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Post Cycle Therapy (PCT)

The Purpose of PCT

The HPTA: How It Works
Determining Factors In Difficulty Recovering the HPTA
Individual Response
Type of Anabolic Steroid(s) Used
Length of Cycle
PCT Medications
SERMs: Nolvadex, Clomid, Toremifene, & Raloxifene
Dosing

Nolvadex: Recommended PCT 10mg/day

Clomid (not recommended)
Torem (not recommended)
SERM Dosing Note
hCG
 Dosing

1. Over The Entire Cycle

2. Weeks Leading Up To PCT
3. 1-2 Weeks Before PCT
4. First 1-2 Weeks Of PCT
Aromatase Inhibitors: Aromasin (Exemestane) Above All Else
Dosing
Drug Interactions
Side Effects
What to Expect from PCT
When NOT to Run PCT
When to Start PCT
Very Long Ester AAS & PCT Transition
Very Long Ester Testosterone & PCT Transition
Important Metabolites Note
When to Start Your Next Cycle
Blood Work
The Danger
PCT for Women
Michael Scally (former) M.D.'s Thoughts:
References
Official /r/steroids PCT Protocols

SERM Dosing Note

Optimal/Primary PCT Options
Nolvadex
 Option 1
Option 2
Clomid

Option 1
Option 2
Torem

Option 1
Option 2
Secondary PCT Options
Nolvadex

Option 1
Option 2
Clomid

Option 1
Option 2
Torem

Option 1
Option 2
Minimalist PCT Options
Nolvadex
Clomid
 Torem
Post Blast & Cruise Recovery Not Endorsed By /r/steroids
ASRM Guidlines For Physicians To Prescribe
Original PoWeR PCT
New PoWeR PCT
Controversy
Jcaesar369 Recommended PCT Protocol
TL;DR:
Controversy
Triptorelin PCT
A Doctor's Recommended PCT (TRT Clinic)
Miscellaneous Findings

Triptorelin/GnRH
Misc.

Post Cycle Therapy (PCT)

Post Cycle Therapy or PCT is a period of medication treatment that follows
the use of anabolic steroids. Post Cycle Therapy is also one of the most
confusing topics for many steroid users; this is largely due to
misconceptions. When to start PCT, which meds to use, how long to use
them and what you should expect, these are all common questions and
ones we’ll address here.

🟢 Recommended PCT: 10mg Nolvadex, 6-8 weeks

The Purpose of PCT

When we supplement with anabolic steroids we suppress our natural

testosterone production. Testosterone, the primary male hormone, is
essential to our very well being. Most men who supplement with anabolic
steroids will always include at least a minimal amount of testosterone in
their cycle due to this suppression factor.

Following the use of exogenous anabolic steroids, the majority of users will
experience what has been dubbed a “hormonal crash” or “post cycle crash”,
which is a bodily environment in which key hormones essential to the
retention of the newly created muscle mass has been suppressed or shut
down. The key hormones in question are LH (Luteinizing Hormone), FSH
(Follicle Stimulating Hormone), and subsequently (and most importantly),
Testosterone. LH and FSH are known as gonadotropins, which are
hormones that signal the gonads (testes) to begin or increase the
manufacture and secretion of Testosterone. Alongside low levels of these
hormones, the overall balance of total hormones will be essentially thrown
off, whereby Testosterone levels will be low, and most of the time
(depending on many factors), Estrogen levels will be higher, and levels of
Cortisol (a steroid hormone that destroys muscle tissue) will be at normal
levels. With Testosterone levels low and Cortisol levels in the normal (or
high) range, Cortisol now becomes a threat to the newly created muscle that
was created during the recent anabolic steroid cycle (Testosterone properly
suppresses and counteracts Cortisol’s catabolic effects on muscle tissue).
SHBG (Sex Hormone Binding Globulin) is also a concern here as well, which
is a protein that binds to sex hormones (Testosterone) and renders them
inactive, essentially ‘handcuffing’ them and preventing them from exerting
their effects. SHBG will also normally be elevated during the post-cycle
weeks as a result of the supraphysiological levels of androgens from the
recent anabolic steroid cycle.

The human body will normally restore this imbalance of hormones and
recover its endogenous Testosterone levels on its own over time with no
assistance, but studies have demonstrated that without the intervention of
Testosterone stimulating agents, this will occur over the course of up to 4
months or so. This is quite evidently enough time for the hormonal
imbalance to wreak havoc on the body and result in any individual losing
most or all of the newly gained muscle during this time. Therefore, all
anabolic steroid users should be concerned with the fastest possible
hormonal recovery, assisted and boosted with the use of Testosterone
stimulating compounds in the proper manner. Furthermore, the attempt to
allow the body to recover on its own will present a very high probability of
long-term endocrine damage to the HPTA over time whereby the individual
will develop anabolic steroid induced hypogonadism (the inability to
manufacture proper levels of Testosterone for the rest of their life). It is
therefore paramount that a proper post cycle therapy that includes multiple
recovery compounds be utilized so as to not only restore the HPTA function
to normal levels as quickly as possible, but to avoid any possible permanent
damage, which takes priority over the concern of maintaining the recently
gained muscle mass.

The HPTA: How It Works

The HPTA is the Hypothalamic Pituitary Testicular Axis, which is an axis of

interconnected endocrine glands in the body that deal with and control
Testosterone production.

Click here For HPTA Diagram

Outlined above is a diagram of the HPTA. The HPTA regulates how much
Testosterone is manufactured and circulating the body at any one given
time. Every individual is essentially programmed by their genetics (DNA) as
to how much maximum Testosterone they will manufacture, and this is the
prime determining factor. There exist other factors that determine how
much Testosterone an individual will produce as well, and these include:
age, diet, body composition, lifestyle habits, and physical activity. All of
these factors play a role in how much Testosterone an individual will
generate overall.

The HPTA functions under what is known as the negative feedback loop,
whereby the body will reduce its manufacture and secretion of
Testosterone if too much Testosterone is detected circulating in the body,
and will also adjust as such if insufficient amounts of Testosterone are
detected. This detection and adjustment, known as the negative feedback
loop, is controlled by the hypothalamus, which is essentially considered the
‘master’ gland for all endocrine and hormonal functions in the body. The
negative feedback loop is ultimately the body’s attempt to maintain
hormonal homeostasis, which refers to the regulation of a system (in this
case, the internal systems of the body) in order to maintain stable and
constant favorable conditions. All endocrine glands operate by way of the
negative feedback loop in one way or another, and to varying degrees. In
the case of post cycle therapy, the concern is primarily with the negative
feedback loop of the HPTA.

Within the HPTA, the concern during PCT is the restoration and regulation
of the following 5 hormones to homeostasis:

GnRH (Gonadotropin Releasing Hormone)

LH (Luteinizing Hormone)
FSH (Follicle Stimulating Hormone)
Testosterone

The HPTA begins with the first axis point, the hypothalamus, which will
detect a need for the human body to manufacture more Testosterone, and
will release varying amounts of GnRH. GnRH is a hormone that signals the
next axis point, the pituitary gland, to begin the manufacture and release of
two important gonadotropins: LH and FSH. LH and FSH are two hormones
that work to signal the third axis point, the testes, to begin production and
secretion of Testosterone. This is the final stage of Testosterone production
in the HPTA.

There are two primary hormonal factors that serve to inhibit, reduce,
suppress, or shut down Testosterone production in the HPTA:

Excess Testosterone
Excess Estrogen

Although there exist other hormones that serve to inhibit and suppress
HPTA function (such as Progestins and Prolactin), these are the two primary
conditional hormones that are of concern. When the hypothalamus detects
excess levels of Testosterone and/or Estrogen in the body (either from the
use of exogenous androgens on an anabolic steroid cycle or otherwise), the
hypothalamus will act to attempt to restore a balance by essentially doing
the opposite of what was previously described. The hypothalamus will
reduce or stop its production of GnRH, which halts production of LH and
FSH, which ultimately reduces or halts production of Testosterone. Until the
hypothalamus’ ideal hormonal environment is restored, the production of
the various signaling hormones within the HPTA will not begin, and this
will often require months of time for the body to do this on its own without
the intervention of any Testosterone stimulating agents. The reason as to
why the recovery of the HPTA naturally takes such a long time should be
very clear due to the described workings of the HPTA.

