DO NOT do PCT. "PCT" is a waste of time and makes zero sense.

[Deleted member 23391]

The traditional roidcel SERM based "PCT" regimens have no basis in logic or reason.

The "PCT" idea is to let your testicles atrophy and destroy themselves then pump your body full of SERMs after the fact and hope this will reverse the damage. An intelligent man replaces the LH signal with HCG the entire time so this atrophy never happens in the first place. This is what smart people do instead of boomer roiders.

The reason your testosterone is low after you've taken steroids is because of atrophy of the testicles themselves due to your endogenous gonadotrophins (LH and FSH) cratering. LH and FSH bounce back quickly unless there's a problem (e.g. secondary hypogonadism - damage to the parts of the brain that start the hormonal cascade resulting in testosterone). This is unlike the testes themselves. The studies parrots cite on various forums and steroid websites are looking at the effects of so called "PCT" drugs on EUGONADAL men - in simple terms, NORMAL men without atrophied testicles. That clomid for example, raises testosterone in normal men is not applicable to men with anabolic steroid induced hypogonadism. Slightly raising gonadotrophin secretion with SERMs and AIs (AIs won't even help much because estradiol will also be low since in men estradiol is produced as a metabolite of testosterone) is not going to do anything - your levels are already crashed and low and your FSH and LH are probably high, the problem is your testicles are unresponsive.

The major roadblock to a fast recovery post cycle is the atrophy and loss of function in the testes. Trying to "trick" your HPTA with SERMs and AIs to raise gonadotrophins doesn't do anything major to solve this problem. LH and FSH bounce back quickly once the system is clear of suppressive drugs and their metabolites. However, the testes have atrophied. They are not responding to the signal - actually, they are, just not as fast as you would like - you will experience some recovery, possibly not a full one depending on your individual genetics and what you took and for how long. Maybe SERMs will at best slightly expedite this process. But even allowing it to transpire in the first place is retarded.

Taking HCG along with SERMs is fucking stupid because HCG is a replacement for leutinizing hormone and thus suppresses your own LH. You may as well have just taken HCG itself, which has minimal sides, instead of drugs that damage your eyesight and mitochondria like clomid and raloxifene.

Read:

H.C.G. During Cycle VS Post Steroid Cycle. BIG DIFFERENCE

H.C.G. During Your Steroid Cycle ~VERSUS~ H.C.G. Post Steroid Cycle. (pct) When To Start Using HCG? Post Cycle Therapy aka "P.C.T." is essential after any steroid cycle. There has been a lot of great PCT protocols over the years, and many bodybuilders , and Athletes alike has garnered success wit...

northernlifters.com

Human Chorionic Gonadotropin (HCg) is a peptide hormone that mimics the action of luteinizing hormone (LH). The testicles (testes) are then Stimulated by this (LH) Luteinizing Hormone to produce testosterone.
NOTE: LH is the primary signal sent from the pituitary to the testes, which stimulates the leydig cells within the testes to produce testosterone.


When steroids (exogenous hormones) are introduces to the body, A QUICK DECLINE in LH Levels Occur. The cessation of an LH signal from the pituitary causes the testes to stop producing testosterone. This process leads to a quick onset of testicular degeneration, by way of a reduction of leydig cell volume, and is then followed by rapid reductions in intra-testicular testosterone (ITT), peroxisomes, and Insulin-like factor 3 (INSL3) – All important bio-markers and factors for proper testicular function and testosterone production.


A small maintenance dosage of HCG ran alongside the steroid cycle can stop this "DEGENERATION" before it ever occurs!
Like myself, most steroid users have been engrained to believe that HCG should be used POST STEROID CYCLE, During Their PCT.

Upon reviewing the science and basic endocrinology you will see that a faster and more complete recovery is possible if hCG is ran during a cycle.
Firstly, we must understand the clinical history of hCG to understand its purpose and its most efficient application. Many popular “steroid profiles” advocate using hCG at a dose of 2500-5000iu once or twice a week. These were the kind of dosages used in the historical (1960’s) hCG studies for hypogonadal men who had reduced testicular sensitivity due to prolonged LH deficiency. A prolonged LH deficiency causes the testes to desensitize, requiring a higher hCG dose for ample stimulation. In men with normal LH levels and normal testicular sensitivity, the maximum increase of testosterone is seen from a dose of only 250iu, with minimal increases obtained from 500iu or even 5000iu. (It appears the testes maximum secretion of testosterone is about 140% above their normal capacity.)


