HCG variances

[MACHI]

After reading DBB's thread, kevin6's, and numerous others regarding HCG I have a question about it...

Way I see it - there are two schools of thought.....
1) (Common/Traditional) Taken during PCT to get boys back up and running...
2) Taken during the cycle to prevent the boys from atrophying at all....

I'm familiar with the first but not with the second. I'm looking for actual research that compares the two. From my foreknowledge and from looking at hundreds of cycles I find that most people prefer number 1.

If anyone has any sources of information for research with this stuff conducted in the manner I'm inquiring for, please post them. Also if you have used it BOTH ways, please enlighten me as to what way you thought was better and why.

Thanks in advance.

 

[Mavy]

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

 

[Mavy]

Ma'fuckin' BUMP!!!!!! Hopefully some mods and vets and smarty-pants like jenetic will chime in on this one.

I also think that duration and drug choice play a nice role in how you use HCG. For example someone running a var only cycle for example, should have less of a hard time recovering and probably wont need HCG throughout the cycle.

A good (but stupid) friend of mine, read somewhere that smoking depelets your stores of vitamin C, so after every smoke he has, he takes a 250mg vitamin C vitamin. lol. He thinks, well maybe its being depleted, but I am refilling it again. This is the same type of scenario I almost see when using HCG during. I guess I am just thinking that, you are going to become supressed while using steroids (whether your nuts shrink or not), you might as well accept this, and let it happen, instead of trying to fight it the whole way through. Let it happen, then address it when you are done your cycle.

 

[MACHI]

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.
.......
Mavy

I agree with what you said. I see some validity in running it during a cycle but it just seems too dangerous. Do you know how HCG and LH are equivilant to each other on a mg/mg or mol/mol basis? What I mean by that is - does one molecule of HCG stimulate as much testosterone production from the Lyedig cells as one molecule of LH? I guess in order to really know if running HCG during a cycle will cause desensitization by overstimulation is to find out that equivilancy and then adjust the HCG dosage to the daily output of LH from the pituitary. Even then though you could run into problems of secretion times and quantities. Is LH secreted all throughout the day or is it like HGH and secreted mostly at night around bedtime. If daily output is 3mg throughout the course of the day and you inject 5mg all at one time EOD for a 12 week cycle I would think that this could (technically) lead to slight desensitization, more specifially because its on a 12 week period. I guess I'm in favor of HCG use druing PCT because you use it for a much shorter duration of time. Shit here is the question to answer then....

Are you more likely to desensitize the lyedig cells with 1 or 2
1) Injecting HCG at 250+% times normal output (LH) for 2-3 weeks
2) Injecting HCG at 100-110% times normal output (LH) for 10-12 weeks

LOL so yeah MAVY I'm hoping this will turn into a compare and contrast discussion as well.....

 

[goldenthree]

What your worried about is atrophy of the leydig cells. Leydig cells produce testosterone in the presence of LH. After doing research I am going to run HCG at low doses during cycle. I think the phrase "use it or lose it" comes to mind. Basically whats happening with steroids is your body does not need to produce testosterone so it tries to save resources by downregulating its testosterone producing capabilities.(= bad ) I don't see why there is any reason not to use physiological doses of HCG during cycle. Desensitisation should not occur if your running physiological doses of HCG.

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.

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.

 

[TheAssholeFomerlyKnownAsDBBT]

I agree with what you said. I see some validity in running it during a cycle but it just seems too dangerous. Do you know how HCG and LH are equivilant to each other on a mg/mg or mol/mol basis? What I mean by that is - does one molecule of HCG stimulate as much testosterone production from the Lyedig cells as one molecule of LH? I guess in order to really know if running HCG during a cycle will cause desensitization by overstimulation is to find out that equivilancy and then adjust the HCG dosage to the daily output of LH from the pituitary. Even then though you could run into problems of secretion times and quantities. Is LH secreted all throughout the day or is it like HGH and secreted mostly at night around bedtime. If daily output is 3mg throughout the course of the day and you inject 5mg all at one time EOD for a 12 week cycle I would think that this could (technically) lead to slight desensitization, more specifially because its on a 12 week period. I guess I'm in favor of HCG use druing PCT because you use it for a much shorter duration of time. Shit here is the question to answer then....

Are you more likely to desensitize the lyedig cells with 1 or 2
1) Injecting HCG at 250+% times normal output (LH) for 2-3 weeks
2) Injecting HCG at 100-110% times normal output (LH) for 10-12 weeks

LOL so yeah MAVY I'm hoping this will turn into a compare and contrast discussion as well.....

BUMP for Mods and Vets

 

[TheAssholeFomerlyKnownAsDBBT]

BUMP for Mods and Vets

~

 

[romoranger]

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

 

[BBig phenom]

cool

 

[tatertoos]

I have read that HCG should not be used during PCT since it inhibits natty test, as well. Any truth?