This very basic understanding of the mechanisms of the HPTA and negative
feedback loop described above is essential to understanding how and why a
proper PCT program must be developed and utilized following an anabolic
steroid cycle.

Determining Factors In Difficulty Recovering the HPTA

With anabolic steroid use, there are several different major determining
factors in how much difficulty an individual will experience in recovery of
their HPTA and endogenous Testosterone function during PCT. They are the
following factors, in no particular order of importance:

1. Individual Response
2. Type of Anabolic Steroid(s) Used
3. Length of Cycle (Degree of Testicular Desensitization)

Individual Response

Every single individual will respond in a different manner to any chemical,

compound, anabolic steroid, food or drug in existence. While some
individuals might experience absolutely no HPTA suppression or shutdown
at all, other individuals might experience severe HPTA suppression and
shutdown to the extent where they might require far longer periods of time
to ensure full recovery than most. This, like anything else, is a spectrum
whereby there are the very ‘lucky’ individuals that recover very quickly
and easily on one end of the spectrum, and the ‘unlucky’ individuals that
have extreme difficulty recovering during post cycle therapy. In between
the two extremes is the average. Once again, this is due to the individual’s
genetic programming as to how the HPTA will respond and attempt to
maintain homeostasis.

Type of Anabolic Steroid(s) Used

All anabolic steroids exhibit suppression or shutdown of the HPTA through

the mechanisms of the negative feedback loop, and there are no exceptions
to this. It’s often said that if you take any anabolic steroid you now produce
no testosterone, but this isn’t exactly true. Various anabolic steroids are
known as being mildly suppressive (something like Anavar), while others
are known as being heavily suppressive (something like Nandrolone
Decanoate). In any case, no matter how mild or severe an anabolic steroid
exerts HPTA suppression, all anabolic steroids when utilized for typical
cycle lengths of weeks at a time will eventually cause the HPTA to shut
down, or at the very least severely suppress its hormonal signal processes.
Even if suppression may not reach 100%, it will still be enough in every
case for there to be a need for testosterone supplementation during
use due to putting your testosterone into a low level state.

Important Note: the need for testosterone supplementation during

anabolic steroid use does not apply to women nor does the need for PCT.
See the PCT For Women Section below.

Length of Cycle

This is perhaps the most important and most influential factor. As the
length of anabolic steroid use continues, the majority of the Leydig cells of
the testes remain dormant and inactive, and the longer these interstitial
cells remain dormant and inactive, the greater the difficulty in essentially
getting these cells to respond to the stimulus of LH and FSH once again. It
has been discovered in studies that the issue of recovery of the Leydig cells
following anabolic steroid use is not due to a lack of LH, but due instead to
the desensitization of the Leydig cells to LH.\1]) In one study in which
exogenous Testosterone was administered to male test subjects for 21
weeks, LH levels were suppressed shortly after beginning administration.
However, at the end of the 21 week period, LH levels were observed to rise
within 3 weeks once the exogenous Testosterone administration stopped,
but Testosterone levels did not rise until many weeks later in most of the
test subjects.

PCT Medications

The main testosterone stimulating agents for HPTA recovery during PCT
are:

Primary

SERMs (Selective Estrogen Receptor Modulators)

Secondary:

hCG (Human Chorionic Gonadotropin)

Aromatase Inhibitors

SERMs: Classes of drugs in the SERM category include: Nolvadex

(Tamoxifen Citrate), Clomid (Clomiphene Citrate), Raloxifene, and Torem
(Toremifene Citrate). The nature of a SERM is that it exhibits mixed
Estrogen agonist and Estrogen antagonist effects on the body. This means
that although a SERM might block the effect of Estrogen at the cellular level
in certain tissues, it can enhance Estrogenic effects in other areas of the
body. These can be positive effects as well as negative effects. In terms of
the effect of SERMs on endogenous Testosterone stimulation, they serve to
act as an Estrogen antagonist at the pituitary gland, triggering the release of
LH and FSH as a result. Elevated levels of Estrogen in men can and does
suppress the output of endogenous Testosterone via the negative feedback
llllll2]) SERMs for this purpose are an absolutely essential addition to any
PCT protocol and are not to be excluded under any circumstance.

hCG: Human Chorionic Gonadotropisynthetic is an LH mimetic. It is a

protein hormone manufactured in high amounts by pregnant females that
contains a protein subunit that is 100% identical to LH, and therefore when
administered to men, it will mimic the action of LH in target tissues, such as
the testes. What results is an increase in Testosterone production via
stimulation of the Leydig cells by hCG. hCG should never be utilized alone,
as its nature as a gonadotropin will itself trigger a negative feedback loop
whereby once hCG is utilized, the pituitary gland will halt output of LH
until hCG use has discontinued. Therefore, hCG must be utilized prior to
PCT or with a SERM, oft-times with an aromatase inhibitor, as hCG has
demonstrated to increase aromatase activity in the testes, resulting in rising
Estrogen levels.\3])

Aromatase inhibitors: These are compounds such as Aromasin

(Exemestane), Arimidex (Anastrozole), and Letrozole (Femara). Rather than
block the activity of Estrogen at the cellular level in different tissues,
aromatase inhibitors (AIs) serve to lower total circulating Estrogen levels in
the body by way of inhibiting the aromatase enzyme, which is the enzyme
responsible for the conversion of androgens into Estrogen. The conversion
of androgens into Estrogen results in excess Estrogen levels, which, as
explained earlier on this wiki page, will trigger the negative feedback loop
leading to suppression of Testosterone production. By way of lowering total
circulating blood plasma Estrogen levels, AIs will engage the negative
feedback loop in a positive manner and result in the release of LH and FSH
for the manufacture and secretion of more Testosterone. This is essentially
due to the hypothalamus realizing that circulating Estrogen levels are too
low, and will attempt to increase circulating levels of Testosterone in order
for a portion of the Testosterone secreted to be able to become aromatized
into Estrogen in order to restore the hormonal balance. The main
importance of aromatase inhibitors is the ability to mitigate the Estrogenic
effects of HCG, if HCG is utilized in certain ways that will be expanded on
later. It is important to note, however, that the majority of aromatase
inhibitors have known drug interactions with Nolvadex that will reduce
blood levels of those AIs. Very specific choices should be made in regards as
to which AI is used during PCT with what SERM.

SERMs: Nolvadex, Clomid, Toremifene, & Raloxifene

The question is often asked among the anabolic steroid using community:
Clomid or Nolvadex? Which one for PCT? But there are also relatively
newer SERMs as well. Toremifene (Torem) & Raloxifene (Ralox).

First of all, we will look at the two main SERMs people use for PCT --
Nolvadex & Clomid. Nolvadex on a mg for mg basis is far more effective
than Clomid in stimulating endogenous Testosterone production, as well as
being a more cost-effective choice than Clomid itself. Studies have
demonstrated that 150mg of Clomid (Clomiphene Citrate) administered
daily raised endogenous Testosterone levels of 10 healthy males by
approximately 150%, while incidentally, 20 mg of Nolvadex (Tamoxifen
Citrate) daily raised endogenous Testosterone levels by the same
amount.\11]) It is very evident here that Clomid is very effective for this
purpose, but Nolvadex seems to be a more cost-effective choice seeing as
though it is more effective than Clomid when compared mg for mg. In the
same study, they directly examined the effects of Nolva and Clomid on the
pituitary. They infused the men with 100 mcg of GnRH and then measured
LH output from the pituitary. The men taking Nolvadex at 20 mg/day had a
significantly increased LH response to GnRH. In contrast, the men taking
Clomid had reduced LH output, a decreased sensitivity to GnRH. The
researchers stated that "a role of the intrinsic estrogenic activity of Clomid
which is practically absent in Tamoxifen (Nolva) seems the most probable
explanation."\11]) Likewise, Clomid actually has been studied to exhibit
Estrogen agonist effects at the pituitary in vitro.\12]) What all this means is
that Clomid potentially will work in varying degrees as an Estrogen at
the pituitary gland, triggering the negative feedback loop and reducing the
output of Testosterone stimulating gonadotropins (LH and FSH). This is a
problem during post cycle therapy, which is a period in which
individuals are trying to recover their HPTA function rather than halt it
even further. Ideally, one would want a SERM that exhibits almost 100%
Estrogen antagonistic effects on the pituitary gland.

