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HCG - Unraveled
PCT is a must upon cessation of steroid use. Many great PCT protocols have been
outlined over the years, and many individuals have had success with following
such protocols. Nevertheless, what works can always work better, and I intend to
show you the most effective way to recover from AAS. This is especially the case
for those that have had a lack of success following popular advice. In this
article I will address the misunderstanding and misuse of Human Chorionic
Gonadotropin (HCG) and show you the most efficient way to use HCG for the
fastest and most complete recovery.
HCG unraveled ???
Human Chorionic Gonadotropin (HCG) is a peptide hormone that mimics the action
of luteinizing hormone (LH). LH is the hormone that stimulates the testes to
produce testosterone . (1) More specifically LH is the primary signal sent from
the pituitary to the testes, which stimulates the leydig cells within the testes
to produce testosterone .
When Steroids are administered, LH levels rapidly decline. The absence of an LH
signal from the pituitary causes the testes to stop producing testosterone ,
which causes rapid onset of testicular degeneration. The testicular degeneration
begins with a reduction of leydig cell volume, and is then followed by rapid
reductions in intra-testicular testosterone (ITT), peroxisomes, and Insulin-like
factor 3 (INSL3) ??? All important bio-markers and factors for proper testicular
function and testosterone production. (2-6,19) However, this degeneration can be
prevented by a small maintenance dose of HCG ran throughout the cycle.
Unfortunately, most steroid users have been engrained to believe that HCG should
be used after a cycle, during PCT. Upon reviewing the science and basic
endocrinology you will see that a faster and more complete recovery is possible
if HCG is ran during a cycle.
Firstly, we must understand the clinical history of HCG to understand its
purpose and its most efficient application. Many popular ???steroid profiles???
advocate using HCG at a dose of 2500-5000iu once or twice a week. These were the
kind of dosages used in the historical (1960???s) HCG studies for hypogonadal men
who had reduced testicular sensitivity due to prolonged LH deficiency. (21,22) A
prolonged LH deficiency causes the testes to desensitize, requiring a higher HCG
dose for ample stimulation. In men with normal LH levels and normal testicular
sensitivity, the maximum increase of testosterone is seen from a dose of only
250iu, with minimal increases obtained from 500iu or even 5000iu. (2,11) (It
appears the testes maximum secretion of testosterone is about 140% above their
normal capacity.) (12-18) If you have allowed your testes to desensitize over
the length of a typical steroid cycle, (8-16 weeks) then you would require a
higher dose to elicit a response in an attempt to restore normal testicular size
and function ??? but there is cost to this, and a high probability that you won???t
regain full testicular function.
One term that is critical to understand is testosterone secretion capacity which
is synonymous to testicular sensitivity. This is the amount of testosterone your
testes can produce from any given LH or HCG stimulation. Therefore, if you have
reduced testosterone secretion capacity (reduced testicular sensitivity), it
will take more LH or HCG stimulation to produce the same result as if you had
normal testosterone secretion capacity. If you reduce your testosterone
secretion capacity too much, then no amount of LH or HCG stimulation will
trigger normal testosterone production ??? and this leads to permanently reduced
testosterone production.
To get an idea of how quickly you can reduce your testosterone secretion
capacity from your average steroid cycle, consider this: LH levels are rapidly
decreased by the 2nd day of steroid administration. (2,9,10) By shutting down
the LH signal and allowing the testis to be non-functional over a 12-16 week
period, leydig cell volume decreases 90%, ITT decreases 94%, INSL3 decreases
95%, while the capacity to secrete testosterone decreases as much as 98%. (2-6)
Note: visually analyzing testes size is a poor method of judging your actual
testicular function, since testicular size is not directly related to the
ability to secrete testosterone . (4) This is because the leydig cells, which are
the primary sites of testosterone secretion, only make up about 10% of the total
testicular volume. Therefore, when the testes may only appear 5-10% smaller, the
testes ability to secrete testosterone upon LH or HCG stimulation can actually
be significantly reduced to 98% of their normal production. (3-5) The point here
is to not judge testosterone secretion capacity by testicular size.
