T Nation

Doing PCT After Fake Gear


hi every one i am 24 years old 180cm tall about 90kg and have been training for about 11 years and turned to the dark side maybe about 4 years ago while being a total ignorant about steroids!

My question/problem is this i believe most of the people in here has purchased fake gear in the past
and this is very similar to what happened t me!to be quick i will say i was on a cycle like this

week1 3x250mg sustanon 2x300boldenone 10mg aromasin

week2 2x250mg sustanon 2x200boldenone >>

week3 >> >> >>

week4 >> >> >>

week5 >> >> >> 3x100mgmasteron 3x75mg trenbolone

week6 >> >> >> >> >>

week7 >> >> >> >> >>

week8 >> >> >> >> >>

week9 >> >> >> >> >>

week10 >> >> >> 2x100mg masteron 2x75mg tren acet.

week 11 off only 10mg aromasin

week 12 500iu hcg every day 10mgaromasin/day 20mgnolva/day 1000iu vitamn E/day

week 13 500iu hcg every day 10mgaromasin/day 20mgnolva/day 1000iu vitamn E/day

week 14 500iu hcg every day 10mgaromasin/day 20mgnolva/day 1000iuvitE/day

week 15 20mg nolva/day 10mgaromasin/day

week 16 20mg nolva/day 10mgaromasin/day

week 17 20mgnolva/day

the problem is that the sustanon and boldenone i used were fake 100% and i only realized it later when i searched on them in the book anabolics 2006 but this had as a result my hpta not shutting down and there was no need for pct but i realized it only when i was at week 17

now my body because of the test produced by hcg and nolva has shutdown my hpta for good and i started having low test symptoms like being sensitive and other i still have some aromasin and i believe i should keep taking it in order to keep estrogen from teking over and add some cabergoline to avoid low test symptoms but i am not sure about it i dont know what is right to do!


i believe it is a fair mistake that could happen to anyone! so please help out!


You and I have talked about this. I am just curious to see if the advice of others mirrors the advice I gave you.

I certainly think the post-cycle hcg was a big mistake, and that the tren may have given you problems with prolactin elevation, which I can say from experience is miserable.

From your post here it is a little hard to tell what is going on. You may want to explain your symptoms a little more.


This post IS confusing - i will have to break it down with questions - i apologise in advance for my opinions, but i dont see any excuse for your fuck ups after 4 years of using:

So at this point, you were planning on a cycle of 500mg/wk Sust and 400mg/wk Eq.. and you frontloaded with 750mg Sust and 600mg Eq?

I assume you continued to use the two drugs here - signified by the arrows?

Does this mean to the Sust and Eq, you added the Tren and Mast?

Was this an attempt at a taper? Did you continue the other drugs including the testosterone at the full dose?

So you decided to use a HELL of a lot of HCG.. with the old style super doses being generally 1000iu up to as much as 2500iu per 5 days, you were using the peak of 2500iu per 5 days! You should 'refresh' your knowledge..

So you have been using steroids for 4 years and you couldn't even tell your frontloaded cycle was doing fuck all until 17 weeks after commencement? I am sorry but that is crazy! Didn't you suspect it to be going badly at any point?
Regardless.. why wasn't the PCT necessary again? Because 2 of the 4 suppressive drugs you used weren't real?

This is not primarily a symptom of low Test. It is a symptom of high Estrogen in comparison to Test.
You are not shutdown 'for good' from using HCG after a cycle.
Tamoxifen doesn't produce Test.

I honestly cannot believe you had the balls or idiocy to state the length of time you have been using!

Anyway, caber is not a drug to 'avoid low test symptoms' i am not even sure what that means (surely low test symptoms are best cured by high test?).
Further AI is not needed.. while dominance of Estrogen is a real threat post cycle, you have been using a suicidal aromatase inhibitor, so what aromatase there was from the higher aromatisable androgens (in this case, Test provided via HCG) was removed, and your levels dropped in days rather than weeks on discontinuation of the HCG - and you continued the Aromasin 2 weeks after the HCG. That is sufficient.
I would expect (without the obvious benefit of bloods) you likely have low Test AND relatively low Estrogen, although likely higher than the Androgen level.

It is a fair mistake that could happen to anyone during the first year or two of using actually, assuming just 2 cycles per year. You have less excuse. You know it is a ridiculour error and that is why you are trying to justify it before a single reply. Just accept you need to read.

You would have been suppressed from the Tren and Mast anyway, so a PCT would have been necessary, would it not? So to that end, you did the 'right thing' whether that was deliberate or accidental is by the by.

