Stopping TRT After 8 Months, PCT Help?

Hey guys,

I have been on TRT for 8 months now, I have been running HCG twice a week at 500IU throughout. I want to come off for various reasons, and am planning a PCT as follows and need advice; I have heard everything from lowering your dose gradually then quitting cold turkey, to just blasting the HCG at higher dose more frequent by itself, to doing a full on HCG/AI/SERM PCT, and I have also read that using an AI like anastrozol will CRASH your E2.

I have read through the stickys on other forums and I think what I have decided to try is this; but obviously want advice

over the last 18 weeks i dropped my dose every 6 weeks from 250 to 200 now to 160.
My last shot of 160MG Test Cyp. will be on Monday the 19th of this month
I will increase my frequency on HCG from 2x a week (days 3-5 post injection) to EOD for 2 weeks, so I will shoot 500IU on the 21,23,25,27,29,31,2, and the 4th.
I will start blasting 1,000IU of Vitamin E ED to try and make the HCG more effective
I will start taking my tamoxifen(nova) at 20MG ED starting the day of my last injection on the 19th and run it with my increased HCG frequency because the nova doesn’t suppress LH and it also helps keep the HCG from desensitizing you to natural LH.

After approximately 2 weeks following my last injection on the 19th, the last AAS should Esther out of my system and I will run out of HCG on the 4th, starting my “real PCT” on the 5th.
I will drop the Vitamin E and start blasting Vitamin C at 1.5G ED to help keep my cortisol lower.
I will continue the tamoxifen(nova) at 20MG ED for 2 weeks, then lower to 10MG ED on weeks 3-4.
I have anastrozole on hand, and am not really sure if I should take 0.25MG twice a week or not, I am also taking DIM currently and dont know if I should continue that throughout PCT either.

You could do that insanely complicated and wildly unnecessary plan, or you could just run a normal pct and save yourself an absolute truckload of aggravation and money.

Nolva 40/40/20/20/10/10

There is no reason why that shouldn’t work just fine. Blasting HCG is just begging for uncontrollable e2 at the same time that you’ll have almost zero testosterone. That is bad news all around. Try a normal pct, get blood work when you’re done, and if you’re not back to some version of normal then you can do the insane version you have laid out. But it’s wise to not send yourself on a hormone roller coaster like the one you’re planning unless you know for a fact that it’s necessary.


Well i already have the HCG on hand, as well as the arimidex. All i would need is the RX for the tamoxifen. If I have the HCG, I am going to use it, and its very beneficial and should be part of any PCT. I would be crazy to sit here with 6,000 units of HCG that i paid $50 for and throw it away and not use it for PCT. HCG is used in huge daily doses, some guys 1-2,000 ED, claiming the desensitization of the leydig cells is a myth. I am using a smaller dose EOD (as its half life is 2-3 days) is very unlikely to cause “uncontrollable” E2 issues, and I can continue the DIM+ at 400mg daily. It will also shorten the recovery time as opposed to just tamoxifen alone.

If you were already going to do it then why bother asking? Why would anyone waste their time trying to answer your questions and correct some of your misunderstandings if your position is “thanks, I’ll do what a I want”?


Personally I would fire up the HCG 1 month after discontinuing the T and not stop until I felt really well on it, and scored well on labs in the TT department.

If you do that, I don’'t even know if you would need a SERM. I wonder if they do more harm than good in the long term, they are really toxic.

If someone corrected my misunderstanding then I would gladly accept their advice, your advice of not using the HCG I already have on hand however was very poor and I am choosing not to follow that poor advice. I am making the choice to continue to use the HCG because I believe it is beneficial and important to PCT. Im not a “wing it” or “good enough” kind of guy. I want to understand the programs and processes and “the why” and do things that are worth doing to the best of my ability and understanding instead of just following some generic or broad “good enough” “just take nolva and youll be fineeeeee” logic. To me a “normal” PCT is the best PCT possible, not just whatever works at the bare minimum. But, I understand what you’re saying, that It might be over kill and just taking the tamoxifen at 40/20/20/10 or whatever would probably be fine.

