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The PCT SERM dosing in this forum is wrong

I salute you KSman,
Thank you to all of the above advices and so your good and altruistic intentions.
I’m interested in your opinion and experience with Aromasin (exemestane)?
As we know, according to previous research, Nolvadex does not change or affect the operation of Aromasin while partially annulle (cancel) the effect of Adex.
As already known, Aromasin is a steroidal AI which keeps it from negatively affecting lipids like other non-steroidal AIs. (Adex or Letro)
Somewhere it is written that it is also not liver toxic, and can be ran for longer lengths of time without negative effect. (which is also in good agreement with your theory of extended PCT)
Also, there’s written that Aromasin will not hurt gains on cycle like other AIs, but may actually help them. Another benefit on cycle is that steroidal AIs (like Aromasin) lower SHBG which increases the ratio of free to bound testosterone which makes your anabolic androgenic steroids more bio-available.
Personally, I do not have a lot of the experience “from the field” about Aromasin, but it seems that, for now, it has at least “theoretical” advantage over other Ais.
Thank you in advance for your review and opinion,

Best regards

Anastrozole and Letro do not have any negative direct effects on lipids. Taking E2 into single digits can do that. So its dosing that is the problem, not the AI. Do not take E2 to low levels. That also robs energy, mood and libido.

Anastrozole mechanically interferes with T at aromatase reaction sites. I do not see how a SERM would mess with that.

SERM doses that create high LH levels lead to high T–>E2 reaction rates inside the testes and because T levels there can be 80 - 100 time higher than serum levels, a competitive AI does not stand a chance. Meanwhile aromatase is working perfectly in peripheral tissues. So the premise that a SERM interferes with these AI’s seems wrong, even though an AI can fail to reduce E2 levels in this situation. Clearly a case of a mistaken assumption, even though the outcome is the same. We have seen guys put on stupid high hCG or SERM doses by idiot doctors, do lab work and E2 is high and keep increasing anastrozole doses. One guy was taking 2mg anastrozole per day, instead of 1mg per week. Doctors do not understand this problem. It was obvious to me knowing what intratesticular T levels are and the nature of a competitive drug. An engineer can figure this out. Doctors are not equipped for deductive reasoning and critical thought.

I don’t like aromasin simply because it does not work well. You need to take around 25 times more mg’s of aromasin to do what 1mg of anastrozole does. I have my doubts that aromasin would work well from high T–>E2 induced in the testes by SERM dosing that is too high. Aromasin is a suicide inhibitor. If that is so great, why do you need to take so much?

I do not have data that bears on whether aromasin fares better inside the testes. But if SERMs are dosed correctly, we don’t need to care about that.

Why do you suggest that anastrozole is liver toxic? A few mg’s per week is not a high chemical load. Some gear is liver toxic, so how do you separate or isolate one effect to anastrozole? Guys take anastrozole for years non-stop for TRT and we do not see any hint of a problem with AST/ALT labs.

AI’s do not lower SHBG. Lower E2 levels lower SHBG and higher T levels lower SHBG. Any effect of an AI on SHBG is an indirect effect.

I agree, more FT improves gains and so does optimal E2 levels. Note that T+SHBG is not bio-available.

The hype about aromasin is nuts. On a mg to mg basis, it does now work well and its more expensive to use. In a TRT context, aromasin shows no advantages except for the rare guy who has a tolerance problem with anastrozole.

So that the way I see things. If “what is written” was accurate, I would not have to do any of this. There is so much misleading stuff on the web.

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KSman, do you have any info on raloxifene? I’m using some to get rid of a gyno flare up and I’ve had to go up to 180mg for the lump to start shrinking, but now you’ve got me scared I’m producing too much E inside my testes. Do you know what sort of doses for ralox are too much? I am also using aromasin to lower my E.

Unfortunately where I live blood work is not an option

I do not have any info for that. Would not be hard to get some data, but someone would have to do this and do labs.

As we know that anastrozole would not stop intratesticular T–>E2, aromasin is not a bad choice. But still do not know if it will work better.

