akn
Musclechemistry Member
It is called the "post cycle crash': and is one of the more
unwelcome aspects of steroid use. As the saying goes,
there is a price to be paid for everything, and in the case of
steroids, one of those prices (a temporary one anyway) is
your natural hormone production. What happens is quite
simple; when you take steroids your body stops making
them. Once you stop taking steroids, you can be left with
a gap until your body starts making its own again. Here,
you can be faced with low levels of androgens and normal
levels of corticosteroids.Your body will (should) eventually
recognize and fix the imbalance, but it can take weeks or
even months.This gap is a bad place to be physiologically,
as without normal androgen levels to balance the
catabolic effects of corticosteroids, a good deal of your
new muscle mass may be 10st.To help your body maintain
its size, you will want to restore endogenous testosterone
production quickly.The methods for doing this seem to be
different everywhere you 100k:"Take HCG, don't take HCG,
use an aromatase inhibitor, just take Clomid, forget Clomid
and just take Nolvadex." What option is really best?
Without an understanding of exactly what is going on in
your body, and why certain compounds help to correct
the situation, choosing the right Post-Cycle Therapy (PCT)
program can be quite confusing. In this section, the roles
of anti-estrogens and HCG during this delicate window of
time are discussed, while detailing an effective strategy for
their use.
The HPTA Axis
The Hypothalamic-Pituitary-Testicular Axis, or HPTA for
short, is the thermostat for your body's natural production
of testosterone. Too much testosterone, and the furnace
will shut off. Not enough, and the heat is turned up (to put
it very simply). For the purposes of our discussion, we can
look at this regulating process as having three levels. At
the top is the hypothalamic region of the brain, which
releases the hormone GnRH (Gonadotropin-Releasing
Hormone) when it senses a need for more testosterone.
GnRH sends a signal to the second level of the axis, the
pituitary, which releases Luteinizing Hormone in
response. LH for short, this hormone stimulates the testes
(level three) to secrete testosterone. The same sex steroids
(testosterone, estrogen) that are produced serve to
counterbalance things, by providing negative feedback
signals (primarily to the hypothalamus and pituitary) to
lower the secretion of testosterone. Synthetic steroids
send the same negative feedback. This quick background
of the testosterone-regulating axis is necessary to
furthering our discussion, as we need to first look at the
underlying mechanisms involved before we can
understand why natural recovery of the HPTA post-cycle is
a slow process. Only then can we implement an ancillary
drug program to effectively deal with it.
The Hypothalamic-Pituitary-Testicular Axis: The
hypothalamus releases Gonadotropin Releasing
Hormone (GnRH), which stimulates the pituitary to
release luteinizing hormone (LH) and follicle
stimulating hormone (FSH). This promotes the
release of testosterone from the testes.
Testosterone, as well as estrogens and progestins,
in turn cause negative feedback inhibition at the
hypothalamus (and to some extent the pituitary),
lowering the output of gonadotropins and
testosterone when too much hormone is present.
Testicular Desensitization
Although steroids suppress testosterone production
primarily by lowering the level of gonadotropic
hormones, the big roadblock to a restored HPTA after we
come off the drugs is surprisingly not LH. This problem
was made clearly evident in a study published back in
1975.348 Here, blood parameters, including testosterone
and LH levels, were monitored in male subjects who were
given testosterone enanthate injections of 250 mg weekly
for 21 weeks. Subjects remained under investigation for
an additional 18 weeks after the drug was discontinued.
At the start of the study, LH levels became suppressed in
direct relation to the rise in testosterone, which was to be
expected. Things looked very different, however, once the
steroids had been withdrawn (see Figure I). LH levels went
on the rise quickly (by the 3rd week), while testosterone
barely budged for quite some time. In fact, on average it
was more than 10 weeks before any noticeable
movement in testosterone production started at all. This
lack of correlation makes clear that the problem in getting
androgen levels restored is not necessarily the level of LH,
but more so testicular atrophy and desensitization to LH.
After a period of inactivation, the testes have lost mass
(atrophied), making them unable to perform the required
workload.The protracted post-cycle window can, likewise,
no longer be looked at as one of low testosterone and low
LH. Much of it actually involves low testosterone and
normal (even high) LH.
The Role 01 Anti-Estrogens
It is important to understand that anti-estrogens alone are
inadequate to restore normal endogenous testosterone
production after a cycle. These agents ordinarily increase
LH levels by blocking the negative feedback of estrogens.
