HCG variances

[mstigi]

my doc, and many others on this site, perscribes HCG during cycle at a low dose of about 20-30 mg every other day. To use it at the end of a cycle will only prevent testes from recovering, use clomid or Nolva for pct.

 

[mstigi]

*correction to last thread, 200-300IU every three days

 

[MACHI]

I cannot find the other study I was looking for but basically it said HCG densensitizies the Leydig cells on an HCG-LH recepetor per cell basis, but because of the hyperplasia, the total number of HCG receptors actually upregulates(just like testosterone, upregulation in the presence of its receptor activator) because of the increase in cells.
Where do you remember seeing this other study?

Luteinizing hormone on Leydig cell structure and function.

Mendis-Handagama SM.

Department of Animal Science, College of Veterinary Medicine, University of Tennessee 37996, USA.

The effects of luteinizing hormone (LH) and human chorionic gonadotrophic hormone (hCG) on Leydig cell structure and function are reviewed in this paper under two main headings; responses to LH and hCG stimulation and responses to LH deprivation. With acute LH stimulation, up to 2 hours following the LH injection, there was no change in the volume of a Leydig cell. However, Leydig cell peroxisomal volume and intraperoxisomal SCP2 content showed a rapid and transient change. These changes can be considered to be specific because: i) no other Leydig cell organelle including smooth endoplasmic reticulum (SER) showed such a change, and ii) only the intraperoxisomal SCP2 but not catalase (a marker enzyme for peroxisomes) showed such a change within 30 minutes of LH stimulation. As these changes occurred prior to the peak testosterone levels following this treatment, it is suggested that SCP2 and peroxisomes may have an association with testosterone biosynthesis prior to cholesterol transport into mitochondria. With LH or hCG stimulation for longer periods, i.e. one day or more, the same morphological changes are produced in Leydig cells irrespective of the age of the species, dosage of LH or hCG, and with single or multiple doses. These changes include, Leydig cells hypertrophy and/or hyperplasia, increase in the cellular organelle content (mostly SER and mitochondria) and depletion of lipid droplets. In addition, a recent study showed that Leydig cell peroxisomal volume, SCP2 content, the amount of intraperoxisomal SCP2 and testosterone secretory capacity were also significantly increased in response to chronic LH treatment. The effects of LH deprivation by whatever means (e.g. hypophysectomy, with testosterone and 17 beta-estradiol silastic implants, LH antisera) on Leydig cell structure and function is generally described as opposite to those observed following LH or hCG stimulation. These include Leydig cell hypotrophy and hypoplasia, reductions in the cytoplasmic organelle content in general and specific reductions in SER and peroxisomal volumes, reductions in total catalase and SCP2 in Leydig cells together with reductions in the intraperoxisomal SCP2 content in Leydig cells and their testosterone secretory capacity.

Morphological and functional responses of rat Leydig cells to a prolonged treatment with human chorionic gonadotropins.

Andreis PG, Cavallini L, Malendowicz LK, Belloni AS, Rebuffat P, Mazzocchi G, Nussdorfer GG.

Department of Anatomy, University of Padua, Italy.

The morphological and functional responses of rat Leydig cells to a 3- and 6-day treatment with human chorionic gonadotropins (hCG) (10 IU/kg/day) were investigated by morphometric and radioimmunological techniques. hCG-administration induced a notable time-dependent enhancement in the steroidogenic capacity and growth of Leydig cells; this last was almost exclusively due to hypertrophy (and not to hyperplasia). The volume of mitochondrial and peroxisome compartments, as well as the surface area per cell of mitochondrial cristae and smooth endoplasmic reticulum (SER) were significantly increased after hCG treatment, and showed a highly significant positive linear correlation with both basal and stimulated testosterone production by isolated Leydig cells of the contralateral testis. Also the volume of nuclei and lipid-droplet compartment and the surface area per cell of Golgi apparatus displayed a notable hCG-induced rise, but they did not correlate with testosterone secretion. These findings suggest that, in addition to mitochondria and SER, in which the enzymes of steroid synthesis are located, peroxisomes are also specifically involved in the secretory activity of rat Leydig cells.

Leydig cell hypertrophy and hyperplasia in adult rats treated with an excess of human chorionic gonadotrophin (hCG).

Lamano-Carvalho TL, Favaretto AL, Silva AA, Antunes-Rodrigues J.