 

[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).

------
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.
------

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.

 

[sigmund]

No worries Mavy - although I included the link it's probably best you cut and paste the Doc's favoured PCT protocol, as it's easier for bro's to read the info from just one thread

So any thoughts on this:

"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."

I'd also be interested to hear what people think about HCG causing permanent damage. Any idea what approx doses / duration could lead to this?

 

[kahbab]

i have been following this thread very closely because i to am confused about HCG doses, needle sizes, and times. i am about to start a 10 week cycle of test enth and i am still not sure about what to do with the HCG. the one thing that i see strange about this post is that i states 1,000 iu HCG IM, meaning intramuscular. everything i have read so far says that HCG needs to be taken subcutaniously so what is really going on? bump for those who know.

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. Remem

ber, the antiestrogens and recovery meds are just as important (or more so) than the AAS.

 

[SuperDawgy]

everything i have read so far says that HCG needs to be taken subcutaniously so what is really going on? bump for those who know.

I just responded to a similar question on another board, according to DrJMW it should be taken IM per the instructions from the manufacturers. I have also called a ob/gyn friend of mine and asked his opinion. He said that it will work both ways, but in his office they go with IM using a 23 ga 1.5 to the glutes.

 

[MACHI]

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)......................

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."

Good post sigmund. Nice info.

I'm getting a really good idea of what doses to take but not when. I still have yet to find which is better, during a cycle or as PCT. In either case. I find that its safe to say use conservative doses (2000-3000IU's per week broken up into increments so as not to overload your testies all at one time) so long as you have your pre cycle test levels measured. In that case, as far as the duration of the HCG doses are concerned you'll definitely know when to stop using it provided you get your test levels measured during PCT to use them as a stop point. I guess it goes contrary to just recommending 3-4 week PCT becuase, as was shown in the drmj thread, different people recover at different times after different cycles. The only definitive way to know when to stop your PCT is to get your endogenous test levels measured and have them compared to your pre cycle levels like was said in drmj's thread. I think your protocol is right on except for its duration. Like I previously said I think duration is dependent on the monitoring of your test levels provided your not taking supraphysiological doses.

Still trying to find info that compare during cycle use to PCT use.....I guess thats the only ? I still have left......

 

[Jenetic]

Leydig cell desensitization from HCG has been shown to be blocked/minimized by Nolvadex. This occurs by supressing HCG's ability to inhibit the conversion of 17 alpha hydroxyprogesterone to testosterone.

Modulation of Leydig Cell Androgen Biosynthesis and Cytochrome P-450 Levels during Estrogen Treatment and Human Chorionic Gonadotropin induced Desensitization

The similarity of estrogen dependent lesions to those produced by hCG treatment further indicates the involvement of endogenous estrogen in the development of the microsomal enzymatic lesions in gonadotropin-induced desensitization of testicular androgen production.

Tamoxifen suppresses gonadotropin-induced 17 alpha-hydroxyprogesterone accumulation in normal men.

Simultaneous administration of hCG and the estrogen antagonist tamoxifen (20 mg twice daily) almost completely abolished the hCG-induced steroidogenic block localized between 17 OHP and T (17 OHP to T ratio at 24 h, 1.1 +/- 0.1 times baseline; P < 0.01 vs. hCG alone). These data indirectly suggest that, in man, the hCG-induced steroidogenic lesion might be mediated through its estrogen-stimulating effect.

Effect of an antiestrogen on the testicular response to acute and chronic administration of hCG in normal and hypogonadotropic hypogonadic men: tamoxifen and testicular response to hCG.

17OHP rose with hCG alone, but not with hCG + Tx in both groups. E, SHBG and 17OHP/T ratio did not change after treatments. hCG tests: E increased 24 h following hCG administration in every test. The ratio 17OHP/T rose at 24 h in the first and second test but in the third test it did not change. These results support the role of E in the acute hCG-induced Leydig cell desensitization.

Bring it? Brought!

Jenetic

 

[DIVISION]

After reading DBB's thread, kevin6's, and numerous others regarding HCG I have a question about it...

Way I see it - there are two schools of thought.....
1) (Common/Traditional) Taken during PCT to get boys back up and running...
2) Taken during the cycle to prevent the boys from atrophying at all....

I'm familiar with the first but not with the second. I'm looking for actual research that compares the two. From my foreknowledge and from looking at hundreds of cycles I find that most people prefer number 1.

If anyone has any sources of information for research with this stuff conducted in the manner I'm inquiring for, please post them. Also if you have used it BOTH ways, please enlighten me as to what way you thought was better and why.

Thanks in advance.

I'm from the school of thought that you're better off doing one round of HCG mid-cycle to retain consistency in your nuts, and then of course doing your PCT as scheduled to recover volume and frequency in your nutsack.

Dr. Weiser, Jenetic both advise that it's best this way.