Its my understanding that HCG suppresses the HTPA, which creates LH and FSH. You want to stop using the HCG after the last AAS Esthers out of your system, otherwise its counter productive. You cant use HCG alone as PCT. Continuing HCG into PCT after that is just hindering and elongating your PCT and keeping your pituitary and hypothalamus suppressed with exogenous hormone. They will continue to see the synesthetic HCG being injected as abundance and lack to kick start their natural LH and FSH production. Once you stop the HCG, you will be back at square one all over again, no LH or FSH, HTPA still shut down. all you did was delay the onset. The point of HCG is to replace that lost signal from the brain to the testes and keep the testes awake, but waking the testes up doesn’t wake the HTPA up, the HTPA sends the LH and FSH to the testes, not the other way around. Thats the point of taking the HCG, wake the testes up so when you start the SERM to wake up the HTPA they’re ready for the signal and don’t take as long to wake up. correct me if I have a misunderstanding on that though.

You are correct but I think your timing is off. Also you are saying there is no PCT without a SERM, I am saying there is no PCT without HCG.

You can’t take HCG too long, it does not desensitize the testes, only gives them a slight refractory period. This is different than long term desensitization.

People underestimate how long it takes for these esters to clear, and since there is no way to do HCG too long, there is nothing wrong with staying on HCG for an entire month or 2.

HCG works to stimulate the pituitary, secondary to suppressing LH, when TT levels drop below 400 ng/dl.

So how high do you think someones TT levels can get while on cycle? Let’s say 5,000. Lets say we are talking about Test E and it is a 7 day half-life (debatable).

So after 1 week with injections your levels will be 2500, after another week they will be 1250, another week 675 and another week to get below 400.

So that’s 4 weeks to get out of someones system and that doesn’t even count the people taking nandrolone decanoate which is a 14 day half life.

So instead of concentrating on when you do the SERM portion, concentrate on when you do your “HCG Blast Phase” this has to be timed correctly. SERM timing doesn’t matter because it is dependent on the resensitization of the testes.

On top of the timing, the dosage is critical, and everyone is different and did different cycles and has different history. So the only way to make sure success is achieved on the first portion of the restart is with how you feel, AND lab work. You don’t stop the HCG until your TT number comes back at MAXIMAL CAPACITY because if high doses of HCG won’t wake up your balls a poorly emitted LH and FSH is sure not going to.

So its all about HCG. We had a guy 55 years old come off TRT after 8 years and get his TT levels up to 900 naturally. This was after 18 months of HCG and peptides, no SERMS.

So we are not sure how helpful SERMS are. Some people need them for the second phase, some people don’t if the first phase is successful.

Hope this makes sense I got interrupted during writing lol. The wife unit.

Now that is the educated, informational response I was looking for, so thank you for that. I am taking 160MG of test cyp per week. I get tested on day 7 in my “trough” and 7 days after my injection my levels are down to 672. I can always ask for my last shot on the 19th to be less as well, say 140MG or whatever, as I have staggered down from 250 to 200 to 160 the last 3 months. So by my thinking, If i get my last shot on Monday the 19th, the next monday on the 26th they will be 672, then the next Monday September 2nd it will be 336. if I run 500IU of HCG from the 21st to the 4th I will be hitting it in that range. I can always purchase more HCG and run it longer if needed, or drop from 500IU to 250IU and stretch this last bottle out a little longer.