In addition to all this, vision sides are common with Clomid and could
may cause irreversible changes.\18]) Nolvadex may potentially cause
some vision sides as well,\19]) but they are known to be far more prominent
in Clomid than Nolvadex.\16]) More on Side Effects below.

Despite all of this, it should still be noted that the FDA actually recommends
Clomid for treatment of male hypogonadism and that high doses are
unnecessary to bring hypogonadal men into range.\14][17])

To touch lightly on Torem & Ralox, they have all been compared and
studied alongside Nolva.\15]) The study looked at the effects of each SERM
in just under 300 infertile men with low sperm count and low testosterone
levels. The men were given 20 mg Nolvadex, 60 mg Toremiefene or 60 mg
Raloxifene every day for three months. See Figure 1 from the study here
showing results month to month or see table below with the medians and
results after three months:

Sperm
FSH LH Testosterone Normal sperm
SERM concentration (x
(mIU/mL) (mIU/mL) (ng/dL) forms (%)
106 / mL)

5.72 to 4.54 to 496.59 to

32.08 to 41.94 18.91 to
Nolvadex 8.42 7.84 763.34
(+30%) 31.64 (+67%)
(+47%) (+72%) (+53%)

5.64 to 4.05 to 498.96 to

25.84 to 37.82 23.09 to
Torem 9.53 6.54 743.92
(+46%) 31.73 (+37%)
(+69%) (+61%) (+49%)

6.39 to 4.18 to 583.55 to

27.01 to 32.64 14.72 to
Ralox 6.87 4.75 604.35
(+20%) 21.86 (+48%)
(+7%) (+13%) (+3%)

As demonstrated, Nolvadex came out on top here in LH, Testosterone &

Normal sperm forms. Torem topped Nolva in FSH and Sperm
concentration. Both are very suitable PCT options (as already known with
Nolva, but this shows Torem as a viable option as well). Ralox was
unfavorable and is probably best used just for gynecomastia treatment.

IMPORTANT NOTE: Also be sure to check out the Drug Interactions section,
as it contains important information for those using SSRIs and SERMs.

Dosing

Nolvadex: Recommended PCT 10mg/day

In all studies involving Nolvadex, for doses used to stimulate endogenous

Testosterone production, only 20–40 mg daily of Nolvadex was utilized, and
it has in fact been shown that doubling the dose to 40 mg or higher will not
produce any significant difference in endogenous Testosterone secretion.

The only reason why many elect to higher daily doses of Nolvadex for the
first 1-2 weeks of a PCT is for the purpose of achieving optimal peak blood
plasma levels more quickly, so as to ensure more rapid HPTA recovery.

This isn't necessary and just further increases your risk of potential sides.

Furthermore, the first week of PCT, there may be lingering suppressive AAS
still in the bloodstream, simply leading to greater oxidative stress on the
body by taking more compounds.

Recent studies have found that even lower doses than traditionally-
prescribed are equally as effective.

A weekly low-dose tamoxifen vs raloxifene vs placebo in

premenopausal women with estrogen receptor-positive breast cancer
— This study examined the efficacy of doses at 1mg and 5mg per day
and found the two lower doses are just as effective as the previous
standard of 20mg per day. “Considering results of our previous studies
we are now focusing on tamoxifen at 5mg per day. A weekly dose of
10mg/week is suggested as an alternative.”

Randomized dose trial of tamoxifen at low doses in hormone

replacement therapy — This study examined the efficacy of tamoxifen at
doses of 1mg, 5mg and 10mg per day. “A dose of 5 mg/day was the most
effective and has been selected for a phase III trial in HRT users.”

Randomized trial of low-dose tamoxifen on breast cancer proliferation

and estrogen biomarkers — “We compared the effects of tamoxifen at 1
mg/day and 5 mg/day with those of the standard dose of 20 mg/day. The
effects of lower doses … were comparable to those achieved with the
standard dose.”

⚠️ PCT dosing with Nolvadex has been updated (2020) as follows:

6–8 Weeks at 10 mg ED. Doses can be taken as low as 5 mg/day if sides
are a concern.

Clomid (not recommended)

According to the study previously mentioned,\14]) and thus recommended
by the FDA, clomid for hypogonadism should be run at 25 mg EOD, 25 mg
ED, or 50 mg EOD. Again, the side effects of Clomid can be quite bothersome
and bad. Why risk vision changes or loss running +50-150 mg ED when you
could just do 25mg ED or 50mg EOD and get fantastic results? Dosing of a
PCT including Clomid is as follows:

6-8 Weeks: 25mg ED or 50mg EOD

Torem (not recommended)

In the study above comparing Nolva, Torem, & Ralox, 60mg was the dosage
used and found to be very sufficient for PCT purposes. 60mg ED is the FDA
recommended dosage and they found no benefit upon doubling the dose in
women with breast cancer. Again, doubling the dose for the purpose of
achieving optimal peak blood plasma levels quicker isn't necessary and just
further increases your risk of potential sides. Dosing of a PCT including
Torem is as follows:

6-8 Weeks: 60mg ED

SERM Dosing Note

Note: As you've noticed above, /r/seroids recommends 6-8 weeks of SERMs.

It is common for a lot of PCT options to only be 4 weeks. These protocols
usually used double the dose for the first week or two. The only reason why
many elect to utilize doubling the dose for the first 1-2 weeks of a PCT
program is for the purpose of achieving optimal peak blood plasma levels
quicker so as to ensure HPTA recovery quicker. This isn't necessary and just
further increases your risk of potential sides. It has been studied that the
longer you are on SERMs, the better your results of stimulating
Testosterone.\15]) So to prevent unwanted sides as well as potentially
achieve better results, we choose to suggest lower dosing over a longer
period than 4 weeks.

hCG
The majority of anabolic steroid users from the 1960s–mid 1980s did not
even utilize any compounds for the purpose of hormonal recovery, and the
term PCT did not even exist at that time. When the use of hCG became
increasingly popular (circa 1980), it was the only compound utilized. Since
then, the medical and scientific understanding of such things has increased
exponentially and there should be no reason for any informed and
properly educated individual to utilize hCG on its own for PCT. When
utilized in conjunction with one of the other two categories of compounds
(an AI and a SERM), the dynamics change considerably.

hCG mimics LH and therefore actually keeps the testicles producing

testosterone even when anabolic steroids are present. However, it does not
induce the production of actual LH. The use of hCG on cycle, this is
primarily done so that post-cycle recovery is easier. hCG is also used on
cycle to prevent or at least minimize testicular atrophy that occurs due to
the use of anabolic steroids. The testicular atrophy that occurs is not
permanent, but will reverse once steroid use is discontinued and natural
testosterone production begins again.

It has been mentioned already that much of the difficulty in recovering the
HPTA following an anabolic steroid cycle is the result of Leydig cell
desensitization. hCG is essentially an analogue of LH, and the testes after a
prolonged anabolic steroid cycle would be as equally desensitized to hCG as
they are to LH. The human body, however, produces LH amounts on its
own that are far too inefficient for proper and rapid Testosterone
production.

The body’s natural increase of LH and FSH following an anabolic steroid

cycle is also not a rapid peak, but a very slow and steady incline, as
evidenced by the study referenced earlier in which it was not until 3 weeks
when LH levels only began to reach the normal physiological
measurements following the cessation of exogenous Testosterone.
Therefore, the body’s own natural LH production does not provide a high
enough dose for stimulation, nor an immediate stimulation to the testes
required for the initial increase in Testosterone needed during the post
cycle therapy weeks.
Now in our PCT will will be utilizing a SERM which will stimulate FSH/LH,
but most will find recovery being a smother transition when hCG is utilized.
Studies have in fact demonstrated the incredible effectiveness of hCG for
this purpose, and it is even suggested clinically that hCG be utilized for the
purpose of treating anabolic steroid induced hypogonadism.\4])

If you choose to include hCG in your PCT protocol, the best possible SERM
for the PCT protocol is Nolvadex, as studies have demonstrated that hCG
and Nolvadex utilized together have exhibited a remarkable synergistic
effect in terms of stimulating endogenous Testosterone production, and that
Nolvadex will actually work to block the desensitization effect on the
Leydig cells of the testes caused by high doses of hCG .\10]) This is very
important, because just as too little LH secretion for extended periods can
cause desensitization to gonadotropins, too much gonadotropin stimulation
(in the form of hCG or otherwise) may likewise cause a desensitization
effect.