I have no studies, get with Jenetic or Juve to get the studies that would confirm validity.

When it comes to PCT, HCG to my nuts only made my balls fatter.




Hope this helps, holmes.







DIV

 

[Jenetic]

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.

This is far from the truth. The reason many endocrinologists have come to this conclusion is due to the fact that very few of them have the experience treating severe forms of secondary aquired hypogonadotropic hypogonadism. They are unfamilar with proper protocols which includes high dosage HCG administration and additional gonadotropin preparations such as HMG or rFSH. This complication puts the patient at risk for potential and unknown side effects in the eyes of the doctor, therefore HRT is a resonable solution since it will quickly alleviate the majority of the uncomfortable symptoms that the patient is experiencing.

There is a thread in the PCT forum which I have recently been addressing. The user did not respond to the typical dosage and schedule of 1,000 IU's 3x/wk. DrJMW is correct. 1,000 IU's is where the therapy begins but he is incorrect by saying that's where it ends. Another alternative I usually recommend for intermediate to advanced AAS users is 1,500 IU's HCG 3x/wk which is based on experience with many of my former training clients. Overall, the goal is 3,000-5000 IU's HCG per week on average. Regardless, if the user does not respond to 1,000 IU's, he will more than likely not respond to a higher degree with the additional 500 IU's included in the 1,500 IU's. The next step taken in this particular case was to change the dosage and schedule of administration. 5,000 IU's HCG every 5 days was selected. This is standard protocol. Note, HCG was not discontinued after 3 weeks and was used for an additional 3-4 weeks until the increase in testicular volume was achieved. If have the time to read the thread, you will see that he has been responding with excellent results and is on his way to recovery.

The most extreme case that I have seen was 10,000 IU's HCG 2x/wk in combination with 150 IU's HMG ED for 120 days. This person previously used AAS for several years and competed at the pro level. The treatment was a sucess and he even concieved a child approximately 7-10 months after cessation.

In most cases the PCT protocol provided by DrJMW is sufficient. One process I recommend which he doesn't necessarily agree with is to incorporate HCG during the cycle when running prolonged or heavy dosages. His reasons are valid in general. My recommendation is to use 500-1000 IU's HCG in combination with Nolvadex for 7 days consecutively mid cycle or intermitently depending on the cycle length. This solution addresses both testicular atrophy and prevention of Leydig cell desensitization associated with HCG usage. There are various factors involved during recovery but it's far from accurate to jump to a conclusion that HRT is needed if one specific recovery protocol is not successful.

Jenetic

 

[Jenetic]

I'm from the school of thought that you're better off doing one round of HCG mid-cycle to retain consistency in your nuts, and then of course doing your PCT as scheduled to recover volume and frequency in your nutsack.

Dr. Weiser, Jenetic both advise that it's best this way.

I have no studies, get with Jenetic or Juve to get the studies that would confirm validity.

From my point of view, I always recommend the appropriate PCT protocol to be utilized post cycle. Also, the previously mentioned mid/intermittent cycle protocol of 500-1,000 IUs HCG and 20 mgs Nolvadex ED for 7 days consecutively can and should be utilized when necessary during prolonged (12+/wks) or heavy dosage (1,000+mgs/wk) cycles.

There is nothing wrong with using HCG at 250-500 IUs 1-2x/wk throughout the cycle. What I don't like about that protocol is that HCG is discontinued once the cycle has completed and the only substances used during PCT are SERMs which consist of Nolvadex and/or Clomid. The reason for my hesitation is that there is no guarantee that this formula prevents testicular atrophy to the extent where the overall volume and function of the testes are in an optimal state. Also, everyone is now aware that Leydig cell desensitization does in fact occur with prolonged or high dosage HCG usage. Therefore, users which follow this protocol whom do not incorporate Nolvadex are now susceptible to Leydig cell desensitization which may render HCG usage post cycle ineffective when and if needed.

Hypothetically speaking, if testicular function and volume have been maintained during cycle with HCG, SERMs are then utilized to counteract the imbalance in the androgen:estrogen ratio encountered post cycle as the exogenous androgens diminish. This results in the prevention of estrogenic side effects while increasing pituitary LH secretion which in turn increases testosterone production.

I can see how this is beneficial during conservative cycles, especially when proper estrogen and prolactin management has been incorporated. However, this conclusion is much more difficult to achieve on heavy or prolonged cycles. Testicular volume should be maintained to an acceptable extent but that does not result in an improved recovery as severe HTPA suppression still exists which is not immediately repairable through the usage of SERMs. The same fact holds true with HCG usage during PCT but the difference is that you are now preventing and/or minimizing the “crash effect” when incorporating HCG.

