AI During PCT Question

I’ve seen some people advise to run an AI all the way through PCT, but this is my understanding. Please excuse my lack of proper terms:

Assuming you weren’t a retard and you used an AI throughout cycle:

End of Cycle: above baseline test, below baseline est
Time between Cycle and PCT: Decreasing test, Low est (from continued AI Use)
PCT: Raising test and est to baseline (stop AI day before SERM PCT starts)

I can understand why you would want to keep running an AI between Cycle and PCT, because your test levels will still be high until the ester clears

But if I use aromasin during cycle there should be no need to run it during PCT, because test levels wouldn’t be high enough to cause aromatization? And because I use aromasin there is no E rebound? I’m not sure how it would work with a non-suicudal AI, but from my understanding it seem that aromasin is superior.

Is this correct or did I miss something?

First understand how a SERM and Ai work.

Aromasin is a suicidal AI, but your body is constantly making aromatase enzymes. So it doesn’t mean just because you take it you wont have anymore for whatever amount of time. So really some become deactivated all while new ones are being made.

An AI stops the conversion of T into E. While a SERM blocks the receptors estrogen bind to.

Now during pct you will still have T in your body, the T just doesn’t disappear in that time frame between last pin and start of pct. You want to start pct when your T is around baseline of normal levels. So really during pct you still have a small amount of T, which will start to aromatize. Now you start your SERM which blocks the receptors, thus making your body think it has no estrogen, which then makes your body want to start making T again.

So during pct your tricking your body into making T by blocking estrogen receptors, so as pct continues and your body starts coming back and making T the AI will stop the conversion so when you stop taking the serm you don’t have a bunch of E floating around waiting to attach to receptors, elimitating any estrogen rebound

[quote]BUDs wrote:

Aromasin is a suicidal AI

Explain

[quote]Paulaner6947 wrote:
I’ve seen some people advise to run an AI all the way through PCT, but this is my understanding. Please excuse my lack of proper terms:

Assuming you weren’t a retard and you used an AI throughout cycle:

End of Cycle: above baseline test, below baseline est
Time between Cycle and PCT: Decreasing test, Low est (from continued AI Use)
PCT: Raising test and est to baseline (stop AI day before SERM PCT starts)

I can understand why you would want to keep running an AI between Cycle and PCT, because your test levels will still be high until the ester clears

But if I use aromasin during cycle there should be no need to run it during PCT, because test levels wouldn’t be high enough to cause aromatization? And because I use aromasin there is no E rebound? I’m not sure how it would work with a non-suicudal AI, but from my understanding it seem that aromasin is superior.

Is this correct or did I miss something?

[/quote]

you need to understand how the half-life applies here…

test e has like a 5 day half-life… so what that means, is each dose is reduced by half every 5 days.

so if i take 500 mg, then it becomes, 250, 125, etc… and so do all the previous doses.

and since most men produce 20-50 mg/wk of testosterone on their own, the exogenous testosterone isn’t even low enough for your HPTA to really start working until 2-4 weeks after your last dose (depending on the dose, ester, etc).

and since estrogen is literally hundreds of times more suppressive to the HPTA than testosterone is, we especially do not want high estrogen in PCT, as it will defeat the whole purpose…

[quote]cycobushmaster wrote:

you need to understand how the half-life applies here…

test e has like a 5 day half-life… so what that means, is each dose is reduced by half every 5 days.

so if i take 500 mg, then it becomes, 250, 125, etc… and so do all the previous doses.

and since most men produce 20-50 mg/wk of testosterone on their own, the exogenous testosterone isn’t even low enough for your HPTA to really start working until 2-4 weeks after your last dose (depending on the dose, ester, etc).

and since estrogen is literally hundreds of times more suppressive to the HPTA than testosterone is, we especially do not want high estrogen in PCT, as it will defeat the whole purpose…
[/quote]

Okay, this makes sense. So would it be wise to run an AI into PCT until enough ester clears so that your test levels would in the baseline range? Or would it be better to just run the AI all the way through PCT?

I’ve often seen that [PCT start day] = [day of last pin] + [half life of ester]. But couldn’t you still be suppressed at this point depending on the dose + ester? Instead of a general formula, shouldn’t you do the math for each cycle to figure when test levels will be around baseline(as suggested by BUDs above), then start PCT with a SERM?

Wait time between last pin and pct depends on the ester of the gear and how much gear you have been running.

Going into pct you will still have T in your body coverting to E. As you go through pct taking your SERM your body will be making T which will Convert into E. So yes it’s wise to run an AI through pct

[quote]cycobushmaster wrote:

and since estrogen is literally hundreds of times more suppressive to the HPTA than testosterone is, we especially do not want high estrogen in PCT, as it will defeat the whole purpose…
[/quote]

So are you saying that one should run an aromasin all the way through PCT and potentially longer? I’m getting confused by your change of thought process in this thread (http://tnation.T-Nation.com/free_online_forum/sports_training_performance_bodybuilding_gear/thoughts_on_planning_pct?id=5898188&pageNo=1#bottom), and I was wondering if you could clarify why you changed your views on PCT? Specifically, why did you go from the view that an AI and SERM should be ran together, to the view that and AI should be ceased a week after SERMs start? I would send a private message but I’ve been reading they don’t work.