If you have allowed your testes to desensitize over the length of a typical steroid cycle, (8-16 weeks) then you would require a higher dose to elicit a response in an attempt to restore normal testicular size and function – but there is cost to this, and a high probability that you won’t regain full testicular function.



One term that is critical to understand is testosterone secretion capacity which is synonymous to testicular sensitivity.
This is the amount of testosterone your testes can produce from any given LH or hCG stimulation. Therefore, if you have reduced testosterone secretion capacity (reduced testicular sensitivity), it will take more LH or hCG stimulation to produce the same result as if you had normal testosterone secretion capacity.

If you reduce your testosterone secretion capacity too much, then no amount of LH or hCG stimulation will trigger normal testosterone production – and this leads to permanently reduced testosterone production.


To get an idea of how quickly you can reduce your testosterone secretion capacity from your average steroid cycle, consider this: LH levels are rapidly decreased by the 2nd day of steroid administration. (2,9,10) By shutting down the LH signal and allowing the testis to be non-functional over a 12-16 week period, leydig cell volume decreases 90%, ITT decreases 94%, INSL3 decreases 95%, while the capacity to secrete testosterone decreases as much as 98%.


Note: visually analyzing testes size is a poor method of judging your actual testicular function, since testicular size is not directly related to the ability to secrete testosterone. This is because the leydig cells, which are the primary sites of testosterone secretion, only make up about 10% of the total testicular volume. Therefore, when the testes may only appear 5-10% smaller, the testes ability to secrete testosterone upon LH or hCG stimulation can actually be significantly reduced to 98% of their normal production. (3-5) The point here is to not judge testosterone secretion capacity by testicular size.




The decreased testosterone secretion capacity caused by steroid use was well demonstrated in a study on power athletes who used steroids for 16 weeks, and were then administered 4500iu hCG post cycle. It was found that the steroid users were about 20 times less responsive to hCG, when compared to normal men who did not use steroids.

In other words, their testosterone secretion capacity was dramatically reduced because they did not receive an LH signal for 16 weeks. The testes essentially became desensitized and crippled. Case studies with steroid using patients show that aggressive long-term treatment with hCG at dosages as high as 10,000iu E3D for 12 weeks were unable to return full testicular size. Another study with men using low dose steroids for 6 weeks showed unsuccessful return of Insulin-like factor-3 (INSL3) concentration in the testes upon 5000iu/wk of HCG treatment for 12 weeks (6) (INSL3 is an important biomarker for testosterone production potential and sperm production.



These studies show that postponing HCG usage until the end of a steroid cycle increases your need for a higher dose of hCG, and decreases your odds of a full recovery.
As a consequence to using a higher dose of hCG at the end of a cycle, estrogen will be increased disproportionately to testosterone, which then causes further HPTA suppression (from high estrogen) while increasing the risk of gyno. For example, high doses of hCG have been found to raise estradiol up to 165%, while only raising testosterone 140%. Higher doses of hCG are also known to reduce LH receptor concentration and degrade the enzymes responsible for testosterone synthesis within the testes -- the last thing someone wants during recovery. While these negative effects of hCG can be partly mitigated by the use of a SERM such as tamoxifen, it will create further problems associated with using a toxic SERM (covered in another article).



In light of the above evidence, it becomes obvious that we must take preventative measures to avoid this testicular degeneration. We must protect our testicular sensitivity. Besides, with hCG being so readily available, and such a painless shot, it makes you wonder why anyone wouldn’t use it on cycle.


Based on studies with normal men using steroids, 100iu HCG administered everyday was enough to preserve full testicular function and ITT levels, without causing desensitization typically associated with higher doses of hCG. It is important that low-dose hCG is started before testicular sensitivity is reduced, which appears to rapidly manifest within the first 2-3 weeks of steroid use. Also, it’s important to discontinue the hCG before you start PCT so your leydig cells are given a chance to re-sensitize to your body’s own LH production. (To help further enhance testicular sensitivity, the dietary supplement Toco-8 may be used)


A more convenient alternative to the above recommendation would be a twice a week shot of 200iu hCG, or possibly a once a week shot of 500iu. However, it is most desirable to adhere to a lower more frequent dose of hCG to mimic the body’s natural LH release and minimize estrogen conversion. If you are starting hCG late in the cycle, one could calculate a rough estimate for their required hCG ‘kick starting’ dosage by multiplying 40iu x days of LH absence, since the testes will be desensitized, thus requiring a higher dose. (ie. 40iu x 60 days = 2400iu HCG dose)


Note: If following the on cycle hCG protocol, hCG should NOT be used for PCT.