I think if you had not used the HCG then you would have recovered. I think that the use of the HCG in massive doses during PCT was your undoing. It wasn't because you weren't suppressed the HCG shut you down, you WERE suppressed from the Tren and Mast. The HCG was too high and used at the wrong time for optimal recovery.

Essentially, you continued suppression upto week 14, and you wonder why you are still suppressed at week 17?
Run a SERM now.. That is all you should need, as essentially your cycle started at week 5 and ended at week 14 - this is 9 weeks.. none too bad.

Run your SERM (Nolvadex in this case) at 40mg a day for 1 week and 20mg a day for another 2-3 weeks.. this should leave you with a better chance at recovery. If you find it useful, continue the Tamoxifen at 10mg a day or EOD for a further week or two - until you feel your libido is strong enough to 'stand alone'.

If you feel more comfortable doing so, add caber - in my experience and opinion Tren has little to no activity as a progestin, and prolactin would not be raised any more than estrogen allows.
So while it is not directly for the tren's effects, Caber would not hurt recovery at around 0.25mg 2x/wk, for the duration you run the SERM (~4 weeks).

HCG should only be run during a cycle, never afterwards as it is suppressive (well, the Testosterone that is eventually secreted in dose dependant levels, is) - especially in the dose at which you used it. If used daily then 100iu is sufficient, but 250iu 2-3x/wk is considered 'the norm' - if you stick to a range of around 5-750iu per week then you shouldn't go wrong.

I hope this helps, and i hope you can take my (utterly astounding) surprise at your error as positive criticism and learn from the mistakes.

If you post or lurk here for any length of time, then there is again no excuse for not knowing how or why to run HCG in the most optimal fashion.

Lastly, next time you run a cycle, then maybe you should post it for criticism, as while it will be painful - you will not only come away with a decent cycle (if your attitude is sound) but some knowledge or sources of where to find the knowledge to build a cycle.



Excellent post Brook. You have a very analytical mind. If you are that quick witted verbally, I say you would be a fine barrister. Very generous contribution.



Very helpful/knowledgeable post Brook. Thanks for putting in the time to write up these detailed responses!


Nope. Short tempered and violent i'm afraid.. ;D


JIM, if you PM me to remind me to do so, i will reply with a good list of sites of articles and info that you will find infinitely useful in furthering your understanding.

I wish you had mentioned a year off (if you did in PM i apologise, it was a while ago and i forget about PM's soon after replying!) as i would not have been quite so critical.

How old was that post of BR's? I would be interested in reading it actually, as a look into what was recommended at that time. I have followed his (BR) work vaguely for a couple of years mow, so it is of interest to me :wink:

You should be aware that following advice that is more than 1-2 years old is a risk in this game, as the knowledge and understanding of these drugs changes rapidly with technology and pure and simple trial and error.

It may be of interest to know that when i joined T-Nation 2 years ago (under my JJ account) i also believed in using HCG post cycle in large doses, among other practices i now sternly frown upon.. However the information here while furthering my knowledge, more importantly furthered my interest and fuelled my desire to fully educate myself on the details of AAS usage. From any source i could. T-Nation steroid forum is but a mere drop in a ocean of information on Bodybuilding/Strength and AAS.. don't limit yourself to any one site on any subject.

A good start is always Google. Google the word(s) you are interested in - in your case 'Anabolic Steroids' and read every relevant article (and research every source, trust me alot will come up) or site in the first 1-5 pages. This will lead to many further links and soon you will be able to refer to the precise links immediately bypassing a search engine.

Listen to Cortes, he is a good guy to take advice from, and i do so regularly.


He is probably referring to the HCG profile on Mesomorphosis, written as a guess 10 years ago.

At the time the standard bb'ing practice was the atrocious business of 5000 IU at at time. I had established that this was not necessary, and in fact was the cause of HCG being considered a harsh drug, and that problems were definitely worse past 1000 IU per day. I meant that as an extreme upper limit. In terms of advice given anyone, or other discussions, I recommended at that time 500 IU 3x/week or every other day, rather than daily. But in terms of the profile I didn't at that time have the basis to say authoritatively that 500 IU per day was necessarily excessive. As it was people thought I was low-balling it, and at least was low compared to other authors.

I would now put the upper limit for daily usage at 250 IU/day, with this again really being more than needed but not problematically so.

The reference to use outside of a cycle is NOT for the PCT period. It is in reference to ongoing use to increase testosterone. It states clearly that the dose should be titrated according to measured testosterone level. In other words, not using more than found necessary and useful.

