Thoughts on Planning PCT

[quote]KSman wrote:

[quote]Vardas wrote:

[quote]KSman wrote:
Same for SERM. [/quote]
So your recommendation is that SERM (Nolvadex) must be used 20 mg of ED throughout the cycle until the end of the PCT?

Sorry, I do not want to be boring … just really interested in your opinion

Cheerful greetings[/quote]

Exactly. If you do not allow the testes to shutdown and shrink, then you do not need to recover form and function during PCT. At that point you transition the testes back to your own natural LH. So PCT then is about tapering off of the SERM and the testes have LH all of the time. You do not want your LH levels dropping * during the transition because that is the wring signal and you use a little anastrozole to ensure that estrogen rebound does not crash the party.

  • by using low doses of SERM, LH will not be excessive and LH level disruption during PCT is reduced. 20mg EOD may be more than enough!

Idealy, one would test LH/FSH during the cycle and might know baseline levels too. But very few will do that.[/quote]

i have never heard of anybody actually getting the SERM to work on cycle…

SERMs work by a false negative feedback mechanism, making the body think there’s low estrogen, so you increase LH/FSH to increase testosterone so it can aromatize into estrogen. however, if you already have a high testosterone level from taking AAS, then the body will have that feedback mechanism triggered as well, which will prevent any increase in LH and FSH.

if anybody has any proof otherwise, feel free to share it, but i thought this had been debunked years ago…

i mean really, if this actually worked, then all you would need to do is take a SERM on cycle, and then once the cycle is done, stop taking both. but it doesn’t work like that, at all…

here’s a link to an old discussion here about this: Why Not SERM on Cycle (w/hcg)? - Pharma - Forums - T Nation

I have seen some blood work from TRT guys doing this as part of an effort to improve sperm count. So there is evidence.
We also see E2 out of control from SERM induced LH getting too high.

SERMs block [some] E2 from acting in the hypothalamus as a feedback signal. That is what a “Selective estrogen-receptor modulator” does.

A SERM cycle has these issues:
The testes can only produce so much T.
High levels of SERM induced LH leads to high T–>E2 inside the testes and a competitive AI cannot work inside the testes because T levels can be 80 time higher than serum in natural guys and probably can get pushed a lot higher. Have seen this blunder in guys’ lab work many times.
High LH risks LH receptor desensitization.

[quote]KSman wrote:
I have seen some blood work from TRT guys doing this as part of an effort to improve sperm count. So there is evidence.
We also see E2 out of control from SERM induced LH getting too high.

SERMs block [some] E2 from acting in the hypothalamus as a feedback signal. That is what a “Selective estrogen-receptor modulator” does.

A SERM cycle has these issues:
The testes can only produce so much T.
High levels of SERM induced LH leads to high T–>E2 inside the testes and a competitive AI cannot work inside the testes because T levels can be 80 time higher than serum in natural guys and probably can get pushed a lot higher. Have seen this blunder in guys’ lab work many times.
High LH risks LH receptor desensitization.[/quote]

TRT is not a real cycle, though. most guys are taking 100-200 mg a week on TRT, not 500 mg+/wk.

anyway, i’m not arguing for high SERM doses, nor have i ever. i’m simply saying that a SERM on cycle is not likely to help prevent testicular atrophy and help recovery much. and it also might reduce one’s gains a bit, due to the decrease in IGF-1, increase in SHBG, etc…

Excellent post Cyco! Should be stickied for sure.

So for a 10 week cycle of 500mg test E could I JUST run
20mg of Nolva ED for 5 weeks?
Or is 6 - 8 weeks safer?

We can’t get stickies. See the 2nd post in this forum’s one sticky for links to topics.

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i think 6 weeks should be the minimum, but honestly doubt if there’s much difference in a week…

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in reference to HCG, i’d like to bring up this point:

some people like to take HCG in varying doses throughout their cycle, anywhere from 250 IU once a week to 500 IU EOD. there is a study where guys were able to avoid suppression of intratesticular testosterone with 500 IU EOD. however, the study was only 3 weeks long, and they were only taking 200 mg a week of tesosterone enanthate.