Shrinking the breast tissue takes time even when the SERM works perfectly. So you may be increasing the dose simply because of the time it takes for the tissue response.

If a 60mg/day dose is used to deal with female breast cancer, one could argue that you might not need more than that.

One sign that dose may be too high is hot flashes. The hypothalamus could hammer the pituitary to produce LH and large LH surges are thought to be the cause of hot flashes. That is the menopausal response of the hypothalamus to very low E2 levels and a SERM can create the same situation. But absence of hot flashes does not indicate that LH levels are reasonable.

Note that high LH levels may also reduce LH receptor sensitivity.

As a SERM increases LH/FSH, in premenopausal women, a SERM will increase E2 levels while hopefully making the E2 less visible to breast tissues. But that is clearly not a good thing. Same happens to males. So its a battle of opposing forces. And anastrozole can’t reduce E2 if LH levels are excessive. Otherwise, an AI will still reduce T–>E2 in peripheral tissues.

In menopausal women where the ovaries have failed [and the hypothalamus and pituitary have stopped trying] , a SERM will not increase E2 and LH/FSH levels may remain low.

[quote]Johnnyrebel87 wrote:
I am starting a cycle soon, I believe I have the adex and Nolvadex dosing fi hi red out, but every hcg dosing I can find looks way too high compared to what you are talking about. What hcg dosing should I use for a 10 week cycle? I am just as concerned with that aspect as the muscle gain…and I don’t need my wife connecting the dots of small nuts and putting on mass. Thanks!!

I’m so glad I found this forum, I read some fucked up doses everywhere. [/quote]

A study was done that showed that 250iu hCG SC EOD was a good replacement dose for LH when HPTA was shutdown by testosterone injections.

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I am starting a cycle soon, I believe I have the adex and Nolvadex dosing fi hi red out, but every hcg dosing I can find looks way too high compared to what you are talking about. What hcg dosing should I use for a 10 week cycle? I am just as concerned with that aspect as the muscle gain…and I don’t need my wife connecting the dots of small nuts and putting on mass. Thanks!!

I’m so glad I found this forum, I read some fucked up doses everywhere.

[quote]KSman wrote:

[quote]Johnnyrebel87 wrote:
I am starting a cycle soon, I believe I have the adex and Nolvadex dosing fi hi red out, but every hcg dosing I can find looks way too high compared to what you are talking about. What hcg dosing should I use for a 10 week cycle? I am just as concerned with that aspect as the muscle gain…and I don’t need my wife connecting the dots of small nuts and putting on mass. Thanks!!

I’m so glad I found this forum, I read some fucked up doses everywhere. [/quote]

A study was done that showed that 250iu hCG SC EOD was a good replacement dose for LH when HPTA was shutdown by testosterone injections.[/quote]
Thank you, that’s the final piece to my serm/pct puzzle

This should be stickied

[quote]KSman wrote:
Anastrozole and Letro do not have any negative direct effects on lipids. Taking E2 into single digits can do that. So its dosing that is the problem, not the AI. Do not take E2 to low levels. That also robs energy, mood and libido.

Anastrozole mechanically interferes with T at aromatase reaction sites. I do not see how a SERM would mess with that.

SERM doses that create high LH levels lead to high T–>E2 reaction rates inside the testes and because T levels there can be 80 - 100 time higher than serum levels, a competitive AI does not stand a chance. Meanwhile aromatase is working perfectly in peripheral tissues. So the premise that a SERM interferes with these AI’s seems wrong, even though an AI can fail to reduce E2 levels in this situation. Clearly a case of a mistaken assumption, even though the outcome is the same. We have seen guys put on stupid high hCG or SERM doses by idiot doctors, do lab work and E2 is high and keep increasing anastrozole doses. One guy was taking 2mg anastrozole per day, instead of 1mg per week. Doctors do not understand this problem. It was obvious to me knowing what intratesticular T levels are and the nature of a competitive drug. An engineer can figure this out. Doctors are not equipped for deductive reasoning and critical thought.