The decreased testosterone secretion capacity caused by steroid use was well
demonstrated in a study on power athletes who used Steroids for 16 weeks, and
were then administered 4500iu HCG post cycle. It was found that the steroid
users were about 20 times less responsive to HCG, when compared to normal men
who did not use Steroids. (8) In other words, their testosterone secretion
capacity was dramatically reduced because they did not receive an LH signal for
16 weeks. The testes essentially became desensitized and crippled. Case studies
with steroid using patients show that aggressive long-term treatment with HCG at
dosages as high as 10,000iu E3D for 12 weeks were unable to return full
testicular size. (7) Another study with men using low dose Steroids for 6 weeks
showed unsuccessful return of Insulin-like factor-3 (INSL3) concentration in the
testes upon 5000iu/wk of HCG treatment for 12 weeks (6) (INSL3 is an important
biomarker for testosterone production potential and sperm production. 20)
These studies show that postponing HCG usage until the end of a steroid cycle
increases your need for a higher dose of HCG, and decreases your odds of a full
recovery. As a consequence to using a higher dose of HCG at the end of a cycle,
estrogen will be increased disproportionately to testosterone , which then causes
further HPTA suppression (from high estrogen) while increasing the risk of gyno.
(11) For example, high doses of HCG have been found to raise estradiol up to
165%, while only raising testosterone 140%. (11) Higher doses of HCG are also
known to reduce LH receptor concentration and degrade the enzymes responsible
for testosterone synthesis within the testes (12,13,19 ) -- the last thing
someone wants during recovery. While these negative effects of HCG can be partly
mitigated by the use of a SERM such as tamoxifen, it will create further
problems associated with using a toxic SERM (covered in another article).
In light of the above evidence, it becomes obvious that we must take
preventative measures to avoid this testicular degeneration. We must protect our
testicular sensitivity. Besides, with HCG being so readily available, and such a
painless shot, it makes you wonder why anyone wouldn???t use it on cycle.
Based on studies with normal men using Steroids, 100iu HCG administered everyday
was enough to preserve full testicular function and ITT levels, without causing
desensitization typically associated with higher doses of HCG. (2) It is
important that low-dose HCG is started before testicular sensitivity is reduced,
which appears to rapidly manifest within the first 2-3 weeks of steroid use.
Also, it???s important to discontinue the HCG before you start PCT so your leydig
cells are given a chance to re-sensitize to your body???s own LH production. (To
help further enhance testicular sensitivity, the dietary supplement Toco-8 may
be used)
A more convenient alternative to the above recommendation would be a twice a
week shot of 200iu HCG, or possibly a once a week shot of 500iu. However, it is
most desirable to adhere to a lower more frequent dose of HCG to mimic the
body???s natural LH release and minimize estrogen conversion. If you are starting
HCG late in the cycle, one could calculate a rough estimate for their required
HCG ???kick starting??? dosage by multiplying 40iu x days of LH absence, since the
testes will be desensitized, thus requiring a higher dose. (ie. 40iu x 60 days =
2400iu HCG dose)
Note: If following the on cycle HCG protocol, HCG should NOT be used for PCT.
Recap ???
For preservation of testicular sensitivity, use 100iu HCG ED starting 7 days
after your first AAS dose. At the end of the cycle, drop the HCG two weeks
before the AAS clear the system. For example, you would drop HCG about the same
time as your last testosterone Enanthate shot. Or, if you are ending the cycle
with orals, you would drop the HCG about 10 days before your last oral dose.
This will allow for a sudden and even clearance in hormone levels, while
initiating LH and FSH production from the pituitary, to begin stimulating your
testes to produce testosterone . Remember, recovery doesn???t begin until you are
off HCG since your body will not release its own LH until the HCG has cleared
the system.
In conclusion, we have learned that utilizing HCG during a steroid cycle will
significantly prevent testicular degeneration. This helps create a seamless
transition from ???on cycle??? to ???off cycle??? thus avoiding the post cycle crash.
Eric M. Potratz has developed his education in the field of endocrinology and
performance enhancement through years of research, counseling, and real world
experience. Over the past five years he has been a private consultant for
hundreds of athletes and bodybuilders alike, and is the founder & president of
Primordial Performance.