^with that being said, it’s possible that this will work with higher androgen doses and for a longer duration, but it’s also possible that it won’t, and the user might end up with some Leydig cell desensitization. if guys on TRT have shown us anything, most of them use 250-500 IU once a week for years, and many report very few issues with testicular shrinkage…

below is a link to the study i mentioned:

Hi @cycobushmaster

That’s an interesting link. I’ve a question regarding leydig cells desensitization with hCG. How much leydig cell sensistization is to be expected with long term use of low dose hCG let’s say 250 iu eod along with regular TRT doses say 100mg/week? And consequently how it could be applicable for a high dose steroids user who’s interested in preserving his fertility as best as he can? Is 250 iu eod hCG use still applicable?
I remember of an old thread where dhickey was discussing hpta restart with KSman and said that 250 iu hCG eod is barely enough for him to maintain his testes. Findings of this study sort of agree with his statement.
Please share if you know of some human trials studying any kind of relationship between leydig cells and hCG which have application for low dose hCG use, I mean high dose hCG is known to produce such desensitization during short periods but what about low dose for long periods.
I really appreciate your thoughts on it.

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honestly, i dunno.

from a logical standpoint, we know that the body is always fighting to get back to homeostasis and is only gonna ignore false signals so long. so if we keep plugging in HCG while testosterone levels are 10x normal, at some point we have to assume that it will ignore the signal from HCG to increase testosterone.

i’ve seen some studies where they claim minimal desensitization while using HCG, but that’s without any extra androgens, so it’s hard to apply that info to TRT or PED use.

i’m gonna do some more digging into this, and will hopefully find some better answers…

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here’s an interesting study, where HCG used at 500 IU EOD maintain fertility:

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^again, this is at TRT doses (the testosterone levels were around 1,000 ng), but still somewhat applicable.

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so is the usual 250iu thrice weekly not enough?

i think it depends what you’re using it for…

based off the study from above, if you’re looking to maintain maximum fertility, then i’d go with 500 IU EOD… maybe even more?

but simply to keep the testes active to be ready for PCT, i think one can get away with as little as 500 IU/wk (and i think we’ve seen plenty of guys go without HCG without many really issues, as well)…

eurgh, I hate how there’s so much conflicting info regarding hCG.

I’ll stick with my 250iu thrice weekly and be done with it.

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some interesting data on PDE5 inhibitors:

Viagra:

Cialis:

another study:

Interesting thread. I’m sure ill have to read it again as I near pct. thanks all for the discussion and citations.

the thread you’re posting in right now answers that question. Did you even read the whole thing? Literally EVERYTHING you’re asking about is explained here. Don’t be so lazy.

The effect of 250iu hCG EOD on the testes does not change with the amount of TRT or gear involved. The idea is to maintain normal testicular activity.

Doses of hCG and LH levels induced by a SERM should not stimulate LH receptors more than normal. If stimulation is high, when PCT ends, you do not want a transition from high LH receptor stimulation to a much lower stimulation from from whatever level of LH your pituitary can produce. If the signal is from high to low, you can expect your testes to do what? And you need to manage E2 after PCT to prevent rebound, cruise 0.25mg twice a week suggested.

High dose SERMs lead to a lot of T–>E2 inside the testes and serum E2 can be very high. And Arimidex/anastrozole can be very ineffective inside the testes, so your AI does not work. Your liver still sees the high E2 and then the liver increases SHBG, opposed by high T to some extent. T+SHBG increases.
E2 still interferes with T at T receptors. High E2 still affects the brain and you may be a mood bitch with some sexual performance issues.

40mg nolva is wrong, 20mg ED could also be too much. Only way to know is to test LH/FSH and also E2.

“you need to manage E2 after PCT to prevent rebound, cruise 0.25mg twice a week suggested.”

How long should one stay on an AI after a PCT? I tapered off the SERMs as well as the AI, at the same time, I don’t believe I ever had a rebound?

Greetings KSman. I posted in another thread. A reply stated you were the man with the best knowledge on this forum. Rather than highjack this one. Can you take a look here and share any of your expertise? Thanks in advance.