Iu?

[SolarTint]

IM reading upon a PCT

Week Nolvadex HCG Aromasin Vitamin E
1 20mgs/day 500iu/day 20-25mgs/day 1000iu/day
2 20mgs/day 500iu/day 20-25mgs/day 1000iu/day
3 20mgs/day 500iu/day 20-25mgs/day 1000iu/day
4 20mgs/day 20-25mgs/day
5 20mgs/day 20-25mgs/day
6 20mgs/day

What is the iu stand for?

[Big]

http://en.wikipedia.org/wiki/International_unit

[Immortal Soldier]

Correct me if I am wrong big, but wouldn't it be stupid to inject 500IU of HCG 3 straight days than take 4 days off? Wouldn't it be better to space each injection out by 2 days?

Thanks

[Big]

Correct me if I am wrong big, but wouldn't it be stupid to inject 500IU of HCG 3 straight days than take 4 days off?

yes that would be wrong, where does it say to do that?

[Big]

IM reading upon a PCT

Week Nolvadex HCG Aromasin Vitamin E
1 20mgs/day 500iu/day 20-25mgs/day 1000iu/day
2 20mgs/day 500iu/day 20-25mgs/day 1000iu/day
3 20mgs/day 500iu/day 20-25mgs/day 1000iu/day
4 20mgs/day 20-25mgs/day
5 20mgs/day 20-25mgs/day
6 20mgs/day

What is the iu stand for?

by the way, this is not how I would run HCG.

[Immortal Soldier]

yes that would be wrong, where does it say to do that?

Sorry I read it wrong, I thought those were days not weeks, even worse now that I found out the format 500iu/day is ridiculous

[Deep_Fried]

Keep HCG out of your PCT window.

HCG is an LH mimetic which will keep your Leydig Cells sensitive throughout a suppresive cycle. This is only to allow a faster HPTA recovery, as the testicular (T) end of the axis will be sensitive and responsive to endogenous LH, and only the HP end will need to regain further sensitivity.

HCG itself WILL keep the Hypothalamus/Pituitary (HP) part of the Axis suppressed via negative feedback which regulates LH levels as well as through the Testosterone and Estrogen levels that will ultimately increase via its action.

So, HCG during actual PCT is pointless obviously, since you cannot restore the Axis while at the same time it is being suppressed further.

I mean, look, you guys oviously understand about using a SERM in PCT to keep E from impacting further negative feedback at the HP which speeds up HPTA revcovery right? So why on earth would you add HCG alongside your PCT ancilliaries, and have it actually cause further negative feedback at the same time?

HCG should ideally be run during cycle and discontinued appropriately along with any AAS before the start of PCT.

[Probably]

Keep HCG out of your PCT window.

HCG is an LH mimetic which will keep your Leydig Cells sensitive throughout a suppresive cycle. This is only to allow a faster HPTA recovery, as the testicular (T) end of the axis will be sensitive and responsive to endogenous LH, and only the HP end will need to regain further sensitivity.

HCG itself WILL keep the Hypothalamus/Pituitary (HP) part of the Axis suppressed via negative feedback which regulates LH levels as well as through the Testosterone and Estrogen levels that will ultimately increase via its action.

So, HCG during actual PCT is pointless obviously, since you cannot restore the Axis while at the same time it is being suppressed further.

I mean, look, you guys oviously understand about using a SERM in PCT to keep E from impacting further negative feedback at the HP which speeds up HPTA revcovery right? So why on earth would you add HCG alongside your PCT ancilliaries, and have it actually cause further negative feedback at the same time?

HCG should ideally be run during cycle and discontinued appropriately along with any AAS before the start of PCT.

whats ur way of running it during cycle? like how many ius every week ?

[Deep_Fried]

As far as HCG , I agree with both Eric Potratz and Dr. Crisler about lower dose HCG throughout cycle. The reasoning is quite clear.
Dr. John Crisler (Swale's) and Eric Potratz's writeups on HCG are below:

HCG - Unraveled
By Eric M. Potratz

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.

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.



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

Swale's HCG advice


Swale's HCG advice

by swale (MD / hrt specailist).