I don’t like aromasin simply because it does not work well. You need to take around 25 times more mg’s of aromasin to do what 1mg of anastrozole does. I have my doubts that aromasin would work well from high T–>E2 induced in the testes by SERM dosing that is too high. Aromasin is a suicide inhibitor. If that is so great, why do you need to take so much?

I do not have data that bears on whether aromasin fares better inside the testes. But if SERMs are dosed correctly, we don’t need to care about that.

Why do you suggest that anastrozole is liver toxic? A few mg’s per week is not a high chemical load. Some gear is liver toxic, so how do you separate or isolate one effect to anastrozole? Guys take anastrozole for years non-stop for TRT and we do not see any hint of a problem with AST/ALT labs.

AI’s do not lower SHBG. Lower E2 levels lower SHBG and higher T levels lower SHBG. Any effect of an AI on SHBG is an indirect effect.

I agree, more FT improves gains and so does optimal E2 levels. Note that T+SHBG is not bio-available.

The hype about aromasin is nuts. On a mg to mg basis, it does now work well and its more expensive to use. In a TRT context, aromasin shows no advantages except for the rare guy who has a tolerance problem with anastrozole.

So that the way I see things. If “what is written” was accurate, I would not have to do any of this. There is so much misleading stuff on the web.

[/quote]

the issue with tamoxifen and anastrozole is a drug interaction that reduces the plasma levels of anastrozole.

i believe the study was done in women, and actually didn’t result in a significant difference in total E2 levels, however. i suspect it would be different in men, tho…

btw, i think aromasin is a little more user friendly than arimidex… a while back, i crashed my E2 on .1 mg/day of A-dex. i’ve used aromasin several times at varying doses (10-25 mg/day), and never had that issue… if cost is a factor, then i’d agree that arimidex is a better option, but otherwise i’ve simply found aromasin easier to use. plus, due to the faster half-life of aromasin, if one needs to make an adjustment to dosing, it takes effect much quicker…

just something to keep in mind.

You appear to be an anastrozole over-responder. We see this a lot in the TRT forum where we have lots of lab work.

Anastrozole over-responders [not rare] need to take 1/4th the amount that others need. We had one guy who needed 1/8th.
There is no way to know in advance. Crashing is the unpleasant path to knowledge. I have never seen this described in any papers, so docs typically would not know this. But we do see a few unthinking docs Rx 1mg/day because the literature states that for female breast cancer.

Can high dose SERM use after cycle, Nolva 40/40/20/20 and Clomid at 50 for 2-3 weeks cause an elevated SHBG after PCT? Is this only caused by the high E2 during SERM use or are they any other factors to influence SHBG. Would the SHBG drop back down after PCT or is it likely to cause a permanent increase in SHBG?

All the AAS using people i know run SERMs at a higher dose than mentioned, would be interested to know the impact on SHBG as my SHBG is high despite any drug use. But haven’t seen high SHBG after SERM use in people i know personally. Interesting from the high E2 inside the testis POV.

Can you describe what the ideal PCT protocol would be with each SERM then? I don’t see it clearly listed out above, unless my eyes aren’t working.

I’m just kicking off a 10 week 400mg/wk Test Cyp cycle with a Tbol kicker. You seem to advocate starting Nolva near the end of the cycle, bridging into PCT and then maintaining a longer-than-4 week low dose if I’m not mistaken?

I have both Clomid and Nolva on hand. Also a member of iSarms.com (Formerly Adrenaline Rush Forums) and they ALL seem to advocate the classic doubling of Clomid and Nolva into:

Clomid- 50/50/25/25 and Nolva- 40/40/20/20 with Aromasin at 12.5mg EOD. This was how I was planning to do my PCT, but if you have a better suggestion with those, I’m ears.

