The PCT SERM dosing in this forum is wrong

It seems like a lot of people are reading this wrong.

Your suggestion is to run low dose SERM+AI OR HCG (+AI) on cycle to prevent testicular shutdown, right? IOW, to put this in specific terms, an 8 week cycle might look like:

W 1-8 Test E 250mg E3D
W 1-10 ADex .5mg E3D
W 11-13 Adex .25 mg E3D
W 1-12 Nolva 20mg ED

T is active in blood stream for at least 10 weeks (dose-dependant, but using simply half life here).

Nolva run the whole course to stimulate LH/FSH production. The first 10 weeks of Nolva are considered ā€œHPTA supportā€ while there is exogenous Test supprressing it, and the final two weeks are run to ensure all Test is flushed from the system.

Adex is run for E2 management throughout the whole course, including slightly longer than Nolva to prevent E2 rebound while running Nolva.

Is this summary accurate? Are my dates and doses wrong? I wanted to codify this into a specific cycle to help people that may be missing the run-PCT-while-on point.

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You have most of the message very well understood.

T may be detectable for 10 weeks, but is definitely depleted in two weeks.

One could taper T going towards PCT.

I would make the PCT phase longer than two weeks if there is any doubt about elevated estrogens or prolactin. Estrogens need time to clear if they were elevated. And typically you do not have lab results.

SERM still needs to be tapered out, even from these low doses.

T think that adex 0.25mg E3D may be stretching the half life a bit too much. EOD is preferable and then a liquid anastrozole product allows for dose increments outside of 1/2 or 1/4 of a tablet. You can dissolve adex in vodka, 1mg/ml, count drops per ml with a dropper bottle and do the math for dispensing by the drop. You will have to shake up the suspended tablet fillers. Many will purchase this prepared.

My approach, with pisses some people off, is to present enough material so they can understand and come up with their program because they know why.

Because adex is a competitive drug, its dose needs to match serum T levels. With 250mg T EOD, 583mg/week] the amount of anastrozole needed may be quite high. In TRT we see a need for 1mg adex per 100mg T per week. I really donā€™t know if that linearity fails with BB T doses. In TRT, one typically has the advantage of oneā€™s lab results and the cumulative experience of others in the TRT forum. May easily need 1mg adex E3D or EOD with suggested cycle.

Adding complexity is the effect of other steroids on aromatization and tying up SHBG with for example SHBG+proviron.

TRT has these objectives, among others:
high normal TT and FT
E2 is the lower 20ā€™s which seems optimal for most; for libido, mood and energy [also less E blocking receptors]
Less SHBG because E2 is lower
Less SHBG reduces T+SHBG [which is not bio-available] thus increasing FT and albumin+T

When I read about BB guys on gear behaving badly [rage], I wonder if its because their estrogen levels are high. We do see that TRT guys with elevated estrogens beating their wives and eating their children and are basically short tempered and intolerant. Get some adex and correct their E2 levels and they are calm and tolerant. When I see guys doing lots of T and nothing for estrogen management bragging about how they are special; I have to wonderā€¦ Sort of freaks me out. Then there is gyno to worry about.

Also, estrogens are really bad for the prostate.

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Awesome, thanks KSMan. This would be a great sticky.

Quick follow up on the dissolving Adex - is this as simple as grinding up the arimidex pills, and swirling it in room temperature 80-proof vodka? Or do you need a higher proof and/or added heat? I havenā€™t done anything vaguely chemistry related in a decade and I have bad memories of doing things wrong.

Thanks!

I have never had to do this. But several have at the TRT forum. The filler of pills will make some kind of sediment or sludge.

Pills are easily crushed between two spoons. But may dissolve anyways. No way to account for what different methods of production are involved.

Shake before dispensing to deal with the solids. The anastrozole will be totally dissolved because of the alcohol. Alcohol also will prevent bacterial growth.

At what point should HCG switch with Nolva for optimal HPTA recovery? Before - After last pin? I was thinking 3 days after last pin. I do plan to continue taking Adex in reducing doses a few weeks past my last SERM.

Unfortunately I have 60 Clomid 50mg and only 20 Nolva 20mg pills. I would prefer a Nolva only approach, but I have what I have.

What would be better starting with Clomid than switching to Nolva?

Possible plans HPTA Restart Protocol

Clomid

W 1-2 Clomid 50mg ED Adex .25mg EOD
W 3-4 Clomid 25mg ED Adex .25mg EOD
W 5-6 Clomid 25mg EOD Adex .25mg E3D
W 7-8 Adex .25mg E3D

Clomid and Nolva

W 1-2 Clomid 50mg ED Adex .25mg EOD
W 3 Clomid 25mg ED Adex .25mg EOD
W 4-5 Nolva 10mg ED Adex .25mg EOD
W 6 Nolva 10mg EOD Adex .25mg E3D
W 7-8 Adex .25mg E3D

The message is not to use high doses and your EOD E3D approach is very reasonable.

I like the idea if getting the top end of the HPTA functioning with a SERM well before PCT so its ready to take over. But your PCT covers a lot of time and things will OK.

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I salute you KSman,
Thank you to all of the above advices and so your good and altruistic intentions.
Iā€™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, thereā€™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 ā€œfrom the fieldā€ about Aromasin, but it seems that, for now, it has at least ā€œtheoreticalā€ 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 Tā€“>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 AIā€™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 donā€™t like aromasin simply because it does not work well. You need to take around 25 times more mgā€™s of aromasin to do what 1mg of anastrozole does. I have my doubts that aromasin would work well from high Tā€“>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 donā€™t need to care about that.

Why do you suggest that anastrozole is liver toxic? A few mgā€™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.

AIā€™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 ā€œwhat is writtenā€ 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? Iā€™m using some to get rid of a gyno flare up and Iā€™ve had to go up to 180mg for the lump to start shrinking, but now youā€™ve got me scared Iā€™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 Tā€“>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 canā€™t reduce E2 if LH levels are excessive. Otherwise, an AI will still reduce Tā€“>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 gainā€¦and I donā€™t need my wife connecting the dots of small nuts and putting on mass. Thanks!!

Iā€™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 gainā€¦and I donā€™t need my wife connecting the dots of small nuts and putting on mass. Thanks!!

Iā€™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 gainā€¦and I donā€™t need my wife connecting the dots of small nuts and putting on mass. Thanks!!

Iā€™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, thatā€™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 Tā€“>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 AIā€™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 donā€™t like aromasin simply because it does not work well. You need to take around 25 times more mgā€™s of aromasin to do what 1mg of anastrozole does. I have my doubts that aromasin would work well from high Tā€“>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 donā€™t need to care about that.

Why do you suggest that anastrozole is liver toxic? A few mgā€™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.

AIā€™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 ā€œwhat is writtenā€ 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 didnā€™t result in a significant difference in total E2 levels, however. i suspect it would be different in men, thoā€¦

btw, i think aromasin is a little more user friendly than arimidexā€¦ a while back, i crashed my E2 on .1 mg/day of A-dex. iā€™ve used aromasin several times at varying doses (10-25 mg/day), and never had that issueā€¦ if cost is a factor, then iā€™d agree that arimidex is a better option, but otherwise iā€™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 quickerā€¦

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 havenā€™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 donā€™t see it clearly listed out above, unless my eyes arenā€™t working.

Iā€™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 Iā€™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, Iā€™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.