Dosing

HCG is ran a couple different ways:

1. Over The Entire Cycle

2. Weeks Leading Up To PCT
3. 1-2 Weeks Before PCT
4. First 1-2 Weeks Of PCT

1. Over The Entire Cycle

This is the preferred option, as it keeps the Leydig cells active, reducing
atrophy and the reactive oxygen species (ROS) free radical damage incurred
by prolonged shutdown. HCG can be ran over the entire length of the cycle
to make PCT easy and efficient, if desired:

Over Entire Length Of Cycle: 250 IU EOD

Stop HCG use before starting PCT (SERM)
Important Note: 250 IU 2x/week is used by some, but there have been
studies on maintaining intra-testicular testosterone in healthy men with
gonadotropin suppression. This study found 125 IU EOD (437.5 iu/week)
was 25% less than baseline. Alternatively, 250 IU EOD (875 iu/week) was
found to only be 7% below baseline.\13])

For this reason, it is recommended to use 250 IU EOD. If desiring to be as

close to baseline as possible, you would need more than 875 IU/week (7%
less than baseline) and less than 1750 IU/week (26% above baseline). This is
where the 500 IU 2x/week comes in, but without a study comparing, we are
only speculating and you could need more. Alternatively, if money is a
factor, it is best to use some hCG rather than no hCG, and you may do less
than the recommended: 500-750 IU/week.

If only taking it for PCT, and not regularly:

2. Weeks Leading Up To PCT

This is the preferred method after Option 1, especially for those that are
coming off a long cycle or blast and cruise.

Starting 6 weeks before PCT:

Weeks 6-4: 500-1000 IU 3x/week

Weeks 3-1: 250-500 IU 3x/week
Week 0: Start PCT (SERM)

3. 1-2 Weeks Before PCT

Typically this will be run in the ~2 weeks leading up to PCT after your last
injection, while you are waiting for your AAS esters to clear (assuming long
esters -- Ex: Test E or C). If using short esters (Prop and/or Ace), nothing
changes. You just start the HCG while on cycle (1-2 weeks before PCT).

If you chose to utilize hCG in this fashion (unless using short esters (Prop
and/or Ace), there is one remaining issues to be addressed:
 The fact that hCG causes increased production of aromatase, leading to
increased Estrogen levels. See Below

This is where the AI is to be utilized as a supportive compound for hCG use

in this 1–2 week period, and after hCG is discontinued early on in PCT, only
the SERM to be used in order to carry along the hormonal recovery process.
hCG utilized in this fashion will be ran:

1-2 Weeks Before PCT: 1000-1500 IU EOD

1-2 Weeks Before PCT: AI will be used only as long as HCG

4. First 1-2 Weeks Of PCT

Some will say hCG shouldn't be ran into PCT as it's suppressive, but as noted
above in the study with Nolvadex, it has shown to be effective when run
simultaneously with Nolvadex.\10])

If you chose to utilize hCG in this fashion, there is one remaining issue to be
addressed:

The fact that hCG causes increased production of aromatase, leading to

increased Estrogen levels. See Below

This is where the AI is to be utilized as a supportive compound for hCG use

in this 1–2 week period, and after hCG is discontinued early on in PCT, only
the SERM to be used in order to carry along the hormonal recovery process.
hCG utilized in this fashion will be run as follows:

First 1-2 Weeks Of PCT: 1000-1500 IU EOD

First 1-2 Weeks Of PCT: AI will be used only as long as HCG

Aromatase Inhibitors: Aromasin (Exemestane) Above All

Else

This Section Is Optional, UNLESS Utilizing hCG dosing 3 or 4.

As noted above in hCG dosing 3 & 4, one issue that needs to be addressed
will be the fact that hCG will trigger increases in testicular aromatase
expression, and result in Estrogen increases in the body. If you are on cycle,
as you would be with HCG dosing 1 & 2, you will already be taking an AI
and be taking care of this. It should also be noted that hCG will also cause
an increase in testicular progesterone levels. Estrogen rising is of course
undesirable during PCT, as it has already been explained that Estrogen will
trigger suppression of endogenous Testosterone production, and there is no
doubt that any individual wishes to encounter Estrogenic side effects
during PCT either.

Therefore, the option here is to include an aromatase inhibitor. However,

there exists a problem in regards to the other two of the three major
aromatase inhibitors (Arimidex and Letrozole). The issue is the fact that in
a PCT program that includes the use of Nolvadex, Arimidex and Letrozole
have direct negative interactions with Nolvadex. The potential problem
here is that Arimidex & Letrozole both have decreased blood plasma
concentrations when used alongside a Nolvadex.\5][20][21]) Aromasin
completely circumvents this problem, as it has been demonstrated to have
no interactions what so ever with Nolvadex, unlike the other two
aforementioned aromatase inhibitors. In one study, Aromasin displayed no
such reduced effectiveness or any reduced blood plasma levels when
utilized with Nolvadex.\6]) The conclusion here is that the use of Arimidex
or Letrozole would be last resort options for controling Estrogen during
hCG dosing 3 & 4 use.

The other benefit of selecting Aromasin over all other AIs is the fact that
Aromasin has demonstrated in several studies to impact cholesterol profiles
in a negative manner far less than other aromatase inhibitors have, where
in one particular study on cancer patients, 24 weeks of Aromasin
(Exemestane) administration held no impact on cholesterol profiles.\7])
Some other studies have also demonstrated a nil effect on cholesterol
profiles from the use of Aromasin.\8]) Although there have also been some
studies that have demonstrated a negative effect on cholesterol profiles
resultant from Aromasin use, it is evident that there is not as a significant
or as a negatively impacting effect from Aromasin on cholesterol as other
aromatase inhibitors.\9])
Finally, in addition to these benefits from Aromasin, it is very clear that
Aromasin holds the ability to increase Testosterone levels in males as
demonstrated by studies. For example, one particularly notable study
selected 12 healthy young male test subjects, and were administered
random Aromasin doses of 25mg and 50mg for a 10 day period, and not
only was Estrogen suppressed by a significant amount (38%), but
Testosterone levels in the test subjects were observed to have increased by
an incredible 60%.\8])

Dosing

Note: This is a lot of Aromasin, but has clinically be shown to be effective.

You may end up experiencing low E2 sides. Most common include the
possibility of stiff joints and lethargy. If you wish to avoid this, consider
skipping the need for this and utilizing hCG dosing 1 or 2

Following these details, Aromasin would be the best possible aromatase

inhibitor of choice in order to combat the increased aromatase activity
caused by hCG. Therefore, Aromasin would then be utilized up to a full
25mg ED, and only while HCG is utilized in hCG dosing 3 or 4. Once hCG
is discontinued, Aromasin too should be halted.

This section is optional, UNLESS utilizing hCG dosing 3 or 4.

Drug Interactions

As with all drugs you use, you should always check for Drug Interactions.
One known issue during PCT is with people taking SSRIs. Nolvadex and
Toremifene have both been shown to have major interactions with one
another.

Most notably, SSRIs have been shown to reduce effectiveness of Nolvadex

and SSRIs when taken with Toremifene have been shown to cause irregular
heart rhythm that may be serious and potentially life-threatening, although
it is a relatively rare side effect. In any case, if you're on a SSRI, it is best to
use Clomid.

Side Effects
Common post-cycle complaints include depressive mood alterations,
fatigue, lethargy, insomnia, and decreased libido.\22]) As stated earlier,
vision sides are common for both Clomid and Nolva, more so with Clomid.
Hot Flashes, Nausea are two common side effects of Clomid, Nolva, &
Torem. Depression is known to affect many in PCT and is an actual listed
side effect of Nolva. Please make sure you are aware of this and in a
good place mentally before ever starting a cycle as you will be faced
with the potential of depression in PCT.

What to Expect from PCT

As stated above in the Side Effects section above, common post-cycle

complaints include depressive mood alterations, fatigue, lethargy,
insomnia, and decreased libido.\22]) You should be fully prepared to go
through these symptoms if you chose to run a cycle.

The biggest problem with most PCT plans is the individual having
unrealistic explanations. Most PCT plans will last 4-8 weeks and many men
expect everything to be back to normal once this 4-8 week period is
complete. PCT does not work this way. Many men also expect for all their
gains be they weight or strength gains to be maintained post-PCT if the PCT
plan was proper and appropriate. Again, PCT does not work this way.