@gunner223 @KSman

I would also like information on this. I am 25, decided to run my first cycle(500mg Test E/week+Dbol 40mg/day ) in september last year, but wanted to stop due to being paranoid about E2 issues despite taking 0.5mg/eod Arimidex, even bumped upto 0.5mg/ed after E2 issues. I was stupid enough to not get baseline labs before starting the cycle. In sum, stopped my cycle in approx. 3 weeks after start and started Nolvadex at 40mg/day on the same day and continued on that for 2 weeks, this was due to my mind playing tricks on me with fear of high e2 & gyno. for 1st week on 40mg nolva i ran arimidex at 0.5mg/eod, then stopped as i was told nolva will do what AI will do (was uneducated on this). After 2 weeks of 40mg tamox/day, i dropped it to 20mg/day for 1 week, after this i ceased nolva and ran clomid 50mg/day for 3 weeks before ending pct. I did not use an AI during PCT as suggested on various pct protocols.

10 weeks after PCT, my TT was 600 ng/dl, FT 6.9 pg/ml(9-28) , E2 : 32 pg/ml (13-42), shbg: 60 nmol/l (12-49), LH : 5 mIU and FSH: 4 mIU.

I did not feel any different than before the cycle, so did not think it was an estrogen rebound after PCT, but SHBG is confusing. I always felt lack of energy, chronic fatigue and lack of muscle gains years before this episode. Body composition has not changed after PCT, and i feel quite the same as before. I had decided i would get these labs after 3 months after PCT jst to look at my hormonal status, always felt something was off. could any of the things i have done with the cycle stop and PCT could have caused high SHBG and low FT?

Thank you.

What if we use armidex instead of anastrozole if we don’t have access to ?
Armidex during cycle and for the pct

@KSman Would Aromasin be effective at keeping E2 in check in the testes, contrary to anastrozole?

Arimidex is anastrazole and vice versa. One is generic and one is name brand, so use either one as they’re the same thing.

KSman wrote:
"I don’t like aromasin simply because it does not work well. You need to take around 25 times more mg’s of aromasin to do what 1mg of anastrozole does. I have my doubts that aromasin would work well from high T–>E2 induced in the testes by SERM dosing that is too high. Aromasin is a suicide inhibitor. If that is so great, why do you need to take so much?

I do not have data that bears on whether aromasin fares better inside the testes. But if SERMs are dosed correctly, we don’t need to care about that."

See above.

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Bumping this up sharing my own protocol - I’m a pharmacist, and I share OP’s opinions 100% after putting in my Extra homework in before dealing with female cancer patients’ drugs. I’ve been blasting and cruising from July 2016 to April 2018.

PCT went like this:

  • April: Nolva 20mg MWF. Asin 12.5mg e14d
  • May: Nolva 10mg MWF. Asin 6.25 e14d
  • June: Nolva 10mg biweekly for 2 weeks then 5mg biweekly. I may have popped one Asin 6.25mg that month.
  • Cialis 10mg 1x/2x per week on demand. Cialis has studies showing an improvement of the T/e2 ratio. Also keeps the missus happy yakno

July bloods: LH&FSH both 4. Total T 420 ng/dL. Free T 12 pg/mL and e2 19 pg/mL. This is compared to 2016 “last natural bloodwork” showing total T 750 ng/dL, free T 8 pg/mL e2 10 pg/mL, LH&FSH both 6.

Feeling absolutely normal, obviously, back to my old self.

FYI I’m now trying to see if I can bump T up a notch (600 is optimal to me), and I’ve just started Clomid 25mg MWF now, with proviron 12.5mg ED for 4 weeks before getting bloods done - I’m VERY curious about the use of low dose Proviron during a “restart”. Will then taper off Clomid.

The debate on asin rather than Adex is probably going to be endless, as of myself I went with the potentially more androgenic activity of Asin, plus its chemical structure is interesting to me.

FYI Asin C20H24O2

https://pubchem.ncbi.nlm.nih.gov/compound/exemestane#section=2D-Structure

And Proviron C20H32O2 - in the grand scheme of chemistry things vastly different, but actually quite damn close.

https://pubchem.ncbi.nlm.nih.gov/compound/Mesterolone#section=2D-Structure