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what is hcg?

chocolatemilk said:
in for sources that say hCG is best used 250iu on cycle...

nobody f*cking knows how to use this sh*t bro. very little studies on it in terms of recovering full testicular stimulation relative to steroid use. theres a vague study i remember but cant pull up on someone who recovered using hCG after long term steroid use left his testes all retarded. some say on cycle some say pct. ive done both ways but i can't determine what's better since i never got bloods for both. just research it for yourself and make your own decision.

How do you feel about Dr scally's power pct program, talked about in anabolics 9th edition?
 
Rhadam said:
Why would you use hcg during PCT? It's suppressive...
Testosterone inhibits GnRH at the hypothalamus. Estrogen inhibits gonadotropin secretion at the pituitary.
Hcg will increase T and E2. Granted though, there is VERY little research done on hcg and most of the stuff is purely anecdotal.

Nope
 
chocolatemilk said:
because all the cool kids are doing it bro

it's recommended by Dr. Michael Scally to use hCG in pct while using clomid/Nolva and continuing the serm use after the hCG for a few weeks

Okay, I got it.
 
chocolatemilk said:
oh I thought you had something better...

you do realize there is more studies done on hCG restoring testes post cycle and hCG curing hypogonadism than there is any piece of literature which shows that hCG on cycle makes you recover faster right?

Yes.
 
chocolatemilk said:
read my first post... i said nobody knows how to use it because there is such little research although there is more research on it used post cycle for recovery. i didn't disprove using it on cycle that's why i asked for literature on why anyone thinks its beneficial on cycle... there isn't

250-500 iu is such a low dose. people fear of desensitizing when Dr's and researchers are giving out 10,000 ius daily for some males. i think the whole 250-500 iu on cycle needs to be re thought. there is no literature to support that it does anything at all

anyone who takes a side on this debate as if they are right is an idiot

Well, I believe Hcg can also be used on cycle to prevent desensitization of the testicles. At what dose? I'm not really sure, there is no data.
 
jamesm11 said:
Why are you so stupid? The hcg argument is based Ina scientific hypothesis and has real science to back up why it has been hypothesized.

You argument is without ANY merit. That's very different.

It's funny though
 
How do you feel about Dr scally's power pct program, talked about in anabolics 9th edition?

was wondering when you'd join the partay... thats the only way i use hCG now...

i dont know if you recognize this study in anabolics and can pull up the name for me to find it online and try to open it for free but there is a study talked about in anabolics which measured LH levels and other hormones and gonadotropins during a full testosterone cycle (Few months) and well past the cycle... they found LH levels rose dramatically post cycle while testosterone levels lagged way behind and took a lot longer to recover normal or pre cycle concentrations. i think the study is mentioned right around Dr. Scally's pct program
 
Have you fellas got any literature to back up this method? I have read numerous studies stating that 250iu twice weekly for the duration of a cycle ceasing a week before pct is the most effective way to use hcg. Anymore than this desensitizes your leydig cells.

lulz

how did i miss this... please post said studies
 
hmmmmmm...

a bodybuilder comes in hasn't touched a steroid in a year has low T, low sperm count, weak erections, and low testicular volume. he is given hCG 10,000iu three times a week, and hMG 75mg daily for a couple months. everything improves back to normal while on treatment. they recheck everything 3 months later and everything is still back to normal range with no treatment. researchers conclude his recovery is not any faster than patients who use hCG alone

Invalid Link Removed

Successful treatment of anabolic steroid–induced azoospermia with human chorionic gonadotropin and human menopausal gonadotropin

Human chorionic gonadotropin used alone has been reported to be successful in treating this group of patients (6, 7). In these cases, testicular function, once back to normal, continued even after the hCG was stopped. Although administering hMG seems appropriate given the hypogonadotropic results in this patient, it is not clear if exactly the same response could not have been achieved using hCG alone. Indeed the speed of recovery of endocrine function in our patient did not seem to be any faster than in reported cases using hCG alone
 
chocolatemilk said:
was wondering when you'd join the partay... thats the only way i use hCG now...

i dont know if you recognize this study in anabolics and can pull up the name for me to find it online and try to open it for free but there is a study talked about in anabolics which measured LH levels and other hormones and gonadotropins during a full testosterone cycle (Few months) and well past the cycle... they found LH levels rose dramatically post cycle while testosterone levels lagged way behind and took a lot longer to recover normal or pre cycle concentrations. i think the study is mentioned right around Dr. Scally's pct program

I'm always last to the party. Lol.
 
10,000 iu 3x a week for two months!!!

lulz @ all the broscience horror stories/theories of desensitization of leydig cells at 500iu/week
 
chocolatemilk said:
hCG does nothing for fat burning there is no scientific data to back that up

Yup.

Only way in men it might indirectly lead to fat loss is with a increase in testosterone.