Keep in mind, HCG is recommended to be used at 1,000-1,500 IUs 3x/wk and is continued with an adjustment in dosage and frequency as necessary until the increase in testicular volume and function have been achieved which is unlike the more typical, yet incorrect belief that HCG is only to be used for a short period of time. Also, this continual usage is not necessary and avoidable in most cases by utilizing the mid/intermittent protocol previously mentioned, but it is much more common with long term (1+/yr) users and/or improper recovery from previous cycles regardless of which protocol is chosen.

The typical argument here when incorporating HCG during PCT is that HCG is itself is suppressive. This is true and occurs though the constant binding of HCG which disrupts the endogenous pulsatile secretion of LH. In this case, your androgens are still elevated. The difference is that the effect is through testicular production which is also minimal compared to that of exogenous hormones. Blood work will display much higher levels of LH, FSH and testosterone in this environment which includes HCG and SERMs during PCT versus HCG during cycle and SERMs only during PCT. This ultimately results in a more comfortable as well as tolerable recovery both physically and psychologically. These results which I have presented are confirmed based upon frequent blood work results of my athletic training clients and I encourage all to do the same if there is any doubt. In conclusion, HCG should always be included during PCT in combination with SERMs regardless of what protocol has been utilized during cycle to prevent testicular atrophy, in order to achieve an optimal recovery.

Jenetic

 

[Mavy]

Damn jenetic! Right when you think you have something figured out. So how does your PCT protocol differ from drjmws? You believe in HCG both during cycle AND in PCT? Where drjmw only reccommends it during PCT? BTW, that HRT statement was what I was told by drjmw, I was just passing it along. I believe that he thought, if his PCT protocal failed more than a few times, that there was a "chance" the patient may require HRT. Obviously it seems there are other methods that can be tried. Epsecially after reading your long shut down thread from what I remember.

So you think that it is a mistake to run HCG during, but after a cycle? Because of the effect is will have on of LH, FSH and T levels. Which is also the reason why nolva is a must as T levels start to go back up to their normal range? Good info bro. I was hoping you would post on this. I still feel somewhat confused, I think that I am just looking for the 1 proven during/PCT formula that is LAW, lol. not the case I guess with all the different cycle people use. HCG does seem like something that can cause more harm than good if used incorrrectly.

Mavy

 

[ATLmuscles]

...My recommendation is to use 500-1000 IU's HCG in combination with Nolvadex for 7 days consecutively mid cycle or intermitently depending on the cycle length. This solution addresses both testicular atrophy and prevention of Leydig cell desensitization associated with HCG usage. There are various factors involved during recovery but it's far from accurate to jump to a conclusion that HRT is needed if one specific recovery protocol is not successful.

Jenetic

Jenetic,

DO you mean 500-1000 iu per day for seven days during cycle?

 

[Jenetic]

Jenetic,

DO you mean 500-1000 iu per day for seven days during cycle?

Yes, that is correct.

Jenetic

 

[Jenetic]

Damn jenetic! Right when you think you have something figured out. So how does your PCT protocol differ from drjmws? You believe in HCG both during cycle AND in PCT? Where drjmw only reccommends it during PCT? BTW, that HRT statement was what I was told by drjmw, I was just passing it along. I believe that he thought, if his PCT protocal failed more than a few times, that there was a "chance" the patient may require HRT. Obviously it seems there are other methods that can be tried. Epsecially after reading your long shut down thread from what I remember.

So you think that it is a mistake to run HCG during, but after a cycle? Because of the effect is will have on of LH, FSH and T levels. Which is also the reason why nolva is a must as T levels start to go back up to their normal range? Good info bro. I was hoping you would post on this. I still feel somewhat confused, I think that I am just looking for the 1 proven during/PCT formula that is LAW, lol. not the case I guess with all the different cycle people use. HCG does seem like something that can cause more harm than good if used incorrrectly.

Mavy

In general, my PCT protocol is about the same as DrJMW's which is 1,000 IUs HCG 3x/wk (mon/wed/fri) in combination with 20 mgs Nolvadex ED for a total of 3 weeks. Then, discontinue HCG and continue with 20 mgs Nolvadex ED for an additional 3 weeks. For the beginner AAS user, this is more than sufficient.

The majority of my experience is with intermediate to advanced athletes whom have completed multiple cycles with higher dosages. Therefore, based upon blood work, we have established that 1,500 IUs 3x/wk (mon/wed/fri) to be the optimal range to begin with. The Nolvadex dosage remains constant, however Clomid is utilized throughout PCT at 50-100 mgs ED during the first 3 weeks and 50 mgs ED for the last 3 weeks.

DrJMW's belief that incorporating HCG during the cycle is not necessary and may result in Leydig cell desensitization is correct for the most part. First, the cycle duration that both he and I recommend is 8 weeks. There is absolutely no reason that significant gains cannot be achieved in 8 weeks. Keeping in mind the 8 week cycle duration and realistic dosages, 500 mgs Testosterone EW and 400 mgs Equipoise EW for example, HCG will not be necessary during the cycle and is best utilized post cycle. Second, if HCG is used without Nolvadex, the prolonged dosage can result in Leydig cell desensitization which may render HCG usage during PCT to be ineffective if and when needed. As I have previously addressed, Nolvadex prevents the Leydig cell desensitization encountered with HCG, therefore there is no problem with using HCG during your cycle as long as Nolvadex is incorporated.