But LH rebounds quickly on its own post-cycle, without
help. Plus, there is not an elevated level of estrogen for
anti-estrogens to block during this window, as
testosterone (now suppressed) is a major substrate used for the synthesis of estrogens in men. Serum estrogen
levels are actually lower here, not higher. Any estrogen
rebound that occurs post-cycle, likewise, happens with a
rebound in testosterone levels, not prior to it (there is an
imbalance in the ratio of androgens to estrogens post
cycle, but this is another topic altogether). On their own,
we are seeing no mechanism in which anti-estrogenic
drugs can effectively help here. I can, however, see why
this fact would be easy to overlook.The medical literature
is filled with references showing anti-estrogenic drugs like
Clomid and Nolvadex to increase LH and testosterone
levels in men, and in normal situations they indeed
perform this function fairly well. Combine this with the
fact that just as many studies can be found to show that
steroid use lowers LH when suppressing testosterone, and
we can see how easy it would be to jump to the
conclusion that we need to focus on LH. We would miss
the true problem, testicular desensitization, unless we
were really looking into the actual recovery rates of the
hormones involved. When we do, we immediately see
little value in focusing solely on anti-estrogenic drugs.
The Role of HCG
With anti-estrogens alone proving to be ineffective, we
are left to focus on a very different level of the HPTA in
order to hasten recovery: the testes. For this we will need
the injectable drug HCG. If you are not familiar, HCG, or
Human Chorionic Gonadotropin, is a prescription fertility
agent that mimics the body's natural LH. Although the
testes are equally desensitized to this drug as they are to
LH (they work through the same receptor), we are
administering it as a measured drug and are, therefore, not
constrained by the limits of our own LH production. In
other words, we can give ourselves a good dose of drug
(as much LH as we need, really), shocking the testes with
unnaturally high levels of stimulation. We want it to reach
a level above what our bodies, even when supported by
anti-estrogens, could do on its own.The result should be a
more rapid restoration of original testicular mass, which
would allow normal levels of testosterone to be output
much sooner than without such an ancillary program in
place. What we are looking at now is HCG actually being
the pivotal post-cycle drug, with anti-estrogens playing
more of a supportive role.
The PoWeR PCT Program
The PCT program outlined below represents what I
consider to be an ideal and effective post-cycle program.
It was developed by the doctors at the Program for
Wellness Restoration (PoWeR), who have a formidable
history helping patients recover normal hormonal
functioning following steroid therapy. One of the key
doctors on this program, Dr. Michael Scally, claims to have
successfully treated more than 100 cases of
hypogonadism/hypogonadotrophic hypogonadism, and
is very well known in the field of androgen replacement
therapy. PoWeR published this program as part of a recent
clinical study, which involved 19 healthy male subjects
who were taking supra physiological (highly suppressive)
doses of testosterone cypionate and nandrolone
decanoate for 12 weeks. Their HPGA Normalization
Protocol focuses on the combined use of HCG, Nolvadex,
and Clomid, and is perhaps the only clinically documented
post-cycle therapy program to be found in the medical
literature (it is amazing how little attention has been paid
to hormone normalization in clinical medicine). The most
notable variation from a classic PCT stack, such that I have
been a longtime supporter of, is the combined use of two
anti-estrogens. In this case I cannot say that there is a
disadvantage to such use; perhaps it is indeed the better
option.
Examining the program closely, we note that the testes
are hit hard with HCG at the onset of therapy. Its intake,
however, is limited to only 16 days. The doctors
undoubtedly recognize that when HCG is taken for too
long or at too high a dosage, it can desensitize the LH
receptor.349 This would only further exacerbate the postcycle
problem, not help it. Anti-estrogens are used during
and after HCG, with a dosage of 10 mg of Nolvadex and
100 mg of Clomid per day rounding out this compliment
of drugs. Clomid is used for a shorter period of time than
Nolvadex, likely because of the desensitizing effect it too
can have (on the pituitary gland) with continued use.
Among other things, these two anti-estrogens will
continue to foster LH release as testosterone levels start to
go back up, as well as combat any potential estrogenic
side effects that may be caused by HCG's up-regulation of
testicular aromatase activity.350 Although in the first
couple of weeks the anti-estrogens probably do very little,
they should be much more helpful towards the middle
and end of the program. During this clinical investigation,
normal hormonal function was restored in all subjects
within 45 days of drug cessation. This is a definite success,
far more favorable than the protracted recovery window
noted in studies without post-cycle therapy, such as the
250 mg/week testosterone enanthate investigation
highlighted in Figure I. For me, I believe such a detailed
recovery program should follow any serious steroid cycle.
It is the best way to maintain your gains at their maximum,
and that is, after all, what we are after.