A morphometric study was undertaken to determine to what extent the increase in LEYDIG cell activity is related to an increase in their number and/or size. An attempt was also made to consider the morphological characteristics of the cells in terms of their probable functional capacity. Following 8 h to 3 d of excess hCG treatment, LEYDIG cells nuclear volume exhibited an increase of 16 to 18% while no significant increase in cells number was observed. By 7 d of hCG treatment, the nuclear hypertrophy (42%) coexisted with hyperplasia (33%). After 14 d of stimulation, a 41% augment in cells number and 31% increase in nuclear volumes were found. Such morphometric parameters were correlated with plasma levels of testosterone. The results suggest that hypertrophy plays a more important role in the enhancement of LEYDIG cells secretory activity in the initial phase of hCG stimulation. A subsequent hyperplasia seems to become relatively more important in longer periods of treatment. Our findings support the statement that both hCG dose and time of treatment, and consequently the plasma level of testosterone, are important parameters to be considered when the functional activity of LEYDIG cells is been evaluated by morphometric techniques.

These are interesting studies but they don't speak of desensitization. In the first, the blue highlight defines 'longer' HCG stimulation as a day or more. I wonder how much longer than a day they conducted the study. To say that the same changes occur regardless of HCG dose or duration deffinitely dosn't take desensitization into account. I think for the ways we are using HCG it's a pointless study. All it shows is that HCG stimulates testosterone production by putting the lyedig cells into 'overdrive'.

In the third study it would be interesting to see a graph which correlates the data highlighted in blue.

Good post though. Thanks. I think the post you can't find would give a lot of answers.

 

[MACHI]

[The role of gonadotropins, cyclic AMP, 22-R-OH-cholesterol and cofactors in regulating endocrine functions of the Leydig cells in rats. III. Mechanisms responsible for "desensitization" of the Leydig cells of rats caused by high doses of hCG]

[Article in Polish]

Grochowski D, Szamatowicz M.

Two groups of rats (a control group and the group examined) were administered intraperitoneally supraphysiological doses of hCG in order to induce a "down regulation" effect on the level of receptors LH and to achieve the desensibilization of Leydig cells. The authors tried to find out at which stage of sequence of changes from receptor stimulation to hormone production there appears a state of cellular resistance to further stimulation. Sections of the nucleus were incubated with various substances influencing steridogenesis (LH, hCG, dbcAMP, 22-R-OH-cholesterol, NAD + NADP + G-6-P + G-6-PDH). An index of the influence of the above substances on the synthesis of androgens were amounts of pregnenolon as the first and testosterone as the final stage of hormonal changes marked radioimmunologically in nucleus homogenates and incubating media. It was shown that the resistance of Leydig cells to further stimulation in the group of animals that were given high doses of hCG is the result of enzymatic blocks in testosterone synthesis. The first block is "late" block of 17 alpha-hydroxylase and 17-20 desmolase, disturbing transforming of 21-carbon steriods into 19-carbon androgens. When the dose of hCG increases, there appears the second block, the so called "early" block, disturbing mitochondrial synthesis of pregnenolon. It was found that exogenic cofactors are in a position, at least partially, to restore the activity of blocked enzymes.(ABSTRACT TRUNCATED AT 250 WORDS)

PMID: 2561360 [PubMed - indexed for MEDLINE]

Studies like this make me think that popular opinion is wrong when it comes to HCG use at least as far as dosage is concerned. I've read a couple more like this and wonder about the traditional HCG approach.

I'm still looking for ones that examin duration of use..........

BUMP FOR MODS AND VETS WHO KNOW THEIR SHIT!

 

[MACHI]

Mavy whats drjmw's recommendation? Can you post a link??

 

[MACHI]

what is size dosage is considered small anough to use during cycle so as to not desensivise (wow, college did wonders for my spelling )

I too am looking for this answer brother. I can't find it anywhere. People just throw out figures but nothing like 5IU's/kg body weight or 10IU's/kg body weight - something like that. I guess the same thing applies to testosterone though. You generally don't see people saying 2.5mgs per lb of body weight or shit like that. Its just 500mg-1000mg's. I don't think you can compare the two though because you can't desensitize your androgen receptors in the same manner you do your HCG receptors. I'm so horribly confused when it comes to HCG

From what I see from all the self medicated doctors on this board and others its more a throw of the dice, trial and error, anecdotal evidence type thing.

 

[Slyder190]

BUMP! I always want to know which way is better. There are always going to be advocates for both. I have yet to run it all the way through a cycle, but am contemplating it. Hopefully this will turn into a huge discussion. I do know that if HCG is taken for too long, or at too high a dosage, the LH receptor will actually become desensitized to LH, so if you go this route, you must be certain of the frequency and dosage you are using.

As it stands right now, I am in favour of using drjmw's recommendation of using it when all steroid has cleared your system, then trying to address the testes with a outside dose of LH. He has stated that this is what endocrinologists have ALWAYS done. Damn I wish we had a few endocrinologists on this board! I am on a waiting list for an endocrinologist to be my family doc. Please let it come true! lol. According to him, there is no reason why this should ever fail. It is proven and tested, and has been applied for years. If the user does not respond to drjmw's PCT protocol, the user either has a failure of the pituitary, or failure of the testes, and will more than likely require HRT indefinately.

I have heard some good info about using during, but I am not sold on it over drjmws protocol. I do see the point though where an once of prevention = a pound of cure.

Mavy

I don't even pretend to know better than the Doc, but I will always use HCG during my cycle, not after.

 

[sigmund]

This is a really good thread, shame DrJMW isn't around anymore to contribute. I've copied the above question / answer from http://www.elitefitness.com/forum/showthread.php?t=330386 (it also contains the Doc's favoured PCT regime).

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Isn't it true that HCG inhibits your body from producing LH? In my limited understanding of the HPTA access and steroids, the one thing that I've read (somewhat conclusively) is the fact that after a steroid cycle it's LH that's suppressed which causes the testosterone suppression, not the other way around. I also recall reading that there are VERY few anabolic steroids that suppress the testicles directly, rather they inhibit LH production.

THERE IS SOME SUPPRESSION, BUT SO WHAT? THE IMMEDIATE GOAL IN THE FIRST THREE WEEKS OF RECOVERY IS TO GET THE TESTES BACK UP TO SIZE. LH SECRETIONS RECOVER VERY RAPIDLY. IF YOU LOOK AT THE CYCLE, YOU SEE THAT NOLVA IS CONTINUED FOR THREE MORE WEEKS. THIS IS TO ENSURE A RAPID RECOVERY OF THE LH SECRETIONS.
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From what I've read / experienced - many doctors are unsure about the proper dosage for HCG. In fact, the AACE clinical guidelines (written in 1996 and considered outdated by many) state HCG dosages should be 1000 to 2000 IU, two or three times a week.

Studies have demonstrated that HCG dosage levels of about 5,000 IU per week or more can cause permanent damage to the testicles (see Medline articles 6210708 and 3583230). These studies have shown that such excessive HCG dosages taken long-term result in testicular desensitization (to future stimulation by LH or HCG). In other words, long-term, such excessive dosages of HCG will result in primary hypogonadism.

Although I am unsure if the following protocol is best for everybody I've come across it before and thought I'd post it for your opinions:

"Safe but effective HCG therapy consists of about 300 to 500 IU, administered before sleep, 2 to 5 times a week depending upon your responsiveness. This protocol more closely mimics the body's natural physiologic rhythm of LH production and should not be run for more than 4 weeks."

 

[Mavy]

Here is Drjmw's PCT protocol.

I have posted this recovery cycle many times. Since this is a new category, I will repost. This recovery cycle works 100% of the time. In extreme cases, it actually needs to be done twice. This recovery cycle is predicated on the fact that the athlete has something to recover. Baseline blood testing of testosterone levels, estradiol levels, and prolactin levels will tell the athlete the whole story. If the athlete's baseline Testos levels are low to low-normal of the range, then recovery is a waste of time. If the athlete's levels are in the middle, then a recovery cycle may be worth it to see the body's reaction.

Begin this cycle the week after last AAS intake.
Weeks one thru three: 1,000U HCG, IM, Monday, Wednesday, Friday; 20mg Nolvadex daily. [50mg clomid daily is added to the cycle if the athlete is coming off a prolonged (12 week+), 600mg+total, weekly AAS dosing (heavy)].

Weeks four thru six: 20mg Nolvadex daily. (50mg Clomid daily if you used it the first three weeks)

Weeks seven, eight: clean. Use this time to evaluate your previous AAS cycle and your recovery. Begin planning your next AAS cycle.

I have posted the following statement a million times, and still 95% of the steroid athletes ignore it: "Blood testing is essential to determine your baseline, see how your body reacts and to see if you recover."

The medications for this cycle are readily available, so there is no excuse. Remember, the antiestrogens and recovery meds are just as important (or more so) than the AAS.

 

[Mavy]

Oops sugmund, didnt see your link there.

I find the "HCG debate" quite confusing also, as there are so many different views on it. Both ways of running it have thier ups and downs. I have also heard of people doing both .. during and postcycle use with HCG which seems like overkill to me.