My protocol does include HCG in combination with Nolvadex during prolonged (12+/wks) and high dosage (1,000+mgs/wk) cycles. In this case, 500-1,000 IUs HCG ED in combination with 20 mgs Nolvadex ED for 7 days consecutively is administered mid cycle or intermittently (every 6-8 weeks) during the cycle. Maintaining testicular volume during cycle does in fact improve recovery when compared to atrophied testes when beginning PCT.

The only other difference in my protocol is when testicular volume has not been restored from HCG post cycle. In this case, HCG is continued with the necessary adjustments in dosage and frequency until an increase in testicular volume has been achieved. Subsequent changes will be based upon the individual’s response to each particular stage. I won’t go into further details here since every case varies and deserves an individualized response.

As you can see by now, I have nothing against HCG usage during a cycle if and when it is warranted, but the emphasis is placed on always incorporating HCG during PCT to insure an optimal recovery.

Jenetic

 

[ATLmuscles]

Yes, that is correct.

Jenetic

Thanks, man. I'm in week-9 of a lnoger cycle, and I just did 1,000 iu HCG last night. I've always been confused about HCG during a cycle and I've done it in one-week or so "spurts" in a longer cycle, as opposed to lower dose throughout. Of course alot of what we do as bosybuilders is using these drugs in a manner that they were not intended, so there is much trial and error. YOu seem really knowledgeable. Is this your field, or just research you've done on your own.

Thanks again. I

 

[Paulo]

Thanks, man. I'm in week-9 of a lnoger cycle, and I just did 1,000 iu HCG last night. I've always been confused about HCG during a cycle and I've done it in one-week or so "spurts" in a longer cycle, as opposed to lower dose throughout. Of course alot of what we do as bosybuilders is using these drugs in a manner that they were not intended, so there is much trial and error. YOu seem really knowledgeable. Is this your field, or just research you've done on your own.

Thanks again. I

I realize this is not my question to answer, but after a good bit of correspondence, I've come to gather that he's actually a 14 year old autistic midget PCT savant.

Needless to say, he's a very special and unique young man who we should all love and treasure.

 

[Mavy]

THese kind of threads are priceless in my mind. And very imporant as well. Thanks for sharing Jenetic.

Would you say that DC (during cycle, lol) HCG usage can really be dependant on what choices of gear a user decides to do?

In MD magazine a couple months ago there was an article and several studies that showed both nandrolone and tren can actually desensitise the leydig cells to pituitary hormones, hence the reason why many people report feeling "shut down hard" while taking tren or Deca. Would you say it would be more important to take DC HCG while running a tren or Deca cycle (even if say it was only a 6 week cycle only of tren) as compared to a longer cycle without these compounds like say 12 weeks of test and EQ for example?

Seems to be a high abundance of people these days running shorter 4-6 week tren cycles or NPP cycles. Would you think these cycles would still justify running HCG during cycle because of the choices of gear being used, even though its only being used for a short time frame?

 

[Jenetic]

THese kind of threads are priceless in my mind. And very imporant as well. Thanks for sharing Jenetic.

Would you say that DC (during cycle, lol) HCG usage can really be dependant on what choices of gear a user decides to do?

In MD magazine a couple months ago there was an article and several studies that showed both nandrolone and tren can actually desensitise the leydig cells to pituitary hormones, hence the reason why many people report feeling "shut down hard" while taking tren or Deca. Would you say it would be more important to take DC HCG while running a tren or Deca cycle (even if say it was only a 6 week cycle only of tren) as compared to a longer cycle without these compounds like say 12 weeks of test and EQ for example?

Seems to be a high abundance of people these days running shorter 4-6 week tren cycles or NPP cycles. Would you think these cycles would still justify running HCG during cycle because of the choices of gear being used, even though its only being used for a short time frame?

Nandrolones are well know for their ability to increase prolactin and prolactin is notorious for it's negative impact on libido and recovery. Therefore, it's not about using HCG during cycle, but more importantly to manage prolactin.

Factors that may complicate and/or delay recovery are elevated levels of estrogen and prolactin. Both of these hormones, when elevated, exert negative feedback on the HPTA. Estrogen and its side effects can be controlled by using an aromatase inhibitor such as Aromasin, Femara and Arimidex during cycles including aromatizing AAS. Prolactin and its side effects can be controlled by using an anti prolactin such as Dostinex or Bromocriptine during cycles containing nandrolones. If these measures have not been addressed during the cycle, they will need to be addressed during PCT.