Overview
For preservation of testicular sensitivity, use 100iu hCG ED starting 7 days after your first AAS dose. At the end of the cycle, drop the hCG two weeks before the AAS clear the system. For example, you would drop hCG about the same time as your last Testosterone Enanthate shot. Or, if you are ending the cycle with orals, you would drop the hCG about 10 days before your last oral dose. This will allow for a sudden and even clearance in hormone levels, while initiating LH and FSH production from the pituitary, to begin stimulating your testes to produce testosterone. Remember, recovery doesn’t begin until you are off hCG since your body will not release its own LH until the hCG has cleared the system.
In conclusion, we have learned that utilizing hCG during a steroid cycle will significantly prevent testicular degeneration. This helps create a seamless transition from “on cycle” to “off cycle” thus avoiding the post cycle crash.

 

[IAMNOTANINCEL]

Never heard of it

 

[Deleted member 28927]

thank you for the looksmaxxing advice nigger​

 

[coispet]

What’s a better alternative?

 

[Deleted member 23391]

Never heard of it

PCT is "post cycle therapy", it's what retarded boomer steroid users do. Basically they let their testicles shrivel to raisins during the steroid cycle then think taking breast cancer drugs to boost their FSH and LH by a little bit after they come off will reverse it. Instead of just preventing the damage from happening in the first place with a drug called HCG that keeps your testicles a normal size.

 

[Deleted member 23391]

What’s a better alternative?

You take HCG the entire time you're taking steroids, low doses several times a week (250-400iu), until a couple half lives after your last injection.

 

[nissan]

too many words

 

[coispet]

You take HCG the entire time you're taking steroids, low doses several times a week (250-400iu), until a couple half lives after your last injection.

Can u find HCG in oral form i plan to take it alongside SARMs

 

[Deleted member 23391]

Can u find HCG in oral form i plan to take it alongside SARMS

 

[Saint Casanova]

What about HMG which is FSH and LH together. Would that completely stop ball shrinkage ?

 

[coispet]

Be grateful i replied to ur thread I’m in genuine and desperate need

 

[Deleted member 23391]

What about HMG which is FSH and LH together. Would that completely stop ball shrinkage ?

You might think that, but FSH receptor agonism isn't necessary. The sertoli cells (the cells which produce sperm) are stimulated by FSH, but they're also stimulated by intratesticular testosterone which HCG provides. This is why HCG is used as a fertility medication, it can boost sperm count. It would be nice if we had FSH receptors also stimulated, but it doesn't matter much.

 

[SubhumanCurrycel]

PCT is "post cycle therapy", it's what retarded boomer steroid users do. Basically they let their testicles shrivel to raisins during the steroid cycle then think taking breast cancer drugs to boost their FSH and LH by a little bit after they come off will reverse it. Instead of just preventing the damage from happening in the first place with a drug called HCG that keeps your testicles a normal size.

Isn’t PCT just damage control and bouncing back a little quicker. I thought it was common sense for people to use HCG during the cycle to prevent testicular atrophy, I believe doctors do that for HRT anyways

 

[Deleted member 23391]

Be grateful i replied to ur thread I’m in genuine and desperate need

HCG is a peptide hormone. Your stomach acid and enzymes would destroy it and turn it into its constituent proteins. No, there is no oral form.

 

[Saint Casanova]

You might think that, but FSH receptor agonism isn't necessary. The sertoli cells (the cells which produce sperm) are stimulated by FSH, but they're also stimulated by intratesticular testosterone which HCG provides. This is why HCG is used as a fertility medication, it can boost sperm count. It would be nice if we had FSH receptors also stimulated, but it doesn't matter much.

So there’s no benefit taking HCG or HMG?

 

[Deleted member 23391]

Isn’t PCT just damage control and bouncing back a little quicker. I thought it was common sense for people to use HCG during the cycle to prevent testicular atrophy, I believe doctors do that for HRT anyways

the problem is that once the testicles shrink due to having no gonadotrophins, they atrophy and become the problem

Your gonadotrophins LH and FSH bounce back very quickly and are produced by your brain again as if almost nothing ever happened. That isn't so for the testes. Now, it might expedite the process, and taking high doses of HCG can reverse some of the atrophy for the people that are really fucked. The problem is you need literally thousands of IUs of HCG to unfuck someone with very atrophied testicles. Since 250ius of HCG keeps intratesticular testosterone somewhat normal (93% according to studies) we can say it's roughly equivalent to your body's natural LH levels in terms of stimulus, and you need 10 times that much for these cases.

Is SERM/AI PCT going to multiply your LH by a factor of 10? No. Is there any use in taking SERMs along with HCG given that HCG replaces natural LH? Also no.