Only thing I would suggest is more HCG, remember you want to maximally stimulate testes. 500 is a low dose, for someone with ASIH

So you ARE saying that it is a myth, you cant desensitize your leydig cells by taking “too much” HCG. How do you know this? I had read that most people who take HCG while on TRT do 250IU, I figured the 500IU twice a week was at the higher end of the range that the DR put me on to maintain fertility. I had heard not to take over 500IU in a single injection or you WILL desensitize them. I respond well to it, my testes were achy, soft and drawn up for maybe the first few weeks when I first started, but right after i started the HCG after the 6th week soon enough cause i didn’t like the atrophy they came back to full size very quick and have remained throughout TRT. And you are also saying that you CAN use HCG by itself for PCT and that it WILL stimulate the HTPA, as long as TT is under 400? So what happens if you continue the HCG and get “maximal capacity” like you said though? The HTPA will be shut down cause your TT went over 400 again and when you stop using the HCG youll crash again, no? Because the HTPA is shut down, so youll have no LH or FSH. In the example of the man who quit TRT after 8 years and took HCG for 18 months, sure, he got his TT to 900 on HCG, but what happens if he quits taking HCG?

If this were true then explain how thousands of users have had multiple successful pct protocols without hcg. It’s the minority that use it. Now I personally like it while I’m on trt and enjoy the benefits of it, but it is by no means a standard pct drug.

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I don’t think they ever recover. How do you know the PCT was successful?

Thanks. This is what I thought and what you describe is probably a similar experience of others who claim hCG desensitization. The point being that the data is anecdotal reports of subjective measures. In my own experience, hCG administration for many causes a subjective feeling within the testicles. many even describe it as similar to “blue balls.” The lack or absence of the subjective symptoms within the testicles over time does not translate into hCG desensitization.

In the area of hCG desensitization, there are no reports in the literature to support this effect clinically, both subjective and objective. That hCG desensitization occurs in the laboratory is unrefuted. It does not occur clinically.

As I posted elsewhere, there is no report anywhere of hCG administration as a cause of primary hypogonadism. If you know of such a case, it would be the first in the entire known body of scientific literature. In other words, “put up or shut up.” This is a continuing myth by those who purport to have knowledge while actually possessing none. This is along the line of the hCG diet, 24-hour urine testing for testosterone replacement therapy (TRT), and FSH monitoring for testosterone replacement therapy (TRT).

hCG desensitization DOES NOT occur clinically. Anyone who says it does, does not know the literature, is trying to advance a myth, and probably believes in the hCG diet! Can hCG desensitization occur? Absolutely. There are many animal models demonstrating this effect, but, again, this effect is NOT seen clinically in FDA approved doses or less. Is there evidence for hCG desensitization in humans for hCG doses higher than FDA approved levels? Indirectly, a single study in does over 5,000 IU exploring testicular response to hCG administration reveals a leveling of T production.

hCG administration does stimulate estradiol and progesterone production. In fact, the estradiol rise occurs before the T rise.

The article "van Bergeijk L, Gooren LJ, van der Veen EA, de Vries CP. Effects of short- and long-term administration of tamoxifen on hCG-induced testicular steroidogenesis in man: no evidence for an oestradiol-induced steroidogenic lesion. Int J Androl 1985;8(1):28-36,: cited as support does nothing of the sort. This is a vain attempt to confuse the issue and by hopefully presenting a peer-reviewed article to win the argument. It ain’t gonna work!

According to the abstract, the study examines the effect of tamoxifen hCG-induced testicular steroidogenesis. They do not use a model of hCG desensitization. The study is exploring a “local” effect of estradiol on T production. In fact, if you even give the slightest thought the study is about hCG desensitization, the study would not work!!! Duh . . . If the cells were desensitized to hCG, they would not produce estradiol or T, thus NO study on tamoxifen effects.

Another study (abstract below) cited by another forum is “Tang P-Z, Tsai-Morris CH, Dufau ML. Regulation of 3{beta}-Hydroxysteroid Dehydrogenase in Gonadotropin-Induced Steroidogenic Desensitization of Leydig Cells. Endocrinology 1998;139(11):4496-505.” THIS IS A STUDY IN RATS!!! This expert is so desperate to prove him/herself. they cite rat studies. If we were to translate this study to humans, which is fraught with so many pitfalls, the easiest method is by dose (IU/kg). The dose for the rats is 100-125 IU/kg. For a 75 kg human, this would be 7,500 IU or more. A dose more than FDA approved, used clinically, and what they claim to cause hCG desensitization.