Protocols: Human chorionic gonadotropin (hCG) is taken at 2500lU every other day for 16 days. Clomiphene
citrate 50 mg is taken twice per day for 30 days. Tamoxifen citrate is taken 20 mg per day for 45 days.
unwelcome aspects of steroid use. As the saying goes,
there is a price to be paid for everything, and in the case of
steroids, one of those prices (a temporary one anyway) is
your natural hormone production. What happens is quite
simple; when you take steroids your body stops making
them. Once you stop taking steroids, you can be left with
a gap until your body starts making its own again. Here,
you can be faced with low levels of androgens and normal
levels of corticosteroids.Your body will (should) eventually
recognize and fix the imbalance, but it can take weeks or
even months.This gap is a bad place to be physiologically,
as without normal androgen levels to balance the
catabolic effects of corticosteroids, a good deal of your
new muscle mass may be 10st.To help your body maintain
its size, you will want to restore endogenous testosterone
production quickly.The methods for doing this seem to be
different everywhere you 100k:"Take HCG, don't take HCG,
use an aromatase inhibitor, just take Clomid, forget Clomid
and just take Nolvadex." What option is really best?
Without an understanding of exactly what is going on in
your body, and why certain compounds help to correct
the situation, choosing the right Post-Cycle Therapy (PCT)
program can be quite confusing. In this section, the roles
of anti-estrogens and HCG during this delicate window of
time are discussed, while detailing an effective strategy for
their use.
The HPTA Axis
The Hypothalamic-Pituitary-Testicular Axis, or HPTA for
short, is the thermostat for your body's natural production
of testosterone. Too much testosterone, and the furnace
will shut off. Not enough, and the heat is turned up (to put
it very simply). For the purposes of our discussion, we can
look at this regulating process as having three levels. At
the top is the hypothalamic region of the brain, which
releases the hormone GnRH (Gonadotropin-Releasing
Hormone) when it senses a need for more testosterone.
GnRH sends a signal to the second level of the axis, the
pituitary, which releases Luteinizing Hormone in
response. LH for short, this hormone stimulates the testes
(level three) to secrete testosterone. The same sex steroids
(testosterone, estrogen) that are produced serve to
counterbalance things, by providing negative feedback
signals (primarily to the hypothalamus and pituitary) to
lower the secretion of testosterone. Synthetic steroids
send the same negative feedback. This quick background
of the testosterone-regulating axis is necessary to
furthering our discussion, as we need to first look at the
underlying mechanisms involved before we can
understand why natural recovery of the HPTA post-cycle is
a slow process. Only then can we implement an ancillary
drug program to effectively deal with it.
The Hypothalamic-Pituitary-Testicular Axis: The
hypothalamus releases Gonadotropin Releasing
Hormone (GnRH), which stimulates the pituitary to
release luteinizing hormone (LH) and follicle
stimulating hormone (FSH). This promotes the
release of testosterone from the testes.
Testosterone, as well as estrogens and progestins,
in turn cause negative feedback inhibition at the
hypothalamus (and to some extent the pituitary),
lowering the output of gonadotropins and
testosterone when too much hormone is present.
Testicular Desensitization
Although steroids suppress testosterone production
primarily by lowering the level of gonadotropic
hormones, the big roadblock to a restored HPTA after we
come off the drugs is surprisingly not LH. This problem
was made clearly evident in a study published back in
1975.348 Here, blood parameters, including testosterone
and LH levels, were monitored in male subjects who were
given testosterone enanthate injections of 250 mg weekly
for 21 weeks. Subjects remained under investigation for
an additional 18 weeks after the drug was discontinued.
At the start of the study, LH levels became suppressed in
direct relation to the rise in testosterone, which was to be
expected. Things looked very different, however, once the
steroids had been withdrawn (see Figure I). LH levels went
on the rise quickly (by the 3rd week), while testosterone
barely budged for quite some time. In fact, on average it
was more than 10 weeks before any noticeable
movement in testosterone production started at all. This
lack of correlation makes clear that the problem in getting
androgen levels restored is not necessarily the level of LH,
but more so testicular atrophy and desensitization to LH.
After a period of inactivation, the testes have lost mass
(atrophied), making them unable to perform the required
workload.The protracted post-cycle window can, likewise,
no longer be looked at as one of low testosterone and low
LH. Much of it actually involves low testosterone and
normal (even high) LH.
The Role 01 Anti-Estrogens
It is important to understand that anti-estrogens alone are
inadequate to restore normal endogenous testosterone
production after a cycle. These agents ordinarily increase
LH levels by blocking the negative feedback of estrogens.