A good PCT plan will help you protect and maintain some of the progress
you made, but if the high influx of hormones is no longer there (the high
influx of hormones that helped you make your gains), without that support
system you will lose some of your gains. A good way to look at is as we look
at food – the nutrients you eat help you buildup your body. The nutrients
you eat become the support system. Take away the nutrients and the
support system goes away with it and the “building” begins to collapse. For
this reason it’s not uncommon for some men to begin consuming extra
calories during PCT in order to protect their gains – in simplistic terms
they’re substituting in nutrients for the hormones that have been taken
away. This can help maintain weight but it’s not always a good idea. Weight
is just weight and if it’s not weight that’s muscle tissue it’s rather useless. It’s
not uncommon for some men to put on a good bit of body fat during this
phase due to their desperation to hang onto gains.
As stated, the primary purpose of PCT is to stimulate natural testosterone
production. Some gains may be lost during this period, but it’s not the end
of the world. For the steroid user he will be on cycle again one day. For the
present period he should focus on his hormone recovery, continue to train
and eat properly protecting the gains he can without putting on excess body
fat.

When NOT to Run PCT

If you’re a steroid user that is on cycle more than you’re off, running a PCT
can be counter productive. For example, a man completes a cycle,
implements PCT and then jumps back on cycle right after or soon after PCT.
This is a very harsh practice and terrible for your body. You are shutting
down your natural testosterone production, stimulating it through PCT and
then shutting it right back down. You’ve put yourself on a never ending
rollercoaster with your hormone levels that’s going to wreak havoc on your
body. For such an individual he would be better off running a low dose of
testosterone, therapeutic levels, during his time between cycles. This is not
an approach most men should take. Most men who use steroids need to
come off and stay off after PCT is complete for a time if long-term health is
important to them.

Another time not to run PCT is if you are prescribed Testosterone

Replacement Therapy (TRT). A low testosterone patient has been found by a
medical professional to no longer have the natural ability to produce
enough testosterone on his own, which is why he needs testosterone
supplementation. If he happens to implement a cycle at some point during
his treatment, once the cycle is over he should simply continue on with his
previous Testosterone Replacement Therapy (TRT). If you implement a PCT
plan, you’re attempting to stimulate your natural ability that medical
professional has deemed to not be enough, and it will serve no purpose.

When to Start PCT

Timing is a very important factor when it comes to PCT. You want to start
PCT around the time the compound will be exiting your body and no longer
a major factor in causing suppression. In the medical field, after 4 half-lives
the amount of drug (6.25%) is considered to be negligible regarding its
therapeutic effects. The chart below is based on known terminal half-lives
of AAS esters, as well as some theoretical half-lives (as some haven't been
studied). You will choose the ester that will require the most amount of
time before starting PCT (SERM).

IMPORTANT NOTE: This is just the time the compound itself will be low
enough to start PCT. This does not take into account for metabolites that
have been found to have a correlation to LH & FSH recovery in
nandrolone.\23]) This could very well happen in other compounds as well.
Be sure to get post PCT blood work to ensure recovery. See Below

Ester Time To Wait After Last Pin Before Starting PCT (SERM)
Acetate 3-4 day

Propionate 3-4 days

Phenylpropionate 5-6 days

Isocaproate 14-16 days

Enanthate 14-18 days

Cypionate 14-20 days

Decanoate 26-30 days

Undecylenate 52-56 days

Undecanoate 80-84 days

As you can see, if using a compound like Nandrolone Decanoate (Deca),

Sustanon (Testosterone Decanoate is its longest ester), Boldenone
Undecylenate (EQ), or Testosterone Undecanote, there is a very long waiting
period before starting PCT.

Very Long Ester AAS & PCT Transition

If using Nandrolone Decanoate or Boldenone Undecylenate, most will opt to

continue running Testosterone up until the point the half-lives will both be
considered negligible at the same time.
*For Example: *In a Testosterone Cypionate and Boldenone Undecylenate
cycle you will continue to run the Testosterone Cypionate for 8 weeks
AFTER your last Boldenone Undecylenate injection.

On cycle, you can are taking supraphysiological doses of Testosterone.

When you are doing this transition into PCT you may either choose to
continue with your supraphysiological doses or drop your Testosterone
down to TRT doses (80-200 mg/week).

Very Long Ester Testosterone & PCT Transition

If you are using Sustanon or Testosterone Undecanote, you may want to

transition into a shorter ester to make the waiting period for the Decanoate
or Undecanoate ester to clear. Otherwise, due to the ester, it will get rid of
the exogenous Testosterone much slower and with that it will be releasing
VERY small minuscule amounts that will get very low at the end and will
not be optimal. Due to this using a Testosterone Enanthate or Propionate
could be very beneficial to you, your well being, and allowing the most
successful PCT possible (you wouldn't want to start early wile the
compound is still aiding in suppression).

Important Metabolites Note

The table above is just the time the compound itself will be low enough to
start PCT. This does not take into account for metabolites that have been
found to have a correlation to LH & FSH recovery—particularly, in one
study involving Nandrolone Decanoate.\23])

In the study researchers found that even after six months LH and FSH were
both still repressed. The recovery of LH and FSH was correlated to the
urinary level of the nandrolone metabolite 19-norandrosterone (19-NA). 19-
NA was detectable for several months after the last nandrolone
administration, and there was a large inter-individual variation in the
excretion rate. Some individuals still tested positive (>2 ng/mL) even one
year after their last nandrolone dose and still sustained suppression of LH
and FSH during that time. Limitations are that this study did not state a post
cycle therapy was used by any of the steroid users. We do not know much a
proper PCT would have sped up recovery.
This could very well happen in other compounds as well. Be sure to get
post PCT blood work to ensure recovery.

When to Start Your Next Cycle

For optimal health the general rule to follow is time on + PCT, equals time
off. If your cycle last 12 weeks, you wait 2 weeks to start PCT, and your PCT
plan lasts 6 weeks, then you will wait 20 weeks before starting a new cycle.
A mistake many men make is saying testosterone levels have recovered
shortly after PCT and it is now okay to start a new cycle. If you do this you
have not allowed your body time to normalize. True recovery means your
levels can hold without any type of supplementation, if not then full
recovery has not been reached.

Blood Work

It’s always a good idea to get blood work done after PCT to see where your
body is at; however, this won’t be the full story. When we run a PCT we are
artificially stimulating natural testosterone production -- the stimulation
would not exist without the implementation of SERMs. The true tale of the
tape is where your numbers are good after a bit of time has passed since
cessation of the SERM; say several months. The earliest time to check blood
work would be a minimum of one month after cessation of SERM's. You will
be looking for LH/FSH returning to fairly normal, as well as total and free
testosterone levels alongside estradiol. How do you know what normal i for
you? If your cycle was run properly, you should have gotten pre-cycle
natural blood work. What were you levels on that blood work? That will be
your base point you are attempting to get back to with PCT.

The Danger

If you’re going to supplement with anabolic steroids there is one single

truth you need to understand: risks exist. One of these risks is
permanently lowering your natural testosterone production and forever
being in need of TRT. Even with the best PCT plan this risk exists. The point
of PCT is to help and minimize this risk; it does not completely remove it. If
this is something you cannot accept then anabolic steroid use is not for you.
PCT for Women

Michael Scally (former) M.D.'s Thoughts:

In the case of pre-menopausal females, tapering the anabolic-

androgenic steroids (AAS) would be the best treatment. Anabolic
steroid administration, like males, causes the HPGA to shutdown.
However, stopping the AAS will produce menopausal like symptoms,
therefore tapering until menses returns is best. The labs follicle
stimulating hormone (FSH), luteneizing hormone (LH), progesterone
(P) and estradiol (E2) will be the best indicator. They will show if the
HPGA is affected adversely. In marked contrast to a man, the period
typically returns within 1-2 months and will occur while tapering.

I would NOT suggest “selective estrogen receptor modulators”

(SERMs) or aromatase inhibitors (AIs) for a woman! NEVER! It is the
equivalency of forcing them into menopausal symptoms. The
HPGA/HPTA are very different. In fact, SERM/AI (such as Nolvadex
and Arimidex) are used in Breast Cancer, which includes a significant
number of adverse effects. Decreasing E2 in a man is far different
from doing the same in a female. E2 and P are the main female
hormones. Just imagine how a man feels that receives Androgen
Deprivation Therapy (ADT) for Prostate Cancer.