Testosterone is regulated by brain signaling through LH. When there is an absence of it the testicles atrophy, and some of the leydig cells undergo apoptosis (death). The LH always bounces back quickly unless there is secondary hypogonadism (damage to the hypothalamus or pituitary gland in the brain).

 

[Saint Casanova]

the problem is that once the testicles shrink due to having no gonadotrophins, they atrophy and become the problem

Your gonadotrophins LH and FSH bounce back very quickly and are produced by your brain again as if almost nothing ever happened. That isn't so for the testes. Now, it might expedite the process, and taking high doses of HCG can reverse some of the atrophy for the people that are really fucked. The problem is you need literally thousands of IUs of HCG to unfuck someone with very atrophied testicles. Since 250ius of HCG keeps intratesticular testosterone somewhat normal (93% according to studies) we can say it's roughly equivalent to your body's natural LH levels in terms of stimulus, and you need 10 times that much for these cases.

Is SERM/AI PCT going to multiply your LH by a factor of 10? No. Is there any use in taking SERMs along with HCG given that HCG replaces natural LH? Also no.

Testosterone is regulated by brain signaling through LH. When there is an absence of it the testicles atrophy, and some of the leydig cells undergo apoptosis (death). The LH always bounces back quickly unless there is secondary hypogonadism (damage to the hypothalamus or pituitary gland in the brain).

How much do you need to take for no ball shrinkage and fertility to remain the same if you’re doing a moderate test cycle for example ?

 

[Deleted member 23391]

How much do you need to take for no ball shrinkage and fertility to remain the same if you’re doing a moderate test cycle for example ?

I take 300ius 2 or 3 times a week which seems to keep my testicles the same size

 

[VeryFuglyNiyguhs]

PCT is a scam that actually hurts you more than it helps you. It's something drug dealers promote to sell even more money.

 

[Deleted member 50579]

The traditional roidcel SERM based "PCT" regimens have no basis in logic or reason.

The "PCT" idea is to let your testicles atrophy and destroy themselves then pump your body full of SERMs after the fact and hope this will reverse the damage. An intelligent man replaces the LH signal with HCG the entire time so this atrophy never happens in the first place. This is what smart people do instead of boomer roiders.

The reason your testosterone is low after you've taken steroids is because of atrophy of the testicles themselves due to your endogenous gonadotrophins (LH and FSH) cratering. LH and FSH bounce back quickly unless there's a problem (e.g. secondary hypogonadism - damage to the parts of the brain that start the hormonal cascade resulting in testosterone). This is unlike the testes themselves. The studies parrots cite on various forums and steroid websites are looking at the effects of so called "PCT" drugs on EUGONADAL men - in simple terms, NORMAL men without atrophied testicles. That clomid for example, raises testosterone in normal men is not applicable to men with anabolic steroid induced hypogonadism. Slightly raising gonadotrophin secretion with SERMs and AIs (AIs won't even help much because estradiol will also be low since in men estradiol is produced as a metabolite of testosterone) is not going to do anything - your levels are already crashed and low and your FSH and LH are probably high, the problem is your testicles are unresponsive.

The major roadblock to a fast recovery post cycle is the atrophy and loss of function in the testes. Trying to "trick" your HPTA with SERMs and AIs to raise gonadotrophins doesn't do anything major to solve this problem. LH and FSH bounce back quickly once the system is clear of suppressive drugs and their metabolites. However, the testes have atrophied. They are not responding to the signal - actually, they are, just not as fast as you would like - you will experience some recovery, possibly not a full one depending on your individual genetics and what you took and for how long. Maybe SERMs will at best slightly expedite this process. But even allowing it to transpire in the first place is retarded.

Taking HCG along with SERMs is fucking stupid because HCG is a replacement for leutinizing hormone and thus suppresses your own LH. You may as well have just taken HCG itself, which has minimal sides, instead of drugs that damage your eyesight and mitochondria like clomid and raloxifene.