3{beta}-hydroxysteroid dehydrogenase/{Delta}5-{Delta}4 isomerases (3{beta}-HSD) are enzymes that catalyze the conversion of {Delta}5 to {Delta}4 steroids in the gonads and adrenal for the biosynthesis of sex steroid and corticoids. In gonadotropin-desensitized Leydig cells, from rats treated with high doses of human CG (hCG), testosterone production is markedly reduced, a finding that was attributed in part to reduction of CYP17 expression. In this study, we present evidence for an additional steroidogenic lesion induced by gonadotropin. Using differential display analysis of messenger RNA (mRNA) from Leydig cells of rats treated with a single desensitizing dose of hCG (2.5 {micro}g), we found that transcripts for type I and type II 3{beta}-HSD were substantially (5- to 8-fold) down-regulated. This major reduction, confirmed by RNase protection assay, was observed at the high hCG dose (2.5 {micro}g), whereas minor or no change was found at lower doses (0.01 and 0.1 {micro}g). In contrast, 3{beta}-HSD mRNA transcripts were not changed in luteinized ovaries of pseudopregnant rats treated with 2.5 {micro}g hCG. The down-regulation of 3{beta}-HSD mRNA in the Leydig cell resulted from changes at the transcriptional level. Western blot analysis showed 3{beta}-HSD protein was significantly reduced by hCG treatment, with changes that were coincidental with the reduction of enzyme activity and temporally consistent with the reduction of 3{beta}-HSD mRNA but independent of LH receptor down-regulation. The reduction of 3{beta}-HSD mRNA resulting from transcriptional inhibition of gene expression, and the consequent reduction of 3{beta}-HSD activity could contribute to the inhibition of androgen production in gonadotropin-induced steroidogenic desensitization of Leydig cells. The gender-specific regulation of 3{beta}-HSD by hCG reflects differential transcriptional regulation of the enzymes to accommodate physiological hormonal requirements and reproductive function

No problem - read the doses!!! I state 10,000 IU. The Desensitization has been shown to occur with 5000IU or higher and less frequently with lower amounts. is not inconsistent but a poor choice of wording. This is from the single study I cite about a leveling of T production, not an absence. These are all non-clinical doses. The key question does this effect occur clinically? I do not refute the ability to show this effect at very high doses. I have not changed my mind. Further, posters are claiming this effect with 1,000 IU. Thanks for reading and helping clarify the post.

I was hoping to obtain the full-text document, but no luck. If anyone has it, either post of forward. This article from 1982 does not show hCG desensitization. In fact, the article states, ”These data indicate that continuous long term hCG administration stimulated T levels in HH.” The only note for “partial desensitization” is a delayed “kinetic” response to hCG administration from 24 to 48 hours! It is also of interest this was over 23 months, almost 2 years with a three times per week schedule. This is a long time, yet they state the above – there continued to be T production. It would be nice to know what the hCG concentration is at this schedule after almost 2 years. The following abstract that used an every 6 day schedule over a year found a consistent T production. Moreover they note that maximal T production occurs 58 hours after injection.

D’Agata R, Vicari E, Aliffi A, Maugeri G, Mongiol A, Gulizia S. Testicular Responsiveness to Chronic Human Chorionic Gonadotropin Administration in Hypogonadotropic Hypogonadism. J Clin Endocrinol Metab 1982;55(1):76-80.