That and messing up your hormonal balance could lead to some imbalances in both men an women possibly causing some weight loss.
All theoretical though
 
Yup.

Only way in men it might indirectly lead to fat loss is with a increase in testosterone.

That and messing up your hormonal balance could lead to some imbalances in both men an women possibly causing some weight loss.
All theoretical though

Indeed, indeed.

I haven't noticed any fat loss @ 450mg per week of test cyp. I'm on week 4. IDK what people talk about when they say it creates fat loss. I eat good too so IDK.
 
lulz

how did i miss this... please post said studies

Heres one. Would you like another?

HCG (Unraveled)



Post-Cycle -Therapy is a must upon cessation of steroid use . Many great Post Cycle Therapy 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.

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 increase testosterone levels . (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 Post-Cycle-Therapy. 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 level of 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 natural 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) So do not judge how "shutdown" you are 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)

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 Post-Cycle-Therapy 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).

Based off the above information, an optimal dose of hCG during the cycle would be 250iu every 4 days, or as a less desirable alternative, once a week shot of 500iu. Keep in mind, that the half-life of hCG is 3-4 days, while the half-life of LH is only 1-2 hours. Considering this difference in excretion time, it is best to space each dose of hCG at least 4 days apart for the optimal "peak and valley" replication. However, going more than 7 days between each hCG shot may promote increase the rate of desensitization from lack of LH or hCG stimulation.

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. (ie. 40iu x 60 days = 2400iu HCG dose) Remember, since the testes will be desensitized later in a cycle, you will require a higher dose. Also, the maximum daily dose of hCG should not exceed 5000iu, and 4-7 days must be taken off between each shot. Generally, a higher dose will require a longer off period between each shot. (eg., 2500iu = 7 days between each shot).

Note: If following the on cycle hCG protocol, hCG should NOT be used for PCT .

Recap

For preservation of testicular sensitivity, use 250iu every 4 day starting 14 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. This will initiate a strong LH and FSH surge 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.
 
Jesus Christ that is not a real published peer-reviewed scientific article it’s from a damn supplement company…


The article is from Eric. I don’t give these articles my time because they're usually just to promote their own companies products--like when he recommends toco-8 alongside hCG :popworm::popworm::popworm:

These types of articles are written knowing the common man won't go fact checking the sources so a lot is missing, a ton is generalized, and sh*t, most of it just isn't even cited. So I'm not gonna sit here and fact check this article for you since I have to study for my test tonight.

But please, feel free to read what it says. If the sentence/paragraph is not cited... dismiss it. If it has a number at the end of it.... go to that study, search it online, find the full article, and see if what he's saying is true (matching the article). If you can't pull up the article, I will gladly do it for you if you ask me. But what you posted means absolutely nothing to me. Fact check it.
 
references?
References as requested
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.

7. Successful treatment of anabolicsteroid -induced azoospermia with human
chorionic gonadotropin and human menopausal gonadotropin
Dev Kumar Menon, et al.
FERTILITY AND STERILITY VOL. 79, SUPPL. 3, JUNE 2003

8. Testicular responsiveness to human chorionic godadotrophin during transient hypogonadotrophic hypogonadism induced by androgenic /anabolic steroids in power athletes
Hannu et al.
J. Steroid Biochem. Vol. 25, No. 1 pp. 109-112 (1986)

9. Comparison of testosterone, dihydrotestosterone, luteinizing hormone, and follicle-stimulating hormone in serum after injection of testosterone enanthate 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 efficacy of high dosage testosterone and parallel dose-dependent suppression of luteinizing hormone, follicle-stimulating hormone, and sperm production.
Matsumoto AM, et al 1990
J Clin Endocrinol Metab 70:282-287

11. Effect of human chorionic gonadotropin on plasma steroid levels in young and old men.
Longcope C et al
Steroids 21:583-590 (1973)

12. Regulation of peptide hormone receptors and gonadal steroidogenesis.
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)

15. The aging Leydig cell III Gonadotropin stimulation in men.
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
 
Jesus Christ that is not a real published peer-reviewed scientific article it’s from a damn supplement company…


The article is from Eric. I don’t give these articles my time because they're usually just to promote their own companies products--like when he recommends toco-8 alongside hCG :popworm::popworm::popworm:

These types of articles are written knowing the common man won't go fact checking the sources so a lot is missing, a ton is generalized, and sh*t, most of it just isn't even cited. So I'm not gonna sit here and fact check this article for you since I have to study for my test tonight.

But please, feel free to read what it says. If the sentence/paragraph is not cited... dismiss it. If it has a number at the end of it.... go to that study, search it online, find the full article, and see if what he's saying is true (matching the article). If you can't pull up the article, I will gladly do it for you if you ask me. But what you posted means absolutely nothing to me. Fact check it.