I really should take the trouble, though it would take a while, to go through all that old Meso stuff and update it -- there actually isn't that much that needs it, but there is some -- and ask Millard to put in the changes. He may also still have somewhere the wrong statement that I got my PhD, though the last several times I checked old articles he'd fixed the headings on those. Need to check that as well.


I'm genuinely flattered, JJ, thanks.

I've learned a massive amount more than I would ever have at this point from your very informative posts, as well. You certainly are one of this board's most valuable assets.

I'm also happy to see that your advice and observations pretty much exactly mirror what he and I discussed via pm. Good stuff.


i have to say i made a major mistake due to being in a hurry i typed bill roberts but it actually was ANTONY ROBERTS SORRY BILL MY MISTAKE this is the article and as you can see it looks preety good for an idea for someone who doesnt know much

                             I APOLOGIZE BILL ROBERTS NO HARD FEELINGS!

Great articles! (read twice!)
Post Cycle Therapy (PCT)
by Anthony Roberts

After a cycle, we have one goal: to hold onto the gains we made during the cycle. Unfortunately, this is easier said than done, because the levels of various hormones and other substances that were circulating around your body during the cycle (huge amounts of testosterone, insulin-like growth factor, growth hormone, and lower amounts of muscle-wasting glucocorticoids) are now changing. Sadly, they are making way for lower amounts of the hormones we want for building muscle, and higher amounts of the catabolic ones. What needs to be done, as quickly as possible, is to get your body to begin production of your own natural anabolic hormones, and produce less of the catabolic ones. Unfortunately, your body has other plans.
But then, so do I?
?and I?m very confident that this protocol will allow you to recover your own natural hormonal levels quickly and lose far less of the gains you worked so hard for on the cycle. This protocol, which is typically implemented after a cycle is called ?Post Cycle Therapy? or ?PCT? for short.
First, I?m going to tell you what anabolic hormones are typically low when a cycle ends, and which catabolic ones are high, then I?ll tell you what drugs can change that condition as fast as possible. Is all of this necessary? No, not at all. You can skip to the end of the article and look for a little chart I made - the extent of my computer skill - which has all of the dosage recommendations and compounds involved to properly recover from your cycle. I think, however, that you?ll see some very odd recommendations if you simply skip to the end, and will find yourself reading through the whole article to find out where they came from - or maybe you?ll just try to find out what?s gotten into me?
I?m not re-inventing the wheel here, and you may have seen a piece of this information elsewhere (possibly in something I?ve written, possibly somewhere else on the internet or in a magazine), but I?m sure of two things:
? You?ve never seen this PCT protocol anywhere
? This is the most effective PCT you?ll ever see
First, I?ll give you a brief explanation on the body and how it works, and why there?s a lag-time after the cessation of Anabolic Steroids before the body returns to normal. Remember, during this lag-time you lose gains, so we really need to make it as short as possible. First, we need to understand a bit of what is going on in your body, what causes it to happen naturally, and what hormones are performing what function. Don?t worry, I?ll try to make it painless.
At the age of puberty, Gonadatropin Releasing Hormone (GnRH) is increasingly released from the Hypothalamus, in turn causing the secretion of Follicle Stimulating Hormone (FSH) and Luetenizing Hormone (LH) from the pituitary, and finally the male gonads (testes) are then stimulated by those pituitary hormones (LH and FSH). (1). FSH, although generally thought to only have a role in production of sperm, actually aids the in regulation of Leydig Cell function (2), while LH directly causes the Leydig Cells in the testes to secrete androgenic hormones such as testosterone (which is causes a surge in other anabolic hormones: Insulin Like Growth Factor, Growth Hormone, etc?). Androgens do this by then targeting other tissues inside the body, either by attaching to the Androgen Receptors (AR), which are found primarily in the cytoplasm of specific cells, or by what?s known as non-receptor mediated effects. When an androgen (your own natural testosterone or an anabolic steroid you?ve injected or ingested) binds to a receptor inside the cell, it activates the transcription of specific genes. What does this mean? Don?t worry, it just means that the steroid molecule gives the cell a message to do something. In the case of testosterone, for example, one of the messages it sends to the cell is to increase nitrogen retention in your body, thus allowing you to use more of the protein you take in, and build more muscle. In the case of testosterone (or anabolic steroids in general), this transcription causes a lot of different anabolic effects to take place: an increase in IGF, a decrease in cortisol, an increase in Red Blood Cell count, and the increased protein synthesis I already told you about. This is not to say that AR binding is the only thing that causes anabolic or androgenic effects, however. Oxymetholone and Methandrostenolone (Anadrol and Dianabol) both bind very weakly to the AR yet are both highly anabolic and androgenic. The diagram below is an example of an androgen?s entry into a target cell, where it (in this case) stimulates protein synthesis, which is a major anabolic effect:

Under the control of this heightened state of androgens, you also go through androgenic development as well as anabolic development. This can be seen in puberty when males grow body hair experience voice changes, as experience genital development and growth.
Another characteristic of androgens in the body is that they are subject to what?s known as a ?negative feedback loop?. Lets review one of the first things I mentioned, ok? Your Hypothalamus secretes GnRH, thus making the pituitary secrete LH & FSH, finally in turn causing the testes to stimulate the Leydig cells to produce testosterone (by conversion of cholesterol), remember? Ok, now, once testosterone is created however, it has the ability to in turn to undergo various metabolic processes that will inhibit GnRH, which in turn inhibits the secretion of LH and FSH, and that brings a halt to natural testosterone production. Once testosterone has stopped being produced, it no longer sends this negative signal, and GnRH eventually begins to do its job again. In this way, your body prevents excess hormones from being secreted and thus maintaining homeostasis (the status quo? in this case a state where you are neither gaining nor losing muscle) (1). This negative feedback loop is partially why we use anabolic steroids?we want more testosterone for anabolic purposes (or more Anavar or whatever) than our body will let us produce (not that our bodies produce Anavar, but you get the idea). When we use that injectable testosterone, it sends the message to our body to begin the negative feedback loop and discontinue producing/secreting the hormones that cause our natural testosterone production. The chart below clearly shows this process, displaying both the negative and positive feedback system(s):

