Low Testosterone?

[Primordial Performance]

no mis-information was being spread. You wrote an article that said do this cause HCG causes desensitization, do this cause HCG causes desensitization.

Then you posted a study on rats to back it up, I guess now i will have to post a study proving you wrong once again that the action of HCG is specie specific. Not to mention the fact the dosesused on the mice balls were comparitive to 7,500iu's on human balls.

I mean I dont understand why you just dont concede that you thought something at one time and apparently you need to re-think it. Thats all, its really not that big of a deal.

You are telling people to do this and do that based on something that you "think" will happen. its a total crock of shit that you are still trying to pass it off.

wether or not your patients recovered fine or not is not the issue, im willing to bet they could recover better though, especilly if they ran a higher dose of HCG on cycle, and ran an even higher dose up until 4 days before SERM treatment.

I have proven my pont and im done arguing with you, since you have now resorted to " Im just right and thats it, just trust me"

Your backing your entire argument on a single excerpt from Dr. Scally whos position on the matter is not very convincing IMO.

Besides, like Ive already pointed out in the other thread, the 250iu dose is more efficient anyway.

Go ahead and run any dose of hCG you like.

-Eric

 

[THE-DET-OAK]

Your backing your entire argument on a single excerpt from Dr. Scally whos position on the matter is not very convincing IMO.

Besides, like Ive already pointed out in the other thread, the 250iu dose is more efficient anyway.

Go ahead and run any dose of hCG you like.

-Eric

actually no its not sufficient, why dont you ask some guys around here the difference between 250iu E4D and 750-1,000 a week..............I know you dont post here much but i do and i recieve feedback ALL the time.

secondly you are saying im basing my argument on a single post post from scally but you dont even have a single post to back up your theory, not one, instead you have the audacity to tell me " common sense"...................gimme a break

lastly thats not all im basing my argument on, I am basing my argument on the FACT (not assumption) that there are hundreds of studies on males using HCG for testosterone replacement therapy (TRT) and moe than a handful on AAS users, and not 1 single study EVER reported HCG induced desensitization of the leydig cells..................not one.

You do realise that although a study sets out to find one thing, it will report any other findings shown right?

So I dont understand why you dont dig deeper, im sure these guys claiming desensitiation are running all kinds of other shit.

Maybe its prolonged use of AAS that causes desensitization? I dont know but I know one thing for sure, its NOT HCG

 

[THE-DET-OAK]

There ae plenty of studies showing that T DOES NOT level off, ive seen them. Im not diggin them up though.....................Ive done enough to prove my point.

 

[THE-DET-OAK]

Maybe this from Scally will finally convince you.

I am appreciative of the qualifications of my posts by others so as to not take my writing out of context. But, it is clear from posts that many believe that hCG desensitization occurs at levels over 500 IU. Even though Crisler does qualify his statement as pointed out, the inference is that doses higher than what he advocates will cause desensitization. He is wrong. Further, I find his grasp and understanding of the literature to be wanting. And that is putting it kindly.

hCG desensitization does occur in cases of prolonged administration of 5,000 IU (Five Thousand). But, even here it is not a given and does not occur often and consistently. I am in total agreement with the immediate posts that this problem is almost never observed in clinical practice. Why the continued worry and hype about this problem is beyond me, but possibly Crisler helps feed this false idea.

I also agree with an earlier post in this threads that the two studies mention do nothing to support or demonstrate desensitization or the use of 250 IU X2 as useful therapy. If you really think about it, what is the purpose of the hCG two days in a row. This is totally and completely bizarre. As before, I challenge anyone to provide literature (article or citations) in support of his treatment(s). If Crisler is so sure of himself, why does he not cite support for the therapy or better publish the treatment. I have a simple answer - it is all in his head.

In the spirit of not repeating myself too much, I will repost some of the information from prior posts on this hCG question.

The study referenced, Coviello AD et al., (2005), Low-dose human chorionic gonadotropin maintains intratesticular testosterone in normal men with testosterone-induced gonadotropin suppression, J Clin Endocrinol Metab. 2005 May;90(5) will give some insight to the current hCG regimen that some of the forum members currently use with their TRT!!!

First, this is a study on intratesticular testosterone (ITT). The participants in this study were treated with T enanthate (TE), 200 mg im weekly, for rapid gonadotropin suppression in conjunction with a variable dose of hCG, delivered sc every other day for 3 wk: 0 (saline placebo), 125, 250, or 500 IU hCG. The placebo group served as the control group. [Note: Do you see a difference already! Even though the study does bot support Crisler, the dosing is much different.]

So, what we have are male subjects with elevated T levels due to exogenous T enanthate. Their endogenous production of T is completely suppressed (theoretically) as are their gonadotropins. ITT is suppressed due to the inhibition of gonadotropins from the exogenous T enanthate.

They found that each dose of hCG (125, 250, and 500 IU) returned the ITT concentration to normal. The data set being measured was not serum T, it was ITT. This should alert one to the stupidity of the research design. This was a waste of resources, in my opinion. The very simple reason is that in a normal male with a normal serum T their ITT will be normal. All this study did was take a normal male and replace his T with exogenous T and than give hCG which replaced his LH. Duh

The one saving grace for the study is that it will be instructive to those using low dose hCG with their TRT. It does tell us something about hCG therapy while on TRT. I mentioned above that if one is going to use hCG while on testosterone replacement therapy (TRT) they should have something to observe, measure, and document. Why? If you are taking a drug, any drug, and do not have a dataset to monitor the effect of the drug you need to seriously think about what you are doing. I would ask them when did you decide to relinquish the control of your body?

It would be of interest to look at the data on serum T changes with each hCG dose . The subjects are on T enanthate so this is very similar to those on hCG with TRT. The finding is that the dose of hCG 125 IU every other day had NO effect on the serum T. The two higher doses did raise the serum T levels above normal. [Note: recall the dosing schedule!!!]

There is no individual data (always a cause for suspicion when reviewing literature) and there are no significance levels. Visual inspection of the graph, however, shows that the serum T level was not significantly different from control until day 21. If I was administering hCG less frequently than every other day and had no dataset to monitor I would be concerned.

Posters will do what they wish regardless of the literature. I respect that, particularly if someone feels they are getting a clinical response. I have treated over a 1000 patients for AIH and more for TRT. I did take the effort to research the treatments. And when I did develop a treatment for AIH, I published and presented the findings. I just happen to be skeptical of others who tout therapies based on their experience that has no basis in the literature. Further, they are treating patients as guinea pigs!

The following downloads are for the above article and another studying hCG administration, including "desensitization."

 

[THE-DET-OAK]

More from Scally.

There are many errors in the above analysis. It is far too lengthy to put them in a post. One will demonstrate: a hCG dose of 300 IU will not normalize T serum T. If you are taking this from the ITT article, you are misinterpreting the article.

If i understand the post, the rational for the hCG two days in a row on Friday and Saturday before the Sunday injection is to assist in the lowest part of the week. If you read the literature on hCG effects, they come about 48-72 hours after injection. This schedule dosing is nonsense. I have a better question: produce literature that supports the use in this manner! Instead, we have theoretical and hypothetical baloney. And even that is based on imagined science.

For all practical purposes, hCG Leydig Cell desensitization does not exist within the clinical framework .

