AI's and Avoiding Estrogen rebound

[Ehren]

Just wondering if Macro and other knowledgeable folks could chime in here.

My question is re: Estrogen rebound and how to avoid it after the cycle is done, and through PCT...I've searched the boards, but with little success.

Other questions are:

Should a shorter cycle protocol be any better re: aromatization? For example, Test Prop or Acetate 100mg/eod 3 weeks on 3 weeks off?

Or switch to Primo for the base with lower-dosed Test (250mg/week)for 12-16weeks?

I'd also like to start using HcG on cycle, but fear the estrogen that comes wth it.

I've tried tapering the AI, (either Aromasin or AIFM at different times with similar results.) Both are great (thank you Macro/AIFM) on cycle at higher doses for me (25mg/ed Aromasin for example).

But even if tapering either of them through PCT, I still get what seems to be, via blood tests, a rebound. 4 weeks after PCT, I'm just out of normal range (high) and 4 months after PCT (before the next cycle), I'm back to the middle of normal range. So it seems like a rebound. Plus, I hold fat in Estro prone places, lower back and glutes...

To add insult to injury, I'm moving among different countries for work and will be for a time. AAS access is legal in many, so this is good, but my access to bloodwork is less available.

The most recent cycle (in an AAS legal country) was:
12 weeks:
500mg Test E/wk.
Anavar: 40mg/day 8 weeks (1-8)
Arimidex: .5 to 1mg/day depending on bloat. (4 weeks at .5mg. then 8 weeks at 1mg.) Didn't like Arimidex. Going back to Aromasin.

Anyway, if I'm doing anything badly wrong, feel free to hammer away. Any advice would be excellent.

For background:
I'm 36y/o, 223lbs, 6'2" 12% (never go higher).
Been training 20 years, PL, Oly lifting, Track and Field, BBing (and losing bodyfat) for the last 5 with no breaks. AAS history 5 cycles. 2 were 15 years ago: Test/Drol X2, Then beginning again 2 years ago: 1)Test only 2)Test/Winnie 3)Test/Var

 

[PsyT]

bump, i have heard there is much less rebound from aromasin compared to other AIs...sorry can't help you out but interested in replies so bumping for you.

 

[Macro]

there is no rebound with exemestane.

not a fan of the taper, and there is still rebound with all competitive inhibitors. they block synthesis, that upregulates production when they remove.

HCG is fine, just keep the doses moderate.

big fan of prolactin suppression, for a whole host of reasons. DOPAMINERGICS will be a staple in this arena, they should be already. particularly compounds like pramipexole and selegiline. because of their protective/restorative effects on the dopaminergic system which is taxed and somewhat readily damaged by strong androgen use (as strong androgen increase dopamine release as well as NE levels, they can decrease MAO-A and increase MAO-b (not a good shift).

if your E levels remain high after cycle, you may have ongoing prolactin issues or have developed fat or breast tissue that is putting out a lot of aromatase (though age and liver strain are also possibles)

 

[Ehren]

PsyT thanks for the bump and MACRO, thanks for the answer! Aromasin it is then.

I'll get full bloods done as in the coming months, and check on the prolactin at that time. I was hoping to save the dopaminergic for Tren use in the distant future. But if I need it, of course I will get some.

Thanks again!

 

[Macro]

PsyT thanks for the bump and MACRO, thanks for the answer! Aromasin it is then.

I'll get full bloods done as in the coming months, and check on the prolactin at that time. I was hoping to save the dopaminergic for Tren use in the distant future. But if I need it, of course I will get some.

Thanks again!

JMHO but PREVENTION rather than treatment should be the emphasis, though when it comes to these issues in bodybuilding (almost a "me too tough to get sides-- me get sides me do something--if bad-- usually me wait till get real bad-- so dont affect my gains" attitude) so many preach the opposite. And can say with absolute certainty that dealing with a DEVELOPED issue is more troublesome and costly (both in time and effort, with estrogen and prolactin it would be fair to say psychologically as well).

as a note- excess estrogen and prolactin dont produce gains--- excess insulin CAN (though there are caveats there)

 

[EDED]

there is no rebound with exemestane.

not a fan of the taper, and there is still rebound with all competitive inhibitors. they block synthesis, that upregulates production when they remove.

HCG is fine, just keep the doses moderate.

big fan of prolactin suppression, for a whole host of reasons. DOPAMINERGICS will be a staple in this arena, they should be already. particularly compounds like pramipexole and selegiline. because of their protective/restorative effects on the dopaminergic system which is taxed and somewhat readily damaged by strong androgen use (as strong androgen increase dopamine release as well as NE levels, they can decrease MAO-A and increase MAO-b (not a good shift).

if your E levels remain high after cycle, you may have ongoing prolactin issues or have developed fat or breast tissue that is putting out a lot of aromatase (though age and liver strain are also possibles)

elaborate 'synthesis' and 'production'

 

[MrCyp]

From what i've heard, LETRO is the only anti-e that can cause any type of a rebound but rebounds are overhyped and not really a big deal. Its a few days with imbalanced estrogen at the most.

 

[Ehren]

Macro,
You mentioned the that strong androgens do a number on the Dopaminergic system. So by "prevention", are you saying it's good practice to include Dopaminergics in regular cycles that don't include Progestins, but a regular test base?

Don't want to put words in your mouth, so just clarifying...

