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Stupid Estrogen / Trestolone Oral Question

This is probably going to sound stupid, but I can’t seem to find an answer to this. I know that an AI inhibits the aromatase enzyme to hinder T->E2 conversion, but, does it completely stop this mechanism from occurring?

It seems to me that if someone crashed their E2 with adex, there are two simple methods to restoring some to feel better again:

  1. Upping the dose of T to provide for more T availability to convert; or
  2. Adding in a high dose of a SERM (Nolva for instance) to get some intratesticular T->E2 conversion that an AI can’t effect.

Has anyone had experience with crashed estrogen, and know if the above two methods would work? Or would tapering down the AI be best?

Not there yet, hopefully never, but I’m scared that it might happen. I’m now running 0.5 mg adex EOD as I’m on trestolone and I hear it aromatises a lot - and from various forums, users have experience of it aromatising more than d-bol (but every body is different).

Couple things:

  1. Yes, upping T will also increase aromatization.
  2. A SERM will not do what you’re suggesting while you’re still on cycle. Estrogen rebound post-cycle is normal, and most cases, one should continue to limit it via an AI.
  3. If you crash your E2, the BEST solution is neither of the above. you should cut your AI dose. If you crashed your E2, you were taking too much adex in the first place.

If you’re ONLY on oral trestolone, then you’re a fucking idiot. Oral trestolone’s halflife is extraordinarily short. You’re going to do bad things to your htpa, with little or no benefit. Oral trestolone should only be used pre-workout, and as a compliment to an injectable cycle.

If you’re using it as a compliment to an injectable cycle, I would not consider it in your AI dosage, because the trestolone dose will be relatively low. Not enough to make a real difference.


No, also on 125mg test-e, 25mg test-p and 100 mg primo administered once a week for TRT. At 0.5mg E3.5D my E2 is at 28.6. So I assumed adding another day of 0.5mg (M,W,F as opposed to M and Thu) wouldn’t hurt as I was underdosing already (to not hit the 22 mark).

This is why I assumed upping Nolvadex could aide in the process of E2 restoration. It seemed too simple to be true I suppose.

I’m taking it 25mg morning, 50mg PWO, and 25mg shortly after workout. There’s no real advice on how to take oral trestolone. But, I can say, in my first week of use, my heavy weight (max lift upper body day WS4SB) on the bench has now doubled for reps. I’m still going for volume though to turn this weight into my repetition day lift post-cycle and gradually move up on the heavy sets. It’s been working for me, but, what would you advise?

Hi Baka,

This theory was shown not to be correct after a forum member got bloodwork whilst on 80mg test and ran a SERM to see it’s effect on LH/FSH

What I’m questioning is whether a SERM could rise crashed E2 levels.

Prior to switching to Clomid, his E2 was 28 and his post-labs show 30. I read this as it could be due to timing, AI dosing, etc. and I would think is a minuscule number to even consider a SERM working. I was just wondering if it was possible though…

It’s also important to note that he was taking 50mg Clomid EOD. Had he chose 50mg per day, or even 100 mg, could the E2 have risen more than that?

I understand what you are questioning.

If a SERM does not increase LH/FSH whilst also using exogenous T then i don’t see how it would cause an increase in E2

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Maybe @KSman will come around and share which studies (for TRT) that was from or clarify whether it can raise E2, and how, without an increase of LH/FSH. I’m no expert and don’t even know if LH/FSH would relate to the intratesticular production of E2 that was being discussed.

I really don’t see a reason to increase the AI dose. You’re not going to be running the trestolone for very long, I’m assuming, so if your E2 is a little elevated for a few weeks, that’s fine. stick with the adex dose you’re currently using, and then you won’t have to worry about any of the things you’re asking about. keep it simple.

From my experience, I am very sensitive from E2 in the ~60+ range. This creates way too much water retention, which slightly increases my BP above my “normal” (which is considered low). With this higher BP, I get intermittent chest pain.

So trying to maintain lower E2 is my overall goal by increasing the AI. I’m not concerned about gyno as I’m concurrently running a SERM.

As of yesterday, I’ve already cut back on dosing trestolone as I’ve started getting these pains again (and my BP is up). While I don’t have labs to see for sure if the E2 is in that range, it’s from my limited experience that it is. My increasing weight could also back that statement up. But, I’d like to run labs to ensure that E2 is the primary cause for higher BP/chest pain as well as possibly a heart valve echo to see if there is any plaque buildup that I don’t know about.

I have seen some guys who cannot resolve gyno with a SERM. Some people are simply wired differently.

I do not understand the other question…

If a SERM such as Nolvadex can make intratesticular T->E2 occur, why isn’t this a preferred method of quickly restoring crashed E2 due to an AI?

Recover from a simple overdose of anastrozole is stopping for 5 days.


I feel like he wanted a less efficient, more complicated answer than this. But yea, that’s what I tried to say earlier. Crashed E2 is easily rectified.

Pretty much. I didn’t know that it was as simple as explained above. But, if people felt like crap during those 5 days, it seems like they could up (or pop a few more) Nolvadex to get E2 kicking right away; though, I don’t know if it would work like that.