So what I?m saying is that anabolic steroids increase androgen levels in the blood, bringing a halt to GnRH, making the pituitary gland (eventually) responds by reducing the release of LH; this loss of LH has the effect of shutting down testosterone, of course, which you know is produced by the Leydig cells in the testes after they are stimulated by LH. Am I being repetitive? Yes. Do you need to understand all of this in order to understand the PCT protocol I?m about to outline? Yes. Remember, the negative feedback loop is, of course, no problem while we are on a cycle. Want more testosterone (or androgens) in your body? Fill up a few more syringes!
But all good things come to an end, and most of us choose to end our cycles at some point. At this point, while there is still some androgens floating around in us, our natural production won?t begin, and even once they are out, there may be some lag time before your body figures out that it needs to start producing its own androgens again. As I said before, this lag time is severely catabolic and it?s where you lose a lot of your gains. SO what we need to do is coax the body into quickly producing its own androgens.
One of the first drugs we?ll consider for this purpose is what is typically called a SERM. Nolvadex (Tamoxifen) is a SERM (Selective Estrogen Receptor Modulator, which means that it has the ability to act as an anti-estrogen with regard to certain genes, yet also acting as an estrogen with respect to others. That?s the ?selective? part I guess. It does this by blocking gene transcription in some cases, and initiating gene transcription in others (3). Luckily for us, it has estrogenic effects on bones (meaning it increases their density), and blood lipids -meaning it lowers cholesterol-, (4)(5)as well as preventing gynocomastia by preventing estrogen gene transcription in breast tissue. However, it acts as an anti-estrogen in the pituitary, thus increasing LH and FSH, which results in an increase in testosterone. 20mgs of Nolvadex will raise your testosterone levels about 150% (6)...Nolvadex actually has quite a few applications for the steroid using athlete. First and foremost, it?s most common use is for the prevention of gynocomastia. Nolvadex does this by actually competing for the receptor site in breast tissue, and binding to it. Thus, we can safely say that the effect of tamoxifen is through estrogen receptor blockade of breast tissue (7).
Estrogen is also important for a properly functioning immune system, and not only that, but your lipid profile (both HDL and LDL) should also show marked improvement with administration of tamoxifen (34).
Nolvadex also has some important features for the steroid using athlete. In hypogonadic and infertile men given nolvadex, increases in the serum levels of LH, FSH, and most importantly, testosterone were all observed (35)It can also block a bit of estrogen in the pituitary, which is a great benefit when used with HCG (more on that later) (36)(37). The increase in testosterone Nolvadex can give someone with a dysfunctional is basically that 20mgs of Nolvadex will raise your testosterone levels about 150% (6)...Why don?t we use Clomid, another SERM? Well, basically because it takes much more to do the same thing. In comparison, it would require 150mgs of Clomid to accomplish that type of elevation in testosterone, but Nolvadex also has the added benefit of significantly increasing the LH (Leutenizing Hormone) response to LHRH (LH-releasing hormone) (6). This most likely indicates some kind of upregulation of the LH-receptors due to the anti-estrogenic effect Nolvadex has at the pituitary. Although both Nolvadex and Clomid are both SERMs, they are actually quite different. As you already know, Nolvadex is highly anti-estrogenic at the hypothalamus and pituitary, while Clomid exhibits weak estrogenic activity at the pituitary (7), which as you can guess, is less than ideal. It should be avoided for the PCT I?m suggesting?and in fact, avoided in general?it?s simply not as good as Nolvadex.
Need I even add that the 150mgs of Clomid you need to get the hormonal increase experienced with 20mgs of Nolvadex is much more expensive? So lets dump the Clomid?and no, using it along with Nolvadex will provide no ?synergy? that I?ve ever seen in any relevant study.
SO how much Nolvadex should you use during PCT? I favor using 20mgs.day, although to be totally honest, you can probably even get away with far less than that. Doses as low as 5mgs/day have proven to be as effective as 20mgs/day for certain areas of gonadal stimulation. (8) 20mgs/day, however, is a dose that myself and others have used with great success, and the research I?ve done in this area typically uses this milligram amount. SO lets stick with 20mgs/day for now.