 

[Macro]

From what i've heard, LETRO is the only anti-e that can cause any type of a rebound but rebounds are overhyped and not really a big deal. Its a few days with imbalanced estrogen at the most.

competitive inhibitors upregulate aromatase MRNA, beyond thier removal. How significant this effects is will likely vary between individuals.


HOWEVER even if there is not a significant upregulation (its only been measured in limited tissues, primarily brain and liver), the shift from low estrogen to even normal can cause issues. even with a taper, the very low doses of letrozole and anastrozole will still be highly suppressing aromatase in central tissues. Thus as that drops there can be basically a spike and then some. ER's are going to generally be upregulated (since you are starving them of the hormone)... hence why its a good idea to use a suicidal inhibitor. necessity.. probably not for most people... but for people that already have estrogen issues.. certainly can be.

technically because of half life and potency there should be LESS rebound from letrozole as compared to anastrozole... but thats gym lore for you.

 

[Macro]

Macro,
You mentioned the that strong androgens do a number on the Dopaminergic system. So by "prevention", are you saying it's good practice to include Dopaminergics in regular cycles that don't include Progestins, but a regular test base?

Don't want to put words in your mouth, so just clarifying...

yes. though need will vary. generally one can only see benefit from limiting potential damage to dopaminergic neurons. Selegiline is another option, less traditional dopaminergic, its primary action is inhibition of mao-b (basically its neuroprotective and allows for greater dopamine levels.)

for people who have the signs of prolactin issues or have had them previously, will go out on the limb and say in general dopaminergics should be a staple.

 

[Kaladryn]

It seems likely to me that a suicidal AI could up-regulate production of Aromatase. I'm not saying it does, just that it seems like it could, I'd be more interested in aromasin (and appreciative) if someone could disprove that for me.

 

[PsyT]

^ what do you mean it seems more likely? Evidence? Or are you just using your 'common sense'? There are lots of counter-intuitive facts in neuroendocrinology....I wouldn't 'go with your gut' here on this one man

but you're right it would be nice to have somebody explain it. I would like to know the mechanism also behind the rebound on letro and why aromasin doesn't get the same rebound...

 

[Macro]

It seems likely to me that a suicidal AI could up-regulate production of Aromatase. I'm not saying it does, just that it seems like it could, I'd be more interested in aromasin (and appreciative) if someone could disprove that for me.

it does not. at least exemestane does not.

 

[Macro]

^ what do you mean it seems more likely? Evidence? Or are you just using your 'common sense'? There are lots of counter-intuitive facts in neuroendocrinology....I wouldn't 'go with your gut' here on this one man

but you're right it would be nice to have somebody explain it. I would like to know the mechanism also behind the rebound on letro and why aromasin doesn't get the same rebound...

letrozole competitive binds to sites to inhibit aromatase synthesis (eg stops them from making aromatase)

exemestane interacts with aromatase enzyme, inactivating it (eg. jacks up the aromatase ENZYME that was produced so that its "done")

 

[MrCyp]

Macro, would clomid act as an anti-e by eliminating total estro or is it just a serm.

 

[Macro]

Macro, would clomid act as an anti-e by eliminating total estro or is it just a serm.

it will generally not lower estrogen... if anything its likely to raise estrogen (as testosterone increases)... there may be tissue specific decreases in estrogen synthesis.

 

[EDED]

it will generally not lower estrogen... if anything its likely to raise estrogen (as testosterone increases)... there may be tissue specific decreases in estrogen synthesis.

tissue specific decresase in E sythesis? what tissue would that be?

clomid sits on estrogen receptor with low agnosim but high antagonism so ER doesnt get activated, no E related specific gets made, estrogen problem 'blocked' right? anti-androgen. much like ATD can be anti androgenic at AR blocking out Test and ATD itself having no agonistic activity


unrelated, can aromasin be used for woman's estrogen dominance symptoms? women with bad PMS are high in E and low in progesterone, if E is reduced without no rebound wont it work? maybe use two weeks prior to period for on week? or low dose E3D for a whole month, and increase/decrease depengind on regularity?

 

[PsyT]

it will generally not lower estrogen... if anything its likely to raise estrogen (as testosterone increases)... there may be tissue specific decreases in estrogen synthesis.

do you mean that as test increases you will drop bodyfat and this will lower the level of aromatase activity your body has (since the enzyme is present in higher concentrations in bodyfat)?

All I know when I jump on clomid, I lose the slight amount of bodyfat I carry on my chest really quickly (after a few days of being on it).

 

[thelix]

yes. though need will vary. generally one can only see benefit from limiting potential damage to dopaminergic neurons. Selegiline is another option, less traditional dopaminergic, its primary action is inhibition of mao-b (basically its neuroprotective and allows for greater dopamine levels.)

for people who have the signs of prolactin issues or have had them previously, will go out on the limb and say in general dopaminergics should be a staple.

Macro, what are the signs of prolactin issues ?

Also, isn't it true that you can't get gyno from prolactin alone ? I've read that suppressing estro would prevent prolactin-based gyno. Not true ?

 

[skulbone]

The rebound may have to deal with the even more extreme changes that Letro causes 99% decrease vs A-sin's 50% decrease. Maybe the body just gets shocked and whatever "handles" E isn't being produced in any significant volume when there are only trace amounts left in the body while on letro. So the kickstart of E is just making the body "spillover" and thus side effects of gyno. But this is speculation.