Jenetic

 

[desman]

i find taking 500iu EOD 3 weeks at end of cycle and following a standard clomid/nolva regime works well for me

 

[LVTitan]

I just responded to a similar question on another board, according to DrJMW it should be taken IM per the instructions from the manufacturers. I have also called a ob/gyn friend of mine and asked his opinion. He said that it will work both ways, but in his office they go with IM using a 23 ga 1.5 to the glutes.

u can use a 29g if you want. i use a 25g for my hcg, and use my quads

 

[MACHI]

Extremely valuable info jenetic. Thanks for taking the time to post. I was away for awhile and just got done thoroughly reading everyones' posts since my last post. I have HCG use and PCT all figured out now, j/k but i have a pretty good idea. Using tamoxifen specifically as a synergist to prevent HCG induced lyedig cell desensitization was a new concept to me. In my next period of free time i'm going to read up more on that. Do you know of any literature you can direct me to on that?

Also, you have clients that you train while monitoring their 'supplement' usage? It sounds as though you really speak from first hand experience with this stuff. I look foward to picking your brain.....

Thanks

 

[GoldenDelicious]

heyas, as usual, didnt read above replies to avoid bias

pharmacist, for those that dont know

id go for doing it during cycle, for a couple of reasons: 1) there is no guarantee that atrophy incurred during cycle is reversible upon LH receptor agonism post cycle, meaning that if yo uuse it post cycle, youre at risk of permanent atrophy that would not occur in teh case of administration during the cycle and 2) hcg will interfere with normal LH regulation as per normal recovery if used post cycle, meaning that recovery will in fact be staggered - your FSH etc will get back online, but LH production should to some degree be supressed. it is non sensical to me to use an LH agonist in the form of HCG post cycle when you are already going to be using testicular stimulants in the form of nolva/clomid, and of course, you are relying on the lack of LH stimulation on the testes to actually precipitate endogenous LH production. if youre going to supplement HCG, then youre going to keep negative pressure on the feedback loop that fucks up your HPTA in the first place, which is the opposite of what you want to do.

just because supplementing HCG is what "endocrinologists have always done" doesnt mean that it is neccessarily the right thing to do, and furthermore, i do not think that there have been too many endocrinologists in the past who have been proactive about integrating HCG use into a steroid users active cycle; for whatever reasons, ethical, moral etc, endocrinologists in the past would have been treating patients in a post cycle setting, and in that context, well, HCG post cycle isnt a bad idea.

long story short: hcg can be useful post cycle, but nowhere near as useful as using it during cycle.

cheers

 

[Mavy]

Hmm ... This could get interesting now. Damn .. how I wish there was an EXPERIENCED endocrinologist who could post on this topic, and try to put some form of closure to this kind of thing, because like I say .. this could go on for years which way is best. And I am sure it there will never be 1 magic formula. I agree with you in the fact that most endocrinologists probably are more skilled at "fixing" a problem, and not "prevention" during a steroid cycle. But really since none of us know either, that is all that we are doing is speculating.

I am on a waiting list for an endocrinologost for a family doctor. Damn is he going to regret it if he accepts me. I will be going in once a week with the studies for him to read, lol.

 

[GoldenDelicious]

mavy, id probably go off what swale says. he sees hundreds of patients, some are post cycle/severely supressed, some are mid cycle, he has bloods from all of them with corresponding info on relevant biological markers, he fiddles with their drug regimes intensely, and what i have read of his makes me think that the during cycle HCG regimen is the way to go for the lowest risk, fastest recovery steroid cycle.

the source of the confusion imo is that HCG post cycle will work to some degree, even well...and so youre going to get some people swearing by it. logically though, the during HCG regimen makes more sense, AND is backed up by real world success as per swales practice. more evidence will become available in the near future, since steroid use is becoming more accepted in the case of various wasting diseases, such as AIDS, cancer, post chemotherapy etc and so there will be a few qualified researchers with decent study protocols who should fairly well put this issue to rest.

for now though, i feel that there is a lack of direct, comparitive evidence, and so at best, youre going to get an incomplete reply imo

cheerios

 

[MACHI]

mavy, id probably go off what swale says. he sees hundreds of patients, some are post cycle/severely supressed, some are mid cycle, he has bloods from all of them with corresponding info on relevant biological markers, he fiddles with their drug regimes intensely, and what i have read of his makes me think that the during cycle HCG regimen is the way to go for the lowest risk, fastest recovery steroid cycle.

the source of the confusion imo is that HCG post cycle will work to some degree, even well...and so youre going to get some people swearing by it. logically though, the during HCG regimen makes more sense, AND is backed up by real world success as per swales practice. more evidence will become available in the near future, since steroid use is becoming more accepted in the case of various wasting diseases, such as AIDS, cancer, post chemotherapy etc and so there will be a few qualified researchers with decent study protocols who should fairly well put this issue to rest.

for now though, i feel that there is a lack of direct, comparitive evidence, and so at best, youre going to get an incomplete reply imo

cheerios

Golden - I'm curious if you know how much more/less potent HCG is than LH on a molecule for molecule basis when it comes to stimulating test production. Also I asked jenetic this next question earlier. Can you direct me towards info that involves tamoxifen being used specifically as a synergist with HCG to prevent lyedig cell desensitization?