Read:

H.C.G. During Cycle VS Post Steroid Cycle. BIG DIFFERENCE

H.C.G. During Your Steroid Cycle ~VERSUS~ H.C.G. Post Steroid Cycle. (pct) When To Start Using HCG? Post Cycle Therapy aka "P.C.T." is essential after any steroid cycle. There has been a lot of great PCT protocols over the years, and many bodybuilders , and Athletes alike has garnered success wit...

northernlifters.com

Apparently hcg increases shbg which in turn decreases t

 

[SomaliMax]

Lnfao just take enclo during your cycle

 

[Chadpreet_]

Don't have access to all that shit anyways

 

[barnmatrix]

Can u find HCG in oral form i plan to take it alongside SARMs

If you too baby to pin then just ropemax bro

 

[Lurkerslep]

retard you take pct to feel better while your balls recover

 

[Deleted member 23558]

Needing much LH and FSH is itself incel trait

 

[Deleted member 52200]

Positive ct is good

 

[Deleted member 23391]

Lnfao just take enclo during your cycle

has that actually worked for you? lol

 

[SomaliMax]

has that actually worked for you? lol

I’m natty but everyone who took sarms told me it works

 

[Deleted member 23391]

I’m natty but everyone who took sarms told me it works

that'll work with something midly suppressive like a SARM cycle, I don't think it could keep your gonadotrophins even remotely high enough on an actual steroid cycle

 

[Deleted member 8365]

@the MOUSE

 

[Orc]

read this summary on the largest study on the subject.

 

[Deleted member 8365]

The traditional roidcel SERM based "PCT" regimens have no basis in logic or reason.

The "PCT" idea is to let your testicles atrophy and destroy themselves then pump your body full of SERMs after the fact and hope this will reverse the damage. An intelligent man replaces the LH signal with HCG the entire time so this atrophy never happens in the first place. This is what smart people do instead of boomer roiders.

The reason your testosterone is low after you've taken steroids is because of atrophy of the testicles themselves due to your endogenous gonadotrophins (LH and FSH) cratering. LH and FSH bounce back quickly unless there's a problem (e.g. secondary hypogonadism - damage to the parts of the brain that start the hormonal cascade resulting in testosterone). This is unlike the testes themselves. The studies parrots cite on various forums and steroid websites are looking at the effects of so called "PCT" drugs on EUGONADAL men - in simple terms, NORMAL men without atrophied testicles. That clomid for example, raises testosterone in normal men is not applicable to men with anabolic steroid induced hypogonadism. Slightly raising gonadotrophin secretion with SERMs and AIs (AIs won't even help much because estradiol will also be low since in men estradiol is produced as a metabolite of testosterone) is not going to do anything - your levels are already crashed and low and your FSH and LH are probably high, the problem is your testicles are unresponsive.

The major roadblock to a fast recovery post cycle is the atrophy and loss of function in the testes. Trying to "trick" your HPTA with SERMs and AIs to raise gonadotrophins doesn't do anything major to solve this problem. LH and FSH bounce back quickly once the system is clear of suppressive drugs and their metabolites. However, the testes have atrophied. They are not responding to the signal - actually, they are, just not as fast as you would like - you will experience some recovery, possibly not a full one depending on your individual genetics and what you took and for how long. Maybe SERMs will at best slightly expedite this process. But even allowing it to transpire in the first place is retarded.

Taking HCG along with SERMs is fucking stupid because HCG is a replacement for leutinizing hormone and thus suppresses your own LH. You may as well have just taken HCG itself, which has minimal sides, instead of drugs that damage your eyesight and mitochondria like clomid and raloxifene.

Read:

H.C.G. During Cycle VS Post Steroid Cycle. BIG DIFFERENCE

H.C.G. During Your Steroid Cycle ~VERSUS~ H.C.G. Post Steroid Cycle. (pct) When To Start Using HCG? Post Cycle Therapy aka "P.C.T." is essential after any steroid cycle. There has been a lot of great PCT protocols over the years, and many bodybuilders , and Athletes alike has garnered success wit...

northernlifters.com

1. The PCT (Post Cycle Therapy) approach involves letting the testicles atrophy and then attempting to reverse the damage with SERMs (Selective Estrogen Receptor Modulators).

2. A more intelligent strategy involves using HCG throughout the cycle to prevent testicular atrophy by replacing the LH signal.

3. Testosterone levels drop post-steroid use due to atrophy caused by decreased LH and FSH production, which bounce back quickly in normal circumstances.

4. Studies on PCT drugs often focus on eugonadal (normal) men, making their applicability to anabolic steroid-induced hypogonadism questionable.

5. Simply raising gonadotrophin secretion with SERMs and AIs is insufficient when the testicles are unresponsive due to atrophy.

6. The major hurdle to a fast post-cycle recovery is the atrophy and loss of function in the testes, not just hormonal levels.

7. Attempting to "trick" the HPTA with SERMs and AIs doesn't effectively address the underlying testicular atrophy issue.

8. Taking HCG alongside SERMs is criticized as counterproductive, as HCG itself can suppress LH, making it akin to using HCG alone without additional damaging drugs like clomid and raloxifene.

 

[PEking]

Blast & Cruise is the way to go with a bit of HCG thrown in to keep your balls going