Copy and pasted, my buddy posted this in another forum thought it might be a useful addition, I will be using this protocol in about 6 weeks or so
COPY AND PASTED
Again copy and pasted
Post Cycle Therapy by Anthony Roberts
Post Cycle Therapy
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 .....20-25mgs/day ..... 1000iu/day
2 ..........20mgs/day .....500iu/day .....20-25mgs/day ..... 1000iu/day
3 ..........20mgs/day .....500iu/day .....20-25mgs/day ..... 1000iu/day
4 ..........20mgs/day ........................20-25mgs/day
5 ..........20mgs/day ........................20-25mgs/day
6 ..........20mgs/day
References
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3- Endocrinology. 1995 Feb;136(2):536-42
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5- Treat Endocrinol. 2004;3(2):105-15. Review.
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7- Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin
release in vitro. Adashi EY, Hsueh AJ, Bambino TH, Yen SS. Am J Physiol
1981 Feb;240(2):E125-30
8- Effect of lower versus higher doses of tamoxifen on pituitary-gonadal
function and sperm indices in oligozoospermic men.m Dony JM, Smals AG,
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Males"
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18- Proc Natl Acad Sci U S A. 1979 Sep;76(9):4460-3
19- Kinetics of the steroidogenic response of the testis to stimulation by
hCG. V. Blockade of 17-20 lyase induced by hCG is an age-dependent
phenomenon inducible by pre-treatment with hCG. Forest MG, Roulier R
20- J Clin Endocrinol Metab 1982 Jul;55(1):76-80
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25- Andrologia 1991 Mar-Apr;23(2):109-14
26- J Clin Endocrinol Metab. 1984 Feb;58(2):327-31
27- Effect of vitamin E on function of pituitary-gonadal axis in male rats and
human subjects. Umeda F, Kato K, Muta K, Ibayashi H.
28- J Steroid Biochem Mol Biol. 2001 Dec;79(1-5):85-91.
29- Clin Cancer Res. 2003 Jan;9(1 Pt 2):468S-72S.
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31- J Steroid Biochem Mol Biol 1997 Nov-Dec;63(4-6):261-7
32- Eur. J. Cancer. 2000, May;36(8):976-82
33- Inhibitory effect of combined treatment with the aromatase inhibitor
exemestane and tamoxifen on DMBA-induced mammary tumors in rats.
34- Bruning PF, Bronfer JMG, Hart AAM, Jong-Bakker M, tamoxifen, serum
lipoproteins and cardiovascular risk, Br. J. Cancer 1988 Oct, 58 (4) 497-9
35- Stimulation of calcitonin secretory capacity by increased serum levels of
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release in vitro. Adashi EY, Hsueh AJ, Bambino TH, Yen SS. Am J Physiol
1981 Feb;240(2):E125-30
37- Hormonal changes in tamoxifen treated men with idiopathic oligozoospermia Exp Clin Endocrinol. 1988 Dec;92(2):211-6
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