So that effectively suggests Nolvadex can not be used at Mega-doses to get a mega-increase in your natural hormones. We can?t use huge doses of any Anti-Estrogen, actually, and expect huge increases in our natural hormones, actually. Arimidex (an Aromatase Inhibitor ?which means it stops the conversion of testosterone into estrogen-another drug used to fight breast cancer like Nolvadex) exhibits basically the same effects when .5mgs or a full 1mg is used (9) and I have even read studies where up to 10mgs/day of Arimidex is studied with no clear benefit over 1mg/day. Letrozole (another Aromatase Inhibitor) is capable of inhibiting Aromatase maximally at a mere 100mcg/day (10.). So clearly we need to add in other compounds to our PCT, because Mega-Doses of one compound will not I think it?s absurdly funny to see people recommending upwards 40-80mgs/day of Nolvadex, or a full milligram (or two!) of Arimidex, in their post-cycle or on-cycle suggestions. I?d steer very clear of listening to anyone who makes those types of recommendations?
All of this tells me that you can?t simply use mega-doses of Anti-Estrogens or SERMS to do anything more than reasonable doses. It must be, therefore, that your body can only respond with so much vigor to any one drug in those families. So lets add in another drug or two, ok? This way we can use reasonable doses of a few drugs and produce some synergy?hopefully decreasing our recovery time.
We?ll need something to go with Nolvadex, which acts in a different manner, and Human Chorionic Gonadatropin (HCG) is the clear choice here. Here?s where things get a bit controversial (no, really?I know you , because I?m pretty much the only person around (currently) who recommends HCG for Post-Cycle Therapy. Although I?m seen as Old School in this respect, really, this is a totally new paradigm for HCG use, made possible only by the inclusion of the other compounds I am introducing to you for PCT. HCG is the natural choice, as it has been used successfully to cure AAS induced (11), and this alone warrants its inclusion to our cycle.
HCG is a peptide hormone manufactured by the embryo in the early stages of pregnancy and later by the placenta to help control a pregnant woman?s hormones (can anything really be said to control a pregnant woman?s hormones except ice-cream and chocolate?). Obviously, as you can guess from the name, it is a substance that stimulates the gonads (hence: gonadotropin). It does this by initiating gene transcription that is identical to that of Luetenizing Hormone, thereby causing the Leydig Cells to produce testosterone. Sounds great right? We can stimulate LH and FSH production with our Nolvadex, and then directly stimulate the Leydig Cells as well, to produce tons of testosterone by different routes! Well...it?s not all that simple.
Unfortunately, while HCG increases Testosterone, it increases estrogen as well(12). As you probably know, estrogen acts directly on the Leydig cells to effect changes in the activities of enzymes important for testosterone synthesis (13) and may actually be considered an important part of that negative feedback loop I mentioned earlier. In addition, an increase in circulating levels of LH have been shown to induce down-regulation of LH-receptors in both rodent studies (14), as well as in human studies (15); since HCG mimics LH, you can expect it to do the same. This LH downregulation can cause an increase in steroidogenic cholesterol (the cholesterol earmarked by your body for conversion into testosterone). (16). Thus, after the initial HCG induced surge in testosterone is over, if you have used enough to downregulate your LH-receptors and increase estrogen too much, then more steroidogenic cholesterol is available. This is telling me that less is being converted to testosterone. In fact, rodent models suggest that if you take a dose large enough to cause a sharp increase of plasma testosterone, you will actually desensitize your Leydig cells to your next shot, and will possibly not experience any rise in testosterone from the second dose at all, or may only experience a very slight one at best (17.). Since this is due to LH-Receptor downregulation, and that occurs in human models too, it is pretty fair to assume that if your first dose of HCG is too large, your second won?t be very effective. Unfortunately, this lack of an increase in testosterone doesn?t necessarily mean that the HCG may be unable to increase circulating levels of Estrogen (18) And remember that increase in Estrogen will (most likely) cause your body ultimately to produce less testosterone. Low LH post-cycle is not the primary cause of slow recovery, because LH generally rises to levels above baseline after a cycle much sooner than testosterone production does. This is probably because the pituitary is working very hard to get your atrophied Leydig cells to start producing testosterone again. HCG should also bring back testicular volume; I feel the need to mention this because it?s important to me and I suspect most men as well. It would also appear that HCG works very well when it?s used on men who have low levels of LH to begin with (as you would be after a cycle), as many studies on pre-pubertal boys and Hypogonadotropic Hypogonadal men would suggest (19)