References

[1] Mauss J, Börsch G, Bormacher K, Richter E, Leyendecker G, Nocke W.

Effect of long-term testosterone enanthate administration on male
reproductive function: Clinical evaluation, serum FSH, LH, Testosterone
and seminal fluid analysis in normal men. Acta Endocrinol (Copenh). 1975
Feb;78(2):373-84. Link

[2] Faloon, W. “Dangers of Excess Estrogen In the Aging Male”. Life

Extension Magazine, November 2008. Link.

[3] Valladares LE, Payne AH. Acute stimulation of aromatization in Leydig

cells by human chorionic gonadotropin in vitro. Proc Natl Acad Sci USA
76:4460-3/1979. Link.
[4] Gill GV. Anabolic steroid induced hypogonadism treated with human
chorionic gonadotropin. Postgrad Med J. 1998 Jan;74(867):45-6. Link.

[5] Boeddinghaus IM, Dowsett M. Comparative clinical pharmacology and

pharmacokinetic interactions of aromatase inhibitors. J Steroid Biochem
Mol Biol. 2001 Dec;79(1-5):85-91. Link.

[6] Zaccheo T, Giudici D, Di Salle E. Inhibitory effect of combined treatment

with the aromatase inhibitor exemestane and tamoxifen on DMBA-induced
mammary tumors in rats. J Steroid Biochem Mol Biol. 1993 Mar;44(4-6):677-
80. Link.

[7] Atalay G, Dirix L, Biganzoli L, Beex L, Nooij M, Cameron D, Lohrisch C,

Cufer T, Lobelle JP, Mattiaci MR, Piccart M, Paridaens R. The effect of
exemestane on serum lipid profile in postmenopausal women with
metastatic breast cancer: a companion study to EORTC Trial 10951,
'Randomized phase II study in first line hormonal treatment for metastatic
breast cancer with exemestane or tamoxifen in postmenopausal patients'.
Ann Oncol. 2004 Feb;15(2):211-7. Link.

[8] Mauras N, Lima J, Patel D, Rini A, di Salle E, Kwok A, Lippe B.

Pharmacokinetics and dose finding of a potent aromatase inhibitor,
aromasin (exemestane), in young males. J Clin Endocrinol Metab. 2003
Dec;88(12):5951-6. Link.

[9] Engan T., Krane J., Johannessen D. C., Kvinnsland S. Plasma changes in
breast cancer patients during endocrine therapy — lipid measurements and
nuclear magnetic resonance (NMR) spectroscopy. Breast Cancer Res. Treat.,
36: 287-297, 1995. Link.

[10] Smals AG, Pieters GF, Drayer JI, Boers GH, Benraad TJ, Kloppenborg
PW. Tamoxifen suppresses gonadotropin-induced 17 alpha-
hydroxyprogesterone accumulation in normal men. J Clin Endocrinol
Metab. 1980 Nov;51(5):1026-9. Link.

[11] Vermeulen A, Comhaire F. Hormonal Effects Of An Antiestrogen,

Tamoxifen, In Normal And Oligospermic men. Fertil Steril. 1978
Mar;29(3):320-7. Link.43160-2/pdf)
[12] Adashi EY, Hsueh AJ, Bambino TH, Yen SS. Disparate effect of
clomiphene and tamoxifen on pituitary gonadotropin release in vitro. Am J
Physiol. 1981 Feb;240(2):E125-30. Link.

[13] Coviello AD, Matsumoto AM, Bremner WJ, Herbst KL, Amory JK,
Anawalt BD, Sutton PR, Wright WW, Brown TR, Yan X, Zirkin BR, Jarow JP.
Low-dose human chorionic gonadotropin maintains intratesticular
testosterone in normal men with testosterone-induced gonadotropin
suppression. J Clin Endocrinol Metab. 2005 May;90(5):2595-602. Epub 2005
Feb 15. Link.

[14] Katz DJ1, Nabulsi O, Tal R, Mulhall JP. Outcomes of clomiphene citrate
treatment in young hypogonadal men. BJU Int. 2012 Aug; 110(4):573-8 Link.

[15] Tsourdi, E., Kourtis, A., Farmakiotis, D., Katsikis, I., Salmas, M., &
Panidis, D. (2009). The effect of selective estrogen receptor modulator
administration on the hypothalamic-pituitary-testicular axis in men with
idiopathic oligozoospermia. Fertility and Sterility, 91(4), 1427–1430.
Link.01280-6/pdf)

[16] Dobbs M. R. (2009). Clinical Neurotoxicology: Syndromes, Substances,

Environments. pg 106. Link.

[17] Teodósio Da Ros C. Twenty-five Milligrams Of Clomiphene Citrate

Presents Positive Effect On Treatment Of Male Testosterone Deficiency - A
Prospective Study. Vol. 38 (4): 512-518, July - August, 2012. Link.

[18] Purvin VA. Visual Disturbance Secondary to Clomiphene Citrate.

1995;113(4):482-484. Link.

[19] Alfred R. Ashford MD Irina Donev MD Ram P. Tiwari MD T. J. Garrett

MD, FRCP(C), FACP. Reversible ocular toxicity related to tamoxifen therapy.
1988. Link.

[20] The ATAC Trialists’ Group. Pharmacokinetics of anastrozole and

tamoxifen alone, and in combination, during adjuvant endocrine therapy
for early breast cancer in postmenopausal women: a sub-protocol of the
‘Arimidex™ and Tamoxifen Alone or in Combination’ (ATAC) trial. British
Journal of Cancer (2001) 85(3), 317–324. Link.
[21] Dowsett M. Drug and hormone interactions of aromatase inhibitors.
Endocrine-Related Cancer (1999) 6 181-185.

[22] Cyrus D. Rahnema, B.S., Larry I. Lipshultz, M.D., Lindsey E. Crosnoe,

B.S., Jason R. Kovac, M.D., Ph.D., and Edward D. Kim, M.D. Anabolic steroid–
induced hypogonadism: diagnosis and treatment

[23] Gårevik, N., Strahm, E., Garle, M., Lundmark, J., Ståhle, L., Ekström, L.,
& Rane, A. (2011). Long term perturbation of endocrine parameters and
cholesterol metabolism after discontinued abuse of anabolic androgenic
steroids. The Journal of Steroid Biochemistry and Molecular Biology, 127(3-
5), 295–300.

Official /r/steroids PCT Protocols

These are the official /r/steroids recomended PCT Protocols. In general, the
longer that you have been on cycle and not producing your own natural
Test, the greater precaution you should take in your PCT.

When something is written as "X/X/Y/Y", think of it as Week 1 daily

dose/Week 2 daily dose/Week 3 daily dose/Week 4 daily dose/etc., etc..

SERM Dosing Note

Note: As you've noticed in our SERMs Dosing section, as well as below,

/r/steroids recommends 6-8 weeks of SERMs. It is common for a lot of PCT
options to only be 4 weeks. These protocols usually used double the dose for
the first week or two. The only reason why many elect to utilize doubling
the dose for the first 1-2 weeks of a PCT program is for the purpose of
achieving optimal peak blood plasma levels quicker so as to ensure HPTA
recovery quicker. This isn't necessary and just further increases your risk of
potential sides. It has been studied that the longer you are on SERMs, the
better your results of stimulating Testosterone.\15]) So to prevent unwanted
sides as well as potentially achieve better results, we choose to suggest
lower dosing over a longer period than 4 weeks.

Optimal/Primary PCT Options

This is the PCT plans you should use if you want PCT to be as as effective as
possible. This is highly recommended to those that have been on cycle a
long time or that are coming off a Blast & Cruise.

Nolvadex

Option 1

Starting at the beginning of the cycle.

Over Entire Length Of Cycle: 250 IU EOD

Stop hCG Before Starting SERM
6-8 Weeks: Nolvadex 10 mg ED = 10/10/10/10/10/10 (10/10)

Option 2

Starting 6 weeks before PCT (SERM).

Weeks 6-4: 500-1000 IU 3x/week

Weeks 3-1: 250-500 IU 3x/week
Week 0: Stop hCG & Starting SERM
6-8 Weeks: Nolvadex 10 mg ED = 10/10/10/10/10/10 (10/10)

Clomid

Option 1

Starting at the beginning of the cycle.

Over Entire Length Of Cycle: 250 IU EOD

Stop hCG Before Starting SERM
6-8 Weeks: Clomid 25mg ED or 50mg EOD = 25/25/25/25/25/25 (/25/25)

Option 2
Starting 6 weeks before PCT (SERM).