Steroidogenic responsiveness to long term hCG administration (1500 U three times a week for 23 months) was characterized in 8 males with hypogonadotropic hypogonadism (HH). During hCG treatment, testosterone (T), which was in the prepuberal range under basal conditions, rose considerably to the upper end of the normal range and remained at that level during the 23 months of observation. A 2.5-fold increase was observed in serum levels of 17{beta}-estradiol (E2) an increment less than seen with T. The increment in 17{alpha}-hydroxyprogesterone was also lower than that in T throughout the study; thus, the 17{alpha}-hydroxyprogesterone to T ratio, despite continuous hCG administration, remained low. Serum androstenedione was slightly increased during hCG therapy. No significant changes were observed in serum levels of dehydroepiandrosterone. These data indicate that continuous long term hCG administration stimulated T levels in HH, with a relatively small change in E2. The kinetics of the T and E2 responses to 2000 U hCG, evaluated after 23 months of therapy, indicated that the testicular response was markedly reduced. No increment in T levels was observed at 24 h; the maximal response occurred at 48 h. This pattern of T response supports the idea that partial testicular desensitization occurs in HH patients receiving chronic treatment with hCG.

Balducci R, Toscano V, Casilli D, Maroder M, Sciarra F, Boscherini B. Testicular responsiveness following chronic administration of hCG (1500 IU every six days) in untreated hypogonadotropic hypogonadism. Horm Metab Res 1987;19(5):216-21.

The observation that the testosterone (T) response to a single intramuscular injection of hCG is prolonged suggests that currently used regimens (2-3 injections per week) to stimulate endogenous androgen secretion in hypogonadotropic hypogonadism (HH) patients have to be reassessed. Moreover, during the last few years, Leydig cell steroidogenic desensitization has been found after massive doses of hCG. The aim of the present investigation, carried out in 6 HH patients who showed no signs of puberty, was to study the effect of 1500 IU hCG administered every six days over a period of one year to induce the onset of pubertal development. To evaluate the kinetics of the response of T, 17 alpha-hydroxyprogesterone (17 alpha-OHP) and 17 beta-oestradiol (E2), blood samples were taken basally and 1, 2, 4 and 6 days after drug injection. This dynamic study was performed after the first injection and after the 4th and 12th month of treatment. During this one year time period, a progressive increase in testicular size was observed. Comparing plasma T levels (mean +/- SE) before the first injection (11.2 +/- 4.7 ng/dl) with the corresponding values at the 4th (38.7 +/- 10.5 ng/dl) and 12th months (99.5 +/- 19.9 ng/dl) of therapy, a progressive and significant increase was observed. T reached a maximum elevation 58 hours after hCG injection at the 4th month (198.3 +/- 42 ng/dl; P less than 0.01) and at the 12th month (415.6 +/- 62.6 ng/dl; P less than 0.05), whereas it remained unchanged following the first hCG injection.(ABSTRACT TRUNCATED AT 250 WORDS)

~ Doc Scally

I imagine the piles of blood work results would be an adequate data point to make this determination.

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So you think the average person doing a cycle, that just does SERM treatment, has lab work 30 days after discontinuing SEMR’s, shows high TT, FT and E2?

I would love to see it. Cause we don’t, we see a crash after SERMS a lot of times.

Maybe thats due to client history, and you are talking about short test only cycles on young people. I don’t know, but we don’t see it, and we def have piles of lab work.

There are other forums that have whole sections dedicated to blood work, both on-cycle and post-pct. Sadly there are not a lot of guys who are running only testosterone, especially the younger ones. The trend is possibly reversing in some corners of the steroid world, but the doses that guys are taking and the complicated stacks they’re using are mildly alarming.

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My next question is WHY does estrogen rise after quitting testosterone? You arent injecting exogenous test into your system, so its not excess going through arimitization.

I talked to my regular doc today, my last 4 shots have been 200, then 160, now 130 and then my last next monday will be 100. He said to just continue the HCG then im done. He wont RX nolva/tamoxifen. He would write me clomid if I really needed it but only at 25mg twice a week. he said HCG isnt synthetic LH/FSH, he said it does stimulate the HTPA to produce its own LH/FSH and it doesnt suppress it.

Sorry if you’ve explained it somewhere but what is the reason you want to come off and what were your pre-TRT levels?