Heres the full study with references etc etc



HCG - Unraveled
By Eric M. Potratz (Email)


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.




Post-Cycle-Therapy is a must upon cessation of steroid use. Many great Post Cycle Therapy 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 increase testosterone levels. (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 Post-Cycle-Therapy. 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.




First, 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 level of 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 natural testosterone production - and this leads to permanently reduced testosterone production. (recovering full testosterone production is a topic for another article)




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) So do not judge how "shutdown" you are 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



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 Post-Cycle-Therapy 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)



Based off the above information, an optimal dose of hCG during the cycle would be 250iu every 4 days, or as a less desirable alternative, once a week shot of 500iu. Keep in mind, that the half-life of hCG is 3-4 days, while the half-life of LH is only 1-2 hours. Considering this difference in excretion time, it is best to space each dose of hCG at least 4 days apart for the optimal "peak and valley" replication. However, going more than 7 days between each hCG shot may promote increase the rate of desensitization from lack of LH or hCG stimulation.

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. (ie. 40iu x 60 days = 2400iu HCG dose)



Remember, since the testes will be desensitized later in a cycle, you will require a higher dose. Also, the maximum daily dose of hCG should not exceed 5000iu, and 4-7 days must be taken off between each shot. Generally, a higher dose will require a longer off period between each shot. (eg., 2500iu = 7 days between each shot)

Note: If following the on cycle hCG protocol, hCG should NOT be used for PCT.




Recap -

For preservation of testicular sensitivity, use 250iu every 4 day starting 14 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. This will initiate a strong LH and FSH surge 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.




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.

7. Successful treatment of anabolic steroid-induced azoospermia with human

chorionic gonadotropin and human menopausal gonadotropin
Dev Kumar Menon, et al.
FERTILITY AND STERILITY VOL. 79, SUPPL. 3, JUNE 2003

8. Testicular responsiveness to human chorionic godadotrophin during transient hypogonadotrophic hypogonadism induced by androgenic/anabolic steroids in power athletes

Hannu et al.
J. Steroid Biochem. Vol. 25, No. 1 pp. 109-112 (1986)

9. Comparison of testosterone, dihydrotestosterone, luteinizing hormone, and follicle-stimulating hormone in serum after injection of testosterone enanthate 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 efficacy of high dosage testosterone and parallel dose-dependent suppression of luteinizing hormone, follicle-stimulating hormone, and sperm production.

Matsumoto AM, et al 1990
J Clin Endocrinol Metab 70:282-287

11. Effect of human chorionic gonadotropin on plasma steroid levels in young and old men.

Longcope C et al
Steroids 21:583-590 (1973)

12. Regulation of peptide hormone receptors and gonadal steroidogenesis.

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)

15. The aging Leydig cell III Gonadotropin stimulation in men.

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
 
chocolatemilk said:
:wtf1: that article is nowhere near a study... everything i said just flew over your head so i will look into myself when i have time

I'm not going to sit here and argue. I'm not going to go through and fact check something against studies as I don't have the time or inclination to do so. What he states does work and I have seen numerous people recover quite easily from heavy cycles dosing it this way. Each to their own but I will continue to dose as stated above.
 
Lukef2000 said:
I'm not going to sit here and argue. I'm not going to go through and fact check something against studies as I don't have the time or inclination to do so. What he states does work and I have seen numerous people recover quite easily from heavy cycles dosing it this way. Each to their own but I will continue to dose as stated above.

ill check it when I have time
 
Lukef2000 said:
References as requested
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.

7. Successful treatment of anabolicsteroid -induced azoospermia with human
chorionic gonadotropin and human menopausal gonadotropin
Dev Kumar Menon, et al.
FERTILITY AND STERILITY VOL. 79, SUPPL. 3, JUNE 2003

8. Testicular responsiveness to human chorionic godadotrophin during transient hypogonadotrophic hypogonadism induced by androgenic /anabolic steroids in power athletes
Hannu et al.
J. Steroid Biochem. Vol. 25, No. 1 pp. 109-112 (1986)

9. Comparison of testosterone, dihydrotestosterone, luteinizing hormone, and follicle-stimulating hormone in serum after injection of testosterone enanthate 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 efficacy of high dosage testosterone and parallel dose-dependent suppression of luteinizing hormone, follicle-stimulating hormone, and sperm production.
Matsumoto AM, et al 1990
J Clin Endocrinol Metab 70:282-287

11. Effect of human chorionic gonadotropin on plasma steroid levels in young and old men.
Longcope C et al
Steroids 21:583-590 (1973)

12. Regulation of peptide hormone receptors and gonadal steroidogenesis.
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)

15. The aging Leydig cell III Gonadotropin stimulation in men.
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

Thanks, now I can read the important stuff.
Written by Eric though for real? Hmmm...
 
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