I advise my AAS patients to use small amounts of HCG (250IU to 500IU) two days each week, right from the beginning of the cycle. This serves to maintain testicular form and function. It makes more sense to me to keep the horse in the barn, so to speak, then to have to chase it across three counties later on. I am also a big fan of maintaining estrogen within physiological ranges. Both therapies have been shown to hasten recovery.

Any more than 500IU of HCG per day causes too much aromatase activity. Some feel aromatase is actually toxic to the Leydig cells of the testes. You are then inducing primary hypogonadism (which is permanent) while treating steroid-induced secondary (hypogonadotrophic) hypogonadism (which is temporary--hopefully).

If 250IU or 500IU on two days each week isn't enough to stave off testicular atrophy, then I recommend using it more days each week (as opposed to taking larger doses). In fact, I wouldn't mind having a guy use 250IU per day ALL THROUGH the cycle. Those that have tell me they thus avoid that edgy, burned-out feeling they usually get. They also say they simply feel better each day. Subjective reports, to be sure, but they are hard not to appreciate. Especially when HCG is so inexpensive.

The testes are then ready, willing and able to again produce testosterone at the end of the cycle. LH levels rise fairly rapidly, but endogenous testosterone production is limited by lack of use. I also want to make sure a SERM, such as Clomid or Nolvadex , is at effective serum dosage (around 100mg QD for Clomid, 20-40mg QD for Nolvadex) when serum androgen levels drop to a concentration roughly equal to 200mg of testosterone per week. That is when androgenic inhibition at the HP no longer dominates over estrogenic antagonism with respect to inducing LH production. Of course, if the fellow has been doing Clomid or Nolvadex all along the way (and I now prefer Nolvadex over Clomid, due to the possibility of negative sides from the Clomid), he is all set to simply continue it at the end (no need to switch from one to the other). BTW, I see no evidence of any benefit in using BOTH SERMs at the same time. I used to think a couple of weeks of the SERM was enough; now I like to see an entire month after the last shot of AAS (and migration of long to short esters as the cycle matures). Tapering the SERM is probably a good idea during the last week, as well.

I want my patients to stop taking HCG within a week after the end of the cycle. The testosterone production it induces will further inhibit recovery, as will using Androgel , or any other testosterone preparation, while in recovery. There is no escaping this, as there is no such thing as a "bridge". Just because you are not inhibiting the HPTA for the entire 24 hours does not mean you are not suppressing it at all. IOW, you can't "fool" the body? it is smarter than you are.

I like Arimidex during the cycle (in fact, consider use of an AI while taking aromatisables a necessity) but it ABSOLUTELY should not be used post cycle (even though it has been shown to increase LH production) because the risk of driving estrogen too low, and therefore further damaging an already compromised Lipid Profile, is too great (this also drives libido back into the ground?and we don?t want that, do we?).

All this is meant to get my guys through recovery as fast as possible (the real goal, yes?). So far, all of them who have tried it have reported they are recovering faster than when they have tried other


JC: Dr. John has updated the original paper you published. Here it is:

My New HCG Protocol Paper
This paper is about to be published in The American Academy of Anti-Aging Medicine 2004 Clinical Updates:

AN UPDATE TO THE CRISLER HCG PROTOCOL

By John Crisler, DO

In my paper “My Current Best Thoughts on How to Administer TRT for Men”, published in A4M’s 2004/5 Anti-Aging Clinical Protocols, I introduced a new protocol where small doses of Human Chorionic Gonadotrophin (HCG) are regularly added to traditional TRT (either weekly IM testosterone cypionate or daily cream/gel). The reasons and benefits of this protocol are as follows, along with a new improvement I wish to share:

Any physician who administers TRT will, within the first few months of doing so, field complaints from their patients because they are now experiencing troubling testicular atrophy. Irrespective of the numerous and abundant benefits of TRT, men never enjoy seeing their genitals shrinking! Testicular atrophy occurs because the depressed LH level, secondary to the HPTA suppression TRT induces, no longer supports them. It is well known that HCG—a Luteinizing Hormone (LH) analog—will effectively, and dramatically, restore the testicles to previous form and function. It accomplishes this due to shared moiety between the alpha subunits of both hormones.