Weeks 6-4: 500-1000 IU 3x/week

Weeks 3-1: 250-500 IU 3x/week
Week 0: Stop HCG & Starting SERM
6-8 Weeks: Clomid 25mg ED or 50mg EOD = 25/25/25/25/25/25 (/25/25)

Torem

Option 1

Starting at the beginning of the cycle.

Over Entire Length Of Cycle: 250 IU EOD

Stop HCG Before Starting SERM
6-8 Weeks: Torem 60mg ED = 60/60/60/60/60/60 (/60/60)

Option 2

Starting 6 weeks before PCT (SERM).

Weeks 6-4: 500-1000 IU 3x/week

Weeks 3-1: 250-500 IU 3x/week
Week 0: Stop hCG & Starting SERM
6-8 Weeks: Torem 60mg ED = 60/60/60/60/60/60 (/60/60)

Secondary PCT Options

This is the PCT plans you should use if you were in a position where hCG
wasn't an option until something changed and you now have access to it at
the VERY end of your cycle.

Note: Aromasin is added in to combat the E2 sides from HCG. Previously

hCG was utilized on cycle and you'd just adjust AI as necessary. Since you
are no longer on cycle, we will use Aromasin. This is a lot of Aromasin, but
has clinically be shown to be effective in aiding to stimulate testicular
function. You may end up experiencing low E2 sides. Most common include
the possibility of stiff joints and lethargy. If you wish to avoid this, consider
skipping the need for this and utilizing the Optimal/Primary PCT Options

Nolvadex

Option 1

Taking hCG right before PCT.

1-2 Weeks BEFORE PCT: hCG 1000-1500 IU EOD

1-2 Weeks BEFORE PCT: Aromasin up to 25mg ED (See Section)
Stop HCG Before Starting SERM
6-8 Weeks: Nolvadex 10 mg ED = 10/10/10/10/10/10 (10/10)

Option 2

Taking HCG and SERM together.

6-8 Weeks: Nolvadex 10 mg ED = 10/10/10/10/10/10 (10/10)

First 1-2 Weeks Of PCT: HCG 1000-1500 IU EOD
First 1-2 Weeks Of PCT: Aromasin up to 25mg ED (See Section)

Clomid

Option 1

Taking HCG right before PCT.

1-2 Weeks BEFORE PCT: HCG 1000-1500 IU EOD

1-2 Weeks BEFORE PCT: Aromasin up to 25mg ED (See Section)
Stop HCG Before Starting SERM
6-8 Weeks: Clomid 25mg ED or 50mg EOD = 25/25/25/25/25/25 (/25/25)
Option 2

Taking HCG and SERM together.

6-8 Weeks: Clomid 25mg ED or 50mg EOD = 25/25/25/25/25/25 (/25/25)

First 1-2 Weeks Of PCT: HCG 1000-1500 IU EOD
First 1-2 Weeks Of PCT: Aromasin up to 25mg ED (See Section)

Torem

Option 1

Taking HCG right before PCT.

1-2 Weeks BEFORE PCT: HCG 1000-1500 IU EOD

1-2 Weeks BEFORE PCT: Aromasin up to 25mg ED (See Section)
Stop HCG Before Starting SERM
6-8 Weeks: Torem 60mg ED = 60/60/60/60/60/60 (/60/60)

Option 2

Taking HCG and SERM together.

6-8 Weeks: Torem 60mg ED = 60/60/60/60/60/60 (/60/60)

First 1-2 Weeks Of PCT: HCG 1000-1500 IU EOD
First 1-2 Weeks Of PCT: Aromasin up to 25mg ED (See Section)

Minimalist PCT Options

This is the PCT plans you should use if you were in a position where HCG
isn't an option. It may not be as effective as the other plans, but it is
sufficient and will aid tremendously.

Nolvadex
 6-8 Weeks: Nolvadex 10 mg ED = 10/10/10/10/10/10 (10/10)

Clomid

6-8 Weeks: Clomid 25 mg ED or 50 mg EOD = 25/25/25/25/25/25 (/25/25)

Torem

6-8 Weeks: Torem 60mg ED = 60/60/60/60/60/60 (/60/60)

Post Blast & Cruise Recovery Not Endorsed By /r/steroids

These are PCT protocols listed are NOT endorsed by /r/steroids and should
be used for information purposes only. They have proven effective for
some, but optimally you will use a PCT protocol listed above

ASRM Guidlines For Physicians To Prescribe

Based on this 2014 paper by the American Society for Reproductive

Medicine this is what they recommend physicians prescribe for anabolic
steroid–induced hypogonadism (ASIH):

Before Starting: Initial blood work will be taken and will include:
hormonal panel (LH, FSH, E2, T, freeT, SHBG, and PRL), complete blood
cell count, lipid profile, prostate-specific antigen, and a comprehensive
metabolic profile.

Week 1-4: For the severely symptomatic patients, a 4-week tapered

course of transdermal or injectable TRT may provide immediate
symptom improvement (i.e. those that have been off for a while and
have not recovered or are experiencing Low T symptoms). Simultaneous
administration of a SERM (such as clomiphene citrate, 25 mg every other
day) will interact at the hypothalamus causing stimulation of LH and
ultimately increase intratesticular T. For patients with ASIH-induced
 gynecomastia, 10–20 mg tamoxifen daily will block the breast estrogen
receptors and stimulate HPG axis recovery.

Week 5-8: After 4 weeks of treatment with TRT and/or a SERM, repeated
hormone panels should be obtained. If the patient has had either a poor
gonadotropin response or a poor T response, the authors commence a 4-
week course of hCG (1,000–3,000 IU, 3 times per week) while continuing
daily treatment with a SERM at the initial starting dose. If a patient
develops gynecomastia while on hCG, Tamoxifen aka Nolvadex 10 mg
b.i.d. (twice a day) or Anastrazole (Arimidex) may be commenced.

After Week 8: After 8 weeks of hCG and adjunctive treatment, you

should get blood work again and hormone levels should once again be
assessed.

If the total serum T remains low and the patient continues to be

symptomatic: primary testicular failure is likely. These patients will
require a longer duration of TRT to avoid permanent ASIH.

If appropriately increased serum T and gonadotropin levels are

observed: the SERM may be reduced to 50% of its starting dose at 10
weeks of treatment and continued through weeks 12–16 or until target
serum T level is achieved. Recovery of hormonal function may be
limited in men with testicular failure, and close monitoring is
recommended.

Original PoWeR PCT

by Michael Scally (former) M.D.

hCG - 2500 IU EOD – first 16 days

Clomid - 100 mg ED - split the dose ½ in the AM, ½ in the PM for the first
30 days
 Nolvadex - 10 mg ED – entire 45 days

NOTE: Clomid and hCG dosing are extremely high, 50 mg Clomid should be
the upper limit as you should never need more. Blasting high doses of hCG
could lead to desensitization of receptors.

The above is a documented and approved PCT plan by former Dr. Scally.
This can be found in Anabolics 10th Edition by William Llewellyn.

New PoWeR PCT

by Michael Scally (former) M.D.

HCG - 2000 IU EOD – (first 20 days)

Clomid - 100 mg ED - split the dose ½ in the AM, ½ in the PM (first 30
days)
Nolvadex - 10 mg ED – (entire 45 days)

NOTE: Clomid and hCG dosing are extremely high, 50 mg Clomid should be
the upper limit as you should never need more. Blasting high doses of hCG
could lead to desensitization of receptors.

The above is a documented and approved PCT plan by former Dr. Scally.

You Can See Both The Original And New PoWeR Protocols: Here

Controversy

Aside from the high Clomid and hCG dosages, it should be noted that there
is some controversy on whether using two SERMs at once is beneficial or
not.

This is one of the explanations that Dr. Scally has given:

Clomid acts as an estrogen, rather than an anti-estrogen, by

sensitizing pituitary cells to the action of GnRH. Although tamoxifen
is almost as effective as Clomid in binding to pituitary estrogen
receptors, tamoxifen has little or no estrogenic activity in terms of its
 ability to enhance the GnRH-stimulated release of LH. The estrogenic
action of Clomid at the pituitary represents a unique feature of this
compound and that tamoxifen may be devoid of estrogenic activity at
the pituitary level.