But LH rebounds quickly on its own post-cycle, without
help. Plus, there is not an elevated level of estrogen for
anti-estrogens to block during this window, as
testosterone (now suppressed) is a major substrate used for the synthesis of estrogens in men. Serum estrogen
levels are actually lower here, not higher. Any estrogen
rebound that occurs post-cycle, likewise, happens with a
rebound in testosterone levels, not prior to it (there is an
imbalance in the ratio of androgens to estrogens post
cycle, but this is another topic altogether). On their own,
we are seeing no mechanism in which anti-estrogenic
drugs can effectively help here. I can, however, see why
this fact would be easy to overlook.The medical literature
is filled with references showing anti-estrogenic drugs like
Clomid and Nolvadex to increase LH and testosterone
levels in men, and in normal situations they indeed
perform this function fairly well. Combine this with the
fact that just as many studies can be found to show that
steroid use lowers LH when suppressing testosterone, and
we can see how easy it would be to jump to the
conclusion that we need to focus on LH. We would miss
the true problem, testicular desensitization, unless we
were really looking into the actual recovery rates of the
hormones involved. When we do, we immediately see
little value in focusing solely on anti-estrogenic drugs.
The Role of HCG
With anti-estrogens alone proving to be ineffective, we
are left to focus on a very different level of the HPTA in
order to hasten recovery: the testes. For this we will need
the injectable drug HCG. If you are not familiar, HCG, or
Human Chorionic Gonadotropin, is a prescription fertility
agent that mimics the body's natural LH. Although the
testes are equally desensitized to this drug as they are to
LH (they work through the same receptor), we are
administering it as a measured drug and are, therefore, not
constrained by the limits of our own LH production. In
other words, we can give ourselves a good dose of drug
(as much LH as we need, really), shocking the testes with
unnaturally high levels of stimulation. We want it to reach
a level above what our bodies, even when supported by
anti-estrogens, could do on its own.The result should be a
more rapid restoration of original testicular mass, which
would allow normal levels of testosterone to be output
much sooner than without such an ancillary program in
place. What we are looking at now is HCG actually being
the pivotal post-cycle drug, with anti-estrogens playing
more of a supportive role.
The PoWeR PCT Program
The PCT program outlined below represents what I
consider to be an ideal and effective post-cycle program.
It was developed by the doctors at the Program for
Wellness Restoration (PoWeR), who have a formidable
history helping patients recover normal hormonal
functioning following steroid therapy. One of the key
doctors on this program, Dr. Michael Scally, claims to have
successfully treated more than 100 cases of
hypogonadism/hypogonadotrophic hypogonadism, and
is very well known in the field of androgen replacement
therapy. PoWeR published this program as part of a recent
clinical study, which involved 19 healthy male subjects
who were taking supra physiological (highly suppressive)
doses of testosterone cypionate and nandrolone
decanoate for 12 weeks. Their HPGA Normalization
Protocol focuses on the combined use of HCG, Nolvadex,
and Clomid, and is perhaps the only clinically documented
post-cycle therapy program to be found in the medical
literature (it is amazing how little attention has been paid
to hormone normalization in clinical medicine). The most
notable variation from a classic PCT stack, such that I have
been a longtime supporter of, is the combined use of two
anti-estrogens. In this case I cannot say that there is a
disadvantage to such use; perhaps it is indeed the better
option.
Examining the program closely, we note that the testes
are hit hard with HCG at the onset of therapy. Its intake,
however, is limited to only 16 days. The doctors
undoubtedly recognize that when HCG is taken for too
long or at too high a dosage, it can desensitize the LH
receptor.349 This would only further exacerbate the postcycle
problem, not help it. Anti-estrogens are used during
and after HCG, with a dosage of 10 mg of Nolvadex and
100 mg of Clomid per day rounding out this compliment
of drugs. Clomid is used for a shorter period of time than
Nolvadex, likely because of the desensitizing effect it too
can have (on the pituitary gland) with continued use.
Among other things, these two anti-estrogens will
continue to foster LH release as testosterone levels start to
go back up, as well as combat any potential estrogenic
side effects that may be caused by HCG's up-regulation of
testicular aromatase activity.350 Although in the first
couple of weeks the anti-estrogens probably do very little,
they should be much more helpful towards the middle
and end of the program. During this clinical investigation,
normal hormonal function was restored in all subjects
within 45 days of drug cessation. This is a definite success,
far more favorable than the protracted recovery window
noted in studies without post-cycle therapy, such as the
250 mg/week testosterone enanthate investigation
highlighted in Figure I. For me, I believe such a detailed
recovery program should follow any serious steroid cycle.
It is the best way to maintain your gains at their maximum,
and that is, after all, what we are after.
Protocols: Human chorionic gonadotropin (hCG) is taken at 2500lU every other day for 16 days. Clomiphene
citrate 50 mg is taken twice per day for 30 days. Tamoxifen citrate is taken 20 mg per day for 45 days.