So, that satisfies an aesthetic consideration which should not be ignored. Now let’s delve into the pharmacodynamics of the TRT medications. For those employing injectable
testosterone cypionate, the cypionate ester provides a 5-8 day half-life, depending upon the specific metabolism, activity level, and overall health of the patient. It is now well-established that appropriate TRT using IM injections must be dosed at weekly intervals, in order to avoid seating the patient on a hormonal, and emotional, roller coaster. Adding in some HCG toward the end of the weekly “cycle” compensates for the drop in serum androgen levels by the half-life of the cypionate ester. Certainly the body thrives on regularity, and supplementing the TRT with endogenous testosterone production at just the right time—without inappropriately raising androgen OR estrogen (more on that later)—approximates the excellent performance stability of transdermal testosterone delivery systems for those who, for whatever reason or reasons, prefer test cyp.

But there’s another metabolic reason to employ this protocol. The P450 Side Chain Cleavage enzyme, which converts CHOL into pregnenolone at the initiation of all three metabolic pathways CHOL serves as precursor (the sex hormones, glucocorticoids and mineralcorticoids), is actively stimulated, or depressed, by LH concentrations. It is intuitively consistent that during conditions of lowered testosterone levels , commensurate increases in LH production would serve to stimulate this conversion from CHOL into these pathways, thereby feeding more raw material for increased hormone production. And vice versa. Thus the addition of HCG (which also stimulates the P450scc enzyme) helps restore a more natural balance of the hormones within this pathway in patients who are entirely, or even partially, HPTA-suppressed.

It is important that no more than 500IU of HCG be administered on any given day. There is only just so much stimulation possible, and exceeding that not only is wasteful, doing so has important negative consequences. Higher doses overly stimulate testicular aromatase, which inappropriately raises estrogen levels, and brings on the detrimental effects of same. It also causes Leydig cell desentization to LH, and we are therefore inducing primary hypogonadism while perhaps treating secondary hypogonadism. 250IU QD is an effective, and safe, dose. After all, we are merely replacing that which is lost to inhibition.

In my previous report I recommended 250IU of HCG twice per week for all TRT patients, taken the day of, along with the day before, the weekly test cyp injection. After looking at countless lab printouts, listening to subjective reports from patients, and learning more about HCG, I am now shifting that regimen forward one day. In other words, my test cyp TRT patients now take their HCG at 250IU two days before, as well as the day immediately previous to, their IM shot. All administer their HCG subcutaneously, and dosage may be adjusted as necessary (I have yet to see more than 350IU per dose required).

I made this change after realizing that the previous HCG protocol was boosting serum testosterone levels too much, as the test cyp serum concentrations rise, approaching its peak at roughly the 72 hour mark. The original goal of supporting serum androgen levels with HCG had overshot its mark.

Those TRT patients who prefer a transdermal testosterone, or even testosterone pellets (although I am not in favor of same), take their HCG every third day. They needn’t concern themselves with diminishing serum androgen levels from their testosterone delivery system. These patients will, of course, notice an increase in serum androgen levels above baseline.

While HCG, as sole TRT, is still considered treatment of choice for hypogonadotrophic hypogonadism by many , my experience is that it just does not bring the same subjective benefits as pure testosterone delivery systems do—even when similar serum androgen levels are produced from comparable baseline values. However, supplementing the more “traditional” TRT of transdermal, or injected, testosterone with HCG stabilizes serum levels, prevents testicular atrophy, helps rebalance expression of other hormones, and brings reports of greatly increased sense of well-being and libido. My patients absolutely love it. As time goes on, we are coming to appreciate HCG as a much more powerful--and wonderful--hormone than previously given credit.

Copyright John Crisler, DO 2004. This article may, in its entirety or in part, be reprinted and republished without permission, provided that credit is given to its author, with copyright notice and 2. http://www.AllThingsMale.com clearly displayed as source. Written permission from Dr. Crisler is required for all other uses.

FYI, swale is AKA crisler
__________________
Dedication is eveything, Impossible is nothing

[yesimussing]

Great stuff.