Thanks

It is kind of a mind bender because it doesn’t seem like you can ever stop taking the AI then.

Would it makes sense to slowly taper the AI over few weeks after the SERM?

I don’t run an AI during PCT. I taper it down in the weeks before as I taper down my test

1 Like

[quote]Igs wrote:
Would it makes sense to slowly taper the AI over few weeks after the SERM?[/quote]

anymore, i typically recommend tapering the AI down when you’ve started the SERM.

[quote]Paulaner6947 wrote:

[quote]cycobushmaster wrote:

you need to understand how the half-life applies here…

test e has like a 5 day half-life… so what that means, is each dose is reduced by half every 5 days.

so if i take 500 mg, then it becomes, 250, 125, etc… and so do all the previous doses.

and since most men produce 20-50 mg/wk of testosterone on their own, the exogenous testosterone isn’t even low enough for your HPTA to really start working until 2-4 weeks after your last dose (depending on the dose, ester, etc).

and since estrogen is literally hundreds of times more suppressive to the HPTA than testosterone is, we especially do not want high estrogen in PCT, as it will defeat the whole purpose…
[/quote]

Okay, this makes sense. So would it be wise to run an AI into PCT until enough ester clears so that your test levels would in the baseline range? Or would it be better to just run the AI all the way through PCT?

I’ve often seen that [PCT start day] = [day of last pin] + [half life of ester]. But couldn’t you still be suppressed at this point depending on the dose + ester? Instead of a general formula, shouldn’t you do the math for each cycle to figure when test levels will be around baseline(as suggested by BUDs above), then start PCT with a SERM?
[/quote]

yeah, that’s kinda what i was explaining as well.

generally, i think it’s easier for most people to just do a quick spreadsheet and plug in the numbers and figure it out there…

I’ve been trying to do more research on the whole aromitization process, but I’m kinda coming up blank trying to find the answers to these questions. I think once I have answers I can totally understand and determine for myself the optimal choice for AI use during PCT. As of now I don’t see how it could be harmful to keep running your AI and taper it off after your finish running your SERM, assuming you adjust the dosage properly in conjunction with your decreasing test levels

  1. Does your body produce more aromatase when attempting to restore the T:E ratio, or does the aromatase already in your body just become active? I suspect the answer to this is “both”, but any specifics would be nice.
  2. Would your body perceive a lack of estrogen and compensate by increased aromatase activity/production? If this is the case, I think it would surely be more beneficial to run an AI until you are finished with your PCT, as excess estrogen could bind to androgen receptors and make recovering your natural test production more difficult.
  3. How long does it take after test levels drop below baseline for your body to cease increased aromatase activity? You should run your AI into your PCT for at least this long, but this is irrelevant if the answer to question 2 is yes.

If anyone could link me to journal abstracts that answer these questions I would love to read them myself, but I’ve been searching for about 30 minutes and haven’t found anything useful.

Thanks

estrogen doesn’t bind to androgen receptors…

here’s a thread i started a while ago about estrogen, etc… http://tnation.T-Nation.com/free_online_forum/sports_training_performance_bodybuilding_gear/thoughts_on_estrogen_and_gyno_management

[quote]cycobushmaster wrote:
estrogen doesn’t bind to androgen receptors…

here’s a thread i started a while ago about estrogen, etc… Thoughts on Estrogen and Gyno Management - Pharma - Forums - T Nation
[/quote]

I will check out the thread, estrogen definitely binds to androgen receptors though.

[quote]Paulaner6947 wrote:

[quote]cycobushmaster wrote:
estrogen doesn’t bind to androgen receptors…

here’s a thread i started a while ago about estrogen, etc… http://tnation.T-Nation.com/free_online_forum/sports_training_performance_bodybuilding_gear/thoughts_on_estrogen_and_gyno_management
[/quote]

I will check out the thread, estrogen definitely binds to androgen receptors though.

http://tnation.T-Nation.com/free_online_forum/sports_training_performance_bodybuilding_trt/estradiol_why_you_should_care

[/quote]

^that study refers to a reduction in the number of androgen receptors. not really binding, but it does affect their number…

that is interesting to see, although that study was referencing the effect of E2 on the AR in breast cancer cells.

anyway, i found this, which claims E cannot bind to the AR:

"Hormones, though, only bind to certain, compatible receptor types. Thyroid hormones and each steroid hormone group - the estrogens, androgens, progestins, glucocorticoids (stress hormones), and mineralocorticoids (water and ion-regulating hormones) - have a matching hormone receptor type. For instance, estrogen hormones, like estrone, bind to estrogen receptors (ER); androgen hormones, such as testosterone, bind to androgen receptors; and so on.

But, steroid hormone receptors for each hormone group can occur in several versions that differ in form, function, and location. So, steroid and thyroid hormones are not restricted to interact with only one receptor, in one tissue, to produce one kind of action. The hormones can easily bind and activate several versions of their matching receptor type. An example is the estrogen 17-beta-estradiol. It binds to both the ER alpha and ER beta receptors but not to androgen, progestin, or thyroid receptors."

however, i’m gonna keep doing some digging, as i think you have any interesting point here, as far as reducing androgen receptors…

http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.327.5377&rep=rep1&type=pdf

^i haven’t had a chance to read this yet, but it seems pertinent to our conversation…