. you are making some sense, but data based studies, and links to those will speak louder.

any how, aside from the type of a.i. you use, rebound is still going to occur. once you start the hpta balancing act, it takes a master to get it under control with little to no side effects like rebound.

lets start with the basics,

you increase T (pick your steroid) and your hpta, sensing the increase, stops natural production of T, and then increases production of E, among other hormones, to balance it out, and return the body back to normal.

skip ahead to end of cycle...

you take, (or should) be taking a serm, which blocks E from it's receptor sites. E ultimately increases, and the hpta ultimately goes back to trying to balance everything out again.

The hpta begins to decrease production of E, and increase T to level out the playing feild.

This is around the time when one should begin taking an A.I. to prevent the newly produced T from aromatizing into E, and also discontinue taking the s.e.r.m.

here is the tricky part where most a.i. users mess up, no matter what type ur using.

one should begin tapering the a.i. immediately, and this is to prevent the hpta from sensing the decrease in aromatase, and increasing production, creating rebound. When one just stops taking the A.I., you will have an abundance of aromatase floating around, with nothing to inhibit it from converting T into E. and your are f*cked.

these are the basics of pct. not bro science, facts. links are posted in my sig.
this isn't even getting into the world of hcg, cortisol control, or growth hormone.

the point is, unless you are prepared to deal with the sides, one should never start the nearly impossible hpta balancing act of hormones.

this is how lawsuits get started, and thing get banned, uninformed, stupid consumers.

[Billton]

When using a suicide inhibitor of aromatase there is no increase in aromatase enzyme. There is a decrease. It then takes some time for the enzyme levels to get back up to normal. That causes a slow rise in estrogen levels. Once E levels are normal your HPTA slows T production to maintain the correct level of estrogen. No rebound should occur.

[DR_P]

When using a suicide inhibitor of aromatase there is no increase in aromatase enzyme. There is a decrease. It then takes some time for the enzyme levels to get back up to normal. That causes a slow rise in estrogen levels. Once E levels are normal your HPTA slows T production to maintain the correct level of estrogen. No rebound should occur.

True, but only one part / fraction of the reality.

What we must not forget is the potential androgenicity / antiandrogenicity of various steroidal AIs and their metabolites.

Another thing that must not be neglected is that ANY disturbance of homeostasis (and aromatase inhibition and reduction of E2 levels is such a disturbance) will evoke counterregulatory mechanisms that will try to re-establish homeostasis. Interestingly, the body does have redundant levels for homeostatic regulation. That means: receptor up- or downregulation and aromatase up- and downregulation are most certainly not the only levels at which the body may try to counterregulate the effects of steroidal AIs.

There is a huge machinery involved in post-receptor signalling, which may have significant influence on the net effects of estradiol reduction. and the exact mechanisms are pretty much unknown. IOW: We don't know what kind of homeostatic (pro-estrogenic) mechanisms non-steroidal AIs are eliciting, and it is absolutely reasonable to postulate that there might be something happening...

We don'T even udnerstand why some steroidal AIs rather increase than decrease estradiol and/or estrone levels, let alone how exactely they influence the incredibly complex hormone and hormone-signalling homeostasis.

[oxo cube]

This is what I don't get about AI's. Used alone, they can be reccomended as otc test boosters, the mechanism of which is that the body supposedly raises test to counter act the decline in estrogen, but then estrogen levels return to the somewhat normal range, as the body produces more test. But then AI's are also reccomended for gyno to reduce estrogen. It can't be both, surely?

[Illadelphia]

So would you say forget the Nolva and get a bottle of Hyperdrol X2 for PCT? (On something that does not aromatize or is an anti estrogen i.e. Epistane?)

Epistane is hardly an anti estrogen. This is where the broscience fails


Someone a year or so back said epistane would have gyno reducing properties. It doesn't, please stop repeating what you hear by portraying it as truth, thanks.

[GeneGnomeX]

Epistane is hardly an anti estrogen. This is where the broscience fails

Epitiostanol (non-methyl) is anti-estrogenic.

[samson08]

Epistane is hardly an anti estrogen. This is where the broscience fails


Someone a year or so back said epistane would have gyno reducing properties. It doesn't, please stop repeating what you hear by portraying it as truth, thanks.

Bro science fails when someone like you tries to portray the wrong image of the truth. Everyone, Epistane is an anti-estrogen. Don't listen to ill. Look it up. It's called research

[Illadelphia]

Bro science fails when someone like you tries to portray the wrong image of the truth. Everyone, Epistane is an anti-estrogen. Don't listen to ill. Look it up. It's called research

Show me the research then, since you portray the "right image of truth"

I bet epistane being an "ai" will cure gyno too?