Thanks for your replies too

 

[Jenetic]

Leydig cell desensitization from HCG has been shown to be blocked/minimized by Nolvadex. This occurs by supressing HCG's ability to inhibit the conversion of 17 alpha hydroxyprogesterone to testosterone.

Modulation of Leydig Cell Androgen Biosynthesis and Cytochrome P-450 Levels during Estrogen Treatment and Human Chorionic Gonadotropin induced Desensitization

The similarity of estrogen dependent lesions to those produced by hCG treatment further indicates the involvement of endogenous estrogen in the development of the microsomal enzymatic lesions in gonadotropin-induced desensitization of testicular androgen production.

Tamoxifen suppresses gonadotropin-induced 17 alpha-hydroxyprogesterone accumulation in normal men.

Simultaneous administration of hCG and the estrogen antagonist tamoxifen (20 mg twice daily) almost completely abolished the hCG-induced steroidogenic block localized between 17 OHP and T (17 OHP to T ratio at 24 h, 1.1 +/- 0.1 times baseline; P < 0.01 vs. hCG alone). These data indirectly suggest that, in man, the hCG-induced steroidogenic lesion might be mediated through its estrogen-stimulating effect.

Effect of an antiestrogen on the testicular response to acute and chronic administration of hCG in normal and hypogonadotropic hypogonadic men: tamoxifen and testicular response to hCG.

17OHP rose with hCG alone, but not with hCG + Tx in both groups. E, SHBG and 17OHP/T ratio did not change after treatments. hCG tests: E increased 24 h following hCG administration in every test. The ratio 17OHP/T rose at 24 h in the first and second test but in the third test it did not change. These results support the role of E in the acute hCG-induced Leydig cell desensitization.

Jenetic

 

[GoldenDelicious]

Golden - I'm curious if you know how much more/less potent HCG is than LH on a molecule for molecule basis when it comes to stimulating test production. Also I asked jenetic this next question earlier. Can you direct me towards info that involves tamoxifen being used specifically as a synergist with HCG to prevent lyedig cell desensitization?

Thanks for your replies too

lol im glad that youre not asking for any, you know, ultra specific info thats going to be a huge pain in the ass to find, or anything

truthfully, i wouldnt know what the molar potency for those drugs is, though nor would it matter, because you could just increase/decrease the dose of either. its not like we dose people with xyz molecules of lh or hcg, we have already established working milligram doses, adn use those. the other thing is, in the case of HCG, it does more than just stimulate LH receptors. its a complicated, versatile little hormone (meaning, its a pain in the ass) that modulates/affects other processes in the body, and is not merely an LH agonist. why, are you thinking of using LH rather than hcg during the cycle? or are you just curious about how effective one is against the other (or worse, are you thinking of using both? )

as for your latter question, well, i couldnt give you any data collected from people trying to do just that...since i dont think anyone has tried it in a clinical setting just yet. I mean, using both at once isnt a bad idea (i have thought of this in the past...but then thought fuck it, save the tamox for when you need rescue from gyno and forget about it) but id have to look at the mechanism of action specifically, and see if it makes sense pharmacologically...dunno...might have to get back to you on this one

(remind me if i dont respond in a day or two, im a bit tardy with things like this, and its late where i am just now )

 

[MACHI]

Jenetic

Thanks jenetic. I read that before but I thought I asked you in one of my earlier posts where you got the info and you never responded. My bad. Where did you get it? I'd like to read the full studies......

MACHI

 

[MACHI]

lol im glad that youre not asking for any, you know, ultra specific info thats going to be a huge pain in the ass to find, or anything

truthfully, i wouldnt know what the molar potency for those drugs is, though nor would it matter, because you could just increase/decrease the dose of either. its not like we dose people with xyz molecules of lh or hcg, we have already established working milligram doses, adn use those. the other thing is, in the case of HCG, it does more than just stimulate LH receptors. its a complicated, versatile little hormone (meaning, its a pain in the ass) that modulates/affects other processes in the body, and is not merely an LH agonist. why, are you thinking of using LH rather than hcg during the cycle? or are you just curious about how effective one is against the other (or worse, are you thinking of using both? )

as for your latter question, well, i couldnt give you any data collected from people trying to do just that...since i dont think anyone has tried it in a clinical setting just yet. I mean, using both at once isnt a bad idea (i have thought of this in the past...but then thought fuck it, save the tamox for when you need rescue from gyno and forget about it) but id have to look at the mechanism of action specifically, and see if it makes sense pharmacologically...dunno...might have to get back to you on this one

(remind me if i dont respond in a day or two, im a bit tardy with things like this, and its late where i am just now )

Golden, sorry lol.
The reason I was curious of the molecular potency of the two cpds is for dosage calculations. Instead of using the trial and error doses I was wondering if you could just match the dosages (much like molar ratios) of HCG to the right ratio of potency to HCG/LH. The purpose of this would be to give greater assurance that you weren't taking supraphysiological doses of HCG DURING your cycle. I was thinking that if this was the case you'd be prone to desensitization. I mean how do we know that 500IU a week is not contributing towards desensitization when 300IU's a week might be the equivilant......