References -
1. Glycoprotein hormones: structure and function.
Pierce JG, Parsons TF 1981
Annu Rev Biochem 50:466???495
2. Low-Dose Human Chorionic Gonadotropin Maintains Intratesticular testosterone
in Normal Men with testosterone -Induced Gonadotropin Suppression
Andrea D. Coviello, et al
J. Clin. Endocrinol. Metab., May 2005; 90: 2595 - 2602.
3. Luteinizing hormone on Leydig cell structure and function.
Mendis-Handagama SM
Histol Histopathol 12:869???882 (1997)
4. Leydig cell peroxisomes and sterol carrier protein-2 in luteinizing
hormone-deprived rats
SM Mendis-Handagama, et al.
Endocrinology, Dec 1992; 131: 2839.
5. Effect of long term deprivation of luteinizing hormone on Leydig cell volume,
Leydig cell number, and steroidogenic capacity of the rat testis.
Keeney DS, et al.
Endocrinology 1988; 123:2906???2915.
6.The Effects of Gonadotropin Suppression and Selective Replacement on
Insulin-like factor 3 Secretion in Normal Adult Men
Katrine Bay, et al
J. Clin. Endocrinol. Metab., Mar 2006; 91: 1108 - 1111.
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Dev Kumar Menon, et al.
FERTILITY AND STERILITY VOL. 79, SUPPL. 3, JUNE 2003
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athletes
Hannu et al.
J. Steroid Biochem. Vol. 25, No. 1 pp. 109-112 (1986)
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of testosterone cypionate.
Schulte-Beerbuhl M, et al 1980
Fertil Steril 33:201???203
10. Effects of chronic testosterone administration in normal men: safety and
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luteinizing hormone, follicle-stimulating hormone, and sperm production.
Matsumoto AM, et al 1990
J Clin Endocrinol Metab 70:282???287
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old men.
Longcope C et al
Steroids 21:583???590 (1973)
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Catt KJ, et al
Rec Prog Horm Res 1980; 36:557???622
13. Effect of human chorionic Gonadotropin on the endocrine function of Papio
testes
GV Katsiia, et al
Probl Endokrinol (Mosk), Sep 1984; 30(5): 68-71.
14. Reproductive function in young fathers and grandfathers.
Nieschlag E, et al.
J Clin Endocrinol Metab 55:676???681 (1982)
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Nankin HR, et al. 1981
J Androl 2:181???189
16. Reproductive hormones in aging men. I. Measurement of sex Steroids, basal
luteinizing hormone, and Leydig cell response to human chorionic Gonadotropin.
Harman SM, et al. 1980
J Clin Endocrinol Metab 51:35???40
17. Prolonged biphasic response of plasma testosterone to single intramuscular
injections of human chorionic Gonadotropin.
Padron RS, et al. 1980
J Clin Endocrinol Metab 50:1100???1104
18. Gonadotrophins and plasma testosterone in senescence. In: James VHT, Serio
M, Martini L, eds. The endocrine function of the human testis.
Mazzi C, et al. 1974
New York: Academic Press, Inc.; 51???66
19. Androgen biosynthesis in Leydig cells after testicular desensitization by
luteinizing hormone-releasing hormone and human chorionic Gonadotropin.
Dufau ML, et al.
Endocrinology 105 1314???1321 (1979)
20. Insulin-like factor 3 Serum Levels in 135 Normal Men and 85 Men with
Testicular Disorders: Relationship to the Luteinizing Hormone-testosterone Axis
K. Bay, S. et al
J. Clin. Endocrinol. Metab., Jun 2005; 90: 3410 - 3418.
21. Stimulation of sperm production by human chorionic Gonadotropin after
prolonged Gonadotropin suppression in normal men.
Matsumoto AM, et al 1985
J Androl 6:137???143
22. Human chorionic Gonadotropin and testicular function: stimulation of
testosterone , testosterone precursors, and sperm production despite high
estradiol levels.
Matsumoto AM, et al. 1983
J Clin Endocrinol Metab 56:720???728
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