This suggests that a pre-exposure to normal LH levels or gonadatropins in general is necessary for HCG-induced Leydig Cell desensitization. This, of course is not a problem for us, as we?ll be using it when LH/Gonadatropin levels are very low anyway ?we just need to stop using it before we regain normal function, or it will work against us eventually. (19) (20). Luckily, the temporary Anabolic steroid induced hypogonadism that is experienced after a cycle basically allows us to respond to HCG like anyone with low LH levels (21), and thus, as I told you, a lot of the possible inhibitory effect of HCG is not going to be relevant because there was no prior ?priming? by circulating gonadotrophins. This is great news for us, because we are going to be using HCG during PCT, when we need to get back some HPTA function, and not when we have levels of gonadatropins high enough to cause HCG-induced desensitization.
But are we still risking some inhibition and possibly delaying our recovery by using HCG? Probably not?you see, some studies in humans have shown that HCG does not actually have a direct effect on inhibiting LH release in men (22)(23), but rather (probably) works to inhibit LH secretion indirectly, simply by stimulating the production of testosterone (thus activating the negative feedback loop). Another factor involved is the induction of testicular aromatase, which raises estrogen levels, again causing inhibition. Unfortunately, yet another process, the downregulation of the Leydig Cell LH receptor itself, seems to also play a role in high dose HCG testicular desensitization. This is also done by HCG actually blocking the conversion of 17 alpha-hydroxyprogesterone (17 OHP) to testosterone (24). Nolvadex actually stops this blocking-action of HCG from taking place (25). Most likely, because of Nolvadex?s direct antiestrogenic effect and LH-upregulating effect on the Pituitary, suppression of gonadotropins via HCG is (25) almost totally stopped with concurrent administration of Nolvadex! So if we Use Nolvadex and we are only using HCG when we are low in gonadatropins, we won?t be inhibited by it at all! Right?
Well?maybe?but there?s still the issue of estrogen caused by that HCG-stimulated surge in testosterone. Well?we can use low doses (300iu or so) to avoid some of that major spike in estrogen, and thus cause far less inhibition from the HCG (26). Of course, I?d want to use a bit more HCG per injection (500iu), if I could, to get my body functioning fully more quickly, and lose less of my gains. Maybe we can get away with taking some Vitamin E with our HCG, since it increases the responsiveness of plasma testosterone levels to HCG, making them significantly higher during vitamin E administration than without it (27). So we can get a better response with our HCG by taking Vitamin E (I recommend 1,000iu/day), but that doesn?t get rid of the problem that we have, which is the estrogen increase the HCG will cause.
Lets solve that pesky estrogen problem now?.
Lets add in an Aromatase Inhibitor! Which one, though? Well, since we are already using Nolvadex, we can?t use Letrozole or Arimidex, as the Nolvadex will actually greatly decrease the blood plasma levels of them (28)!
So we have to use Aromasin (exemestane) as our AI, because it?s an aromatase inactivator, meaning it makes estrogen receptors useless, and instead of just inhibiting production (as an anti-aromatase would do) it cuts off production totally. Aromasin can also cause androgenic sides (29)(30)(31), which may help to elevate your mood while you are on PCT. This final drug in my recommended PCT can effectively remove up to about 85%+ of estrogen from your body (32). Most importantly, using Aromasin together with Nolvadex doesn?t reduce exemestane?s effectiveness (33). So now, I think the problem of ANY inhibition possible with HCG is solved, and we can use that 500iu/day dose that I wanted to use previously.
With this PCT, there will be a rapid increase in LH, FSH, and testosterone, as well as almost a complete block on all the factors that could be causing your natural hormones to be delayed in returning to baseline. For this reason, I feel that the second your cycle is over is when you should start this PCT (a week after your last shot, or the day after your last pill is fine). Remember, waiting for some of the extra androgens you?ve been taking to leave your body is nonsensical, as we want to start recovery as soon as possible to retain maximum gains. There is no evidence to suggest waiting any length of time after your cycle is over will increase PCT effectiveness?it simply prolongs the time you aren?t doing anything positive to regain your natural hormones. And how long do we run this for? Well?we need to stop the HCG relatively soon for reasons discussed earlier. But the Nolvadex, and Aromasin can be used for awhile longer. Ideally, we?d be getting weekly blood work, but we could also get it done monthly, and just running this PCT until we see our natural hormones restored?but weekly bloodwork isn?t really an option for most of us. Failing the option of monitoring recovery with blood-work, I?m going to give you my best thoughts on the time you should be running your PCT. It?s important to note I haven?t discussed nutrition or other compounds that may be beneficial?this is because in this article, I am primarily concerned with the restoration of hormonal function, nothing else. And with no further delays, here are my recommendations for PCT:
Week Nolvadex HCG Aromasin Vitamin E
1 20mgs/day 500iu/day 20mgs/day 1,000iu/day
2 20mgs/day 500iu/day 20mgs/day 1,000iu/day
3 20mgs/day 500iu/day 20mgs/day 1,000iu/day
4 20mgs/day 20mgs/day
5 20mgs/day
6 20mgs/day