Some strongly disagree with Dr. Scally's reasoning behind the use of
Clomid. What he is describing here is believed to be "estrogen priming," the
concept that estrogen makes the pituitary more sensitive to GnRH from the
hypothalamus, so that more LH is released for a given GnRH stimulus. This
is well known to occur in females leading up to ovulation. Unlike females,
however, men don't have a preovulatory period or spikes in LH. The
research is fairly clear that estrogen priming does not occur in males. For
starters, take a look at an authoritative reference work like Grossman's
Clinical Endocrinology, which states (pg. 99):

Progesterone, acting synergistically with oestrogens, exerts negative

feedback on the hypothalamus during the luteal phase, thus limiting
GnRH pulsatility and slowing LH pulse frequency. The mechanism of
positive oestrogen feedback at the time of the LH surge has been
much debated. There is now evidence that enhancement of both
hypothalamic GnRH pulse generator activity and pituitary
responsiveness to GnRH are involved. All species so far studied have
shown an increased 'self-priming' effect of GnRH on the pituitary
during the preovulatory period... In males, the situation is more
straightforward. Since LH surges do not occur, only negative
feedback effects are relevant. testosterone (and its active metabolite
dihydrotestosterone, DHT) exerts major suppressive effects on both
LH and FSH secretion, largely by inhibiting the GnRH pulse frequency
generator, but possibly also by direct pituitary actions. Oestrogens in
the male reduce pituitary responsiveness to GnRH.

That states clearly that there is no priming in males, only negative

feedback. The last emboldened sentence in this quote directly contradicts
Dr. Scally's quote above. If Clomid were to produce estrogenic action in the
pituitary, it would only serve to inhibit LH secretion.

Grossman's statement is corroborated by the more recent research on the

specific effects of androgens and estrogen on the pituitary and
hypothalamus of healthy men. Here, it was shown that estrogenic action at
the pituitary has an inhibitory effect on LH output. In other words, estrogen
decreases pituitary sensitivity to GnRH. Estrogen does not produce positive
feedback as seen in estrogen priming in females. The paper stated in its
conclusion that: "These data confirm previous work from our group which
... showed [estrogen] has both hypothalamic and pituitary sites of negative
feedback in the male." In fact, "negative feedback at the pituitary requires
aromatization," as testosterone itself doesn't produce negative feedback at
the pituitary.

This older paper had a very interesting finding:

The positive estrogen feedback was found to be a relatively sex-

specific reaction of the hypothalamo-hypophyseal system in rats as
well as in human beings. It is dependent--most of all--on the estrogen
convertible androgen level during sexual brain differentiation, but
also on an estrogen priming effect in adulthood. The lower the
estrogen convertible androgen or primary estrogen level during brain
differentiation, the higher is the evocability of a positive estrogen
action on LH secretion in later life. In clinical studies, we were able to
induce a positive estrogen feedback on LH secretion in most intact
homosexual men in clear-cut contrast to intact hetero- or bisexual
men. These findings were strongly confirmed by Gladue and
associates.

In other words, estrogen levels during brain development are responsible

for the sex-specific differences in gonadotrophin secretion and estrogen
feedback at the pituitary. The important point of this research is that males
(with the exception of homosexuals) were not found to have any positive
feedback from estrogen. Those results that were "strongly confirmed."

Finally, there's this research (that was referenced above), which couldn't
have been any more relevant. It directly examined the effects of Nolva and
Clomid on the pituitary of human males. They infused the men with 100
mcg of GnRH and then measured LH output from the pituitary. The men
taking Nolvadex at 20 mg/day had a significantly increased LH response to
GnRH. In contrast, the men taking Clomid had reduced LH output, a
decreased sensitivity to GnRH. The researchers stated that "a role of the
intrinsic estrogenic activity of Clomid which is practically absent in
Tamoxifen seems the most probable explanation."

Jcaesar369 Recommended PCT Protocol

Please Read The Original Post Here

TL;DR:

Last 6 Weeks of Your Cycle / Blast & Cruise:(including the time needed to
allow all compounds to clear)

We will count down the last 6 weeks (plus 3 days - 45 days total). You will
start the SERM's after day 0.

T-minus 45 to 24 Days: 500–1000 IU HCG 3x weekly (IM) for 3 weeks

T-minus 23 to 2 Days: 250-500 IU HCG 3x weekly (IM) for 3 weeks

T-minus 2 to 0 Days: Wait 3 days before starting SERM's

Starting The SERMs

SERMs should be run for a much longer time period, depending on the time
of your Cycle or Blast and Cruise (i.e., total time on steroids). Use your head
and think about this one. If a standard 12–16 week cycle uses 4 weeks of
SERM's, how long should a 3-year BnC PCT be? There is no right answer, but
you will probably want to err on the side of caution and run at least 8–12
weeks of SERMs.

10 mg Nolvadex (Tamoxifen) everyday OR 60 mg Toremifene everyday

AND

25 mg Clomid (Clomiphene) everyday

Controversy

It should be noted that there is some controversy on whether using two

SERMs at once is beneficial or not, with consensus leaning towards the
latter.

How long to wait to check blood work to see if you've recovered?

Answer: ONE MONTH after cessation of SERM's. You will be looking for
LH/FSH returning to fairly normal, as well as total and free testosterone
levels. How do you know what normal is? What your levels were that you
got with your pre-cycle natural self blood work.

Disclaimer: All of these RECOMMENDATIONS (not mandatory) are to be

used as advice. All of the suggestions by Jcaesar369 are based off of clinical
FDA trials and studies, found in the original post for reference.

Triptorelin PCT

Triptorelin 50–100 mcg injected intramuscular ONCE

Pick one:

Nolvadex 10/10/10/10
Toremifine 30/30/15/15

The reason for the Nolvadex or Toremifine is to prevent the estrogen

rebound that is common with Triptorelin, one may also use an AI such as
Armidex or Aromasin.

A Doctor's Recommended PCT (TRT Clinic)

/u/DeludedOldMan's TRT doctor recommend this plan when coming off a 9-

month cruise:

Weeks 1-2 (last 2 weeks of injecting test)

Test C/E (normal TRT dose)

 400 IU HCG E3D
20 mg Clomid EOD

Weeks 3-4

400 IU HCG E3D

20 mg Clomid EOD

Weeks 5 - 6

20 mg Clomid EOD

Week 7-8

20 mg Clomid E3D

Miscellaneous Findings

Triptorelin/GnRH

A newer approach receiving recent attention is Triptorelin, the GnRH

agonist. This is used in a continuous manner to chemically castrate a man,
but in a one off dose, has been reported to kick start the PTA in a
hypogonadic BB. Triptorelin is a synthetic analogue of GnRH. It causes
constant stimulation of the pituitary gland and by acting as such, it
stimulates the pituitary gland to pump out LH and FSH. The dose needed to
cause chemical castration is much greater than the dose one would use to
restart HPTA.

The way Triptorelin hinders gonadotropin release is similar to how hCG

will hinder test production in the testes. A small amount of hCG will
stimulate the Leydig cells to produce testosterone, but too much will
desensitize the Leydig cells. This is what GnRH does, but with the pituitary
gland. Triptorelin has been studied to restore full HPTA function in a
steroid user who cycled for 13 years. Due to it's nature it is advised that
Triptorelin only be used if coming off long-term blasting and cruising or if
one plans to cease AAS forever.

Anecdotal evidence claims that Triptorelin is capable of restoring HPTA

function to those diagnosed with hypogonadism.

Anabolic steroids purchased on the Internet as a cause of prolonged

hypogonadotropic hypogonadism
Pituitary gonadotropin-releasing hormone receptors. Effects of
castration, steroid replacement, and the role of gonadotropin-releasing
hormone in modulating receptors in the rat
Effects of castration on luteinizing hormone and follicle-stimulating
hormone secretion by pituitary cells from male rats

Misc.

Mechanism by which Nolvadex works:

While the literature is scant in this field, a recent paper has shed some
light on this mechanism: Short-Term Aromatase-Enzyme Blockade
Unmasks Impaired Feedback Adaptations in Luteinizing Hormone and
Testosterone Secretion in Older Men

How Clomid affects the eyes: Effect of clomiphene on [Ca2+]i rises and
cell viability in rabbit corneal epithelial cells

Explains the possible cause behind vision effects: Oxidative stress

plays an important role in the pathogenesis of drug-induced retinopathy