For the second question I actually was looking for the exact chemical mechanism of action. Jenetic posted something damned close if not 'it' but the description wasn't as detailed as what I was looking for.

Thanks bro

 

[GoldenDelicious]

Golden, sorry lol.
The reason I was curious of the molecular potency of the two cpds is for dosage calculations. Instead of using the trial and error doses I was wondering if you could just match the dosages (much like molar ratios) of HCG to the right ratio of potency to HCG/LH. The purpose of this would be to give greater assurance that you weren't taking supraphysiological doses of HCG DURING your cycle. I was thinking that if this was the case you'd be prone to desensitization. I mean how do we know that 500IU a week is not contributing towards desensitization when 300IU's a week might be the equivilant......

i would follow the swale protocol, because he has used a bit of trial and error to arrive at the doses he suggests.

by the way, HCG isnt endogenous to men, so youre supraphysiological no matter waht you do but i get what youre talking about (what, me ballbreaker?)

For the second question I actually was looking for the exact chemical mechanism of action. Jenetic posted something damned close if not 'it' but the description wasn't as detailed as what I was looking for.

Thanks bro

i looked for it once, didnt find it. granted i could ahve tried harder

 

[ocisbomb]

I've been waiting for this thread. Awesome.

 

[Mavy]

mavy, id probably go off what swale says. he sees hundreds of patients, some are post cycle/severely supressed, some are mid cycle, he has bloods from all of them with corresponding info on relevant biological markers, he fiddles with their drug regimes intensely, and what i have read of his makes me think that the during cycle HCG regimen is the way to go for the lowest risk, fastest recovery steroid cycle.

the source of the confusion imo is that HCG post cycle will work to some degree, even well...and so youre going to get some people swearing by it. logically though, the during HCG regimen makes more sense, AND is backed up by real world success as per swales practice. more evidence will become available in the near future, since steroid use is becoming more accepted in the case of various wasting diseases, such as AIDS, cancer, post chemotherapy etc and so there will be a few qualified researchers with decent study protocols who should fairly well put this issue to rest.

for now though, i feel that there is a lack of direct, comparitive evidence, and so at best, youre going to get an incomplete reply imo

cheerios

gd, who is this swale character that I always here people talk about? I have heard very conflucting things about this guy, and the general concensus I have heard about the guy is that he is really nothing more than a business man? Is this where you are getting your theories from, or these your own? Can you post his PCT protocol here? Or his during cycle HCG usage protocol? Just curious to see what he has to say. Also, where does he post? And why is there so much 'dis' towards the guy? Some folks on VIP have told me that he had taken info that has been around for years, and started pimping it out as his special recovery theory, and is somehow making quite a bit of cash from it. I am not trying to dis the guy, this is just some of the rumors I have heard from a few people on the subject, maybe you can shed some light.

Cheers,
Mavy

 

[GoldenDelicious]

gd, who is this swale character that I always here people talk about? I have heard very conflucting things about this guy, and the general concensus I have heard about the guy is that he is really nothing more than a business man? Is this where you are getting your theories from, or these your own? Can you post his PCT protocol here? Or his during cycle HCG usage protocol? Just curious to see what he has to say. Also, where does he post? And why is there so much 'dis' towards the guy? Some folks on VIP have told me that he had taken info that has been around for years, and started pimping it out as his special recovery theory, and is somehow making quite a bit of cash from it. I am not trying to dis the guy, this is just some of the rumors I have heard from a few people on the subject, maybe you can shed some light.

Cheers,
Mavy

long story short
hes the guy behind allthingsmale.com, was involved with cutting edge muscle, there was a falling out with mods there, which led to a lot of them talking badly about him

my take on the guy is that he does a really good job. a lot of people think that he is making good money from his dealing with steroid users, but these people dont realise just how much money a specialist makes regardless of who he works with. frankly i think he could do better not dealing with the roiders, and would do well telling them all to F off, and making more money dealing with normal patients coming through the door.

he posts on ology here and there

oh and yes, i was talking about the during cycle hcg use with as needed nolva/clomid, and the timing of nolva/clomid use post cycle, and tapering them off. its simple, but very sound, imo

cheers