Rationale for the Use of Aromasin with Tamoxifen During Post Cycle Therapy

Aromasin (Exemestane) is one of those weird compounds that nobody really knows what to do with. What we generally hear about it makes it very uninteresting?It?s a third generation Aromatase Inhibitor (AI) just like Arimidex (Anastrozole) and Femera (Letrozole). Both of those two drugs are very efficient at stopping the conversion of androgens into estrogen, and since we have them, why bother with Aromasin? It?s a little harder to get than the other two commonly used aromatase inhibitors, because it?s not in high demand, and there?s never been a readily apparent advantage to using it. And I mean?lets face it: It?s awkward-sounding. Aromasin doesn?t have much of a ring to it, and exemestane is even worse. Arimidex has a bunch of cool abbreviations ("A-dex" or just ?dex) and even Letrozole is just "Letro" to most people. Where?s the cool nickname for
Aromasin/exemestane? A-Sin? E-Stane? It just doesn?t work. It?s the black sheep of AIs. And why do we even need it when we have Letrozole, which is by far the most efficient AI for stopping aromatization (the process by which your body converts testosterone into estrogen)? Letro can reduce estrogen levels by 98% or greater; clinically a dose as low as 100mcgs has been shown to provide maximum aromatase inhibition (2)!
So why would we need any other AIs? Well, first of all, estrogen is necessary for healthy joints (3) as well as a healthy immune system (4). So getting rid of 98% of the estrogen in your body for an extended period of time may not be the best of ideas. This may be useful on an extreme cutting cycle, leading up to a bodybuilding contest, or if you are particularly prone to gyno, but certainly can?t be used safely for extended periods of time without compromising your joints and immune system.
That leaves us with Arimidex, which isn?t as potent as Letrozole, but at .5mgs/day will still get rid of around half (50%) of the estrogen in your body. Problem solved, right? Use Arimidex on your typical cycles, and if you are very prone to gyno or are getting ready for a contest, use Letro.
But what about Post Cycle Therapy (PCT)?
I think at this point most people are sold on the use of Nolvadex (Tamoxifen Citrate) instead of Clomid for post cycle therapy (PCT), since both compete estrogen at the receptor site, both increase serum test levels, and both drugs may also alter blood lipid profiles favorably (6). But since 20mgs of Tamoxifen is equal to 150mgs of clomid for purposes of testosterone elevation, FSH and LH, but Tamoxifen doesn?t decrease the LH response to LHRH (6) I think most people agree to Nolvadex?s superiority for PCT.
Aromasin with Nolvadex
I?ve always been in favor of using Nolvadex during PCT, along with an AI, because reducing estrogen levels has been positively correlated with an increase in testosterone (7) so in my mind, it?s be beneficial to increase testosterone by as many mechanisms as possible while trying to recover your endogenous testosterone levels after a cycle. SO which AI do we use? Letro or A-dex? Well, why don?t we just keep using whichever one we used during the cycle, and add in some Nolvadex? Unfortunately, Nolvadex will significantly reduce the blood plasma levels of both Letrozole as well as Arimidex (8). So if we choose to use one of them with our Nolvadex on PCT, we?re throwing away a bit of money as the Nolvadex will be reducing their effectiveness.
This, of course, is where Aromasin comes in, at 20-25mgs/day.
Aromasin, at that dose, will raise your testosterone levels by about 60%, and also help out your free to bound testosterone ratio by lowering levels of Sex Hormone Binding Globulin (SHBG), by about 20% (12)?SHBG is that nasty enzyme that binds to testosterone and renders it useless for building muscle. But what about using it along with Nolvadex for PCT?
Difference Between Type-I and Type-II Aromatase Inhibitors
To understand why Aromasin may be useful in conjunction with Nolvadex while both Letro and A-dex suffer reduced effectiveness, we?ll need to first understand the differences between a Type-I and Type-II Aromatase Inhibitor. Type I inhibitors (like Aromasin) are actually steroidal compounds, while type II inhibitors (like Letro and A-dex) are non-steroidal drugs. Hence, androgenic side effects are very possible with Type-I AIs, and they should probably be avoided by women. Of course, there are some similarities between the two types of AIs?both type I & type II AIs mimic normal substrates (essentially androgens), allowing them to compete with the substrate for access to the binding site on the aromatase enzyme. After this binding, the next step is where things differ greatly for the two different types of AI?s. In the case of a type-I AI, the noncompetitive inhibitor will bind, and the enzyme initiates a sequence of hydroxylation; this hydroxylation produces an unbreakable covalent bond between the inhibitor and the enzyme protein. Now, enzyme activity is permanently blocked; even if all unattached inhibitor is removed. Aromatase enzyme activity can only be restored by new enzyme synthesis. Now, on the other hand, competitive inhibitors, called type II AI?s, reversibly bind to the active enzyme site, and one of two things can happen: 1.) either no enzyme activity is triggered or 2.) the enzyme is somehow triggered without effect. The type II inhibitor can now actually disassociate from the binding site, eventually allowing renewed competition between the inhibitor and the substrate for binding to the site. This means that the effectiveness of competitive aromatase inhibitors depends on the relative concentrations and affinities of both the inhibitor and the substrate, while this is not so for noncompetitive inhibitors. Aromasin is a type-I inhibitor, meaning that once it has done its job, and deactivated the aromatase enzyme, we don?t need it anymore. Letrozole and Arimidex actually need to remain present to continue their effects. This is possibly why Nolvadex does not alter the pharmacokinetics of Aromasin (11).
Before we close the book on Aromasin, it?s worth noting that you can (and should) still use one of the non-steroidal AIs during your cycle to reduce estrogen, if necessary. When you are ready for PCT, you can then switch over to Aromasin and still experience the full effects of an AI, since there is no cross-over tolerance experienced between steroidal and non-steroidal AIs (9). Since Aromasin is about 65% efficient at suppressing estrogen (10), it?s certainly a very powerful agent, especially considering you won?t experience reduced effectiveness because of your concurrent use of Nolvadex or from any sort of tolerance developed by using other AIs on your cycle(9). There is also a decent amount of preclinical data suggesting that Aromasin has a beneficial effect on bone mineral metabolism that is not seen with non-steroidal agents, and it may also have beneficial effects on lipid metabolism that are not found in the non-steroidal Letro and A-dex (9).
Finally, as we?re going to be using Nolvadex for PCT anyway, and we ought to be using an AI with it for maximum recovery?I think Aromasin- considering it?s compatibility with Nolvadex and beneficial effects on bone mineral content and lipid profile, has finally stopped being the black sheep of AIs and found a home in our cycles.


Easy enough mistake to make I suppose.

Inasmuch as "Anthony Roberts" is a fake name anyway, it was confusing of him to decide to choose that, and it seems a strange decision as well. I mean who that wants to be a steroid guru comes up with pen names for themselves such as John Duchaine, David Kneller, Bruce Palumbo, John Starr, etc? If the thought were even to come into the mind, it would be rejected by most. But, no accounting for taste.

Maybe he thought it would make him sound science-y.



I personally think it is likely that he wanted the connection to your work.. as having your work mixed up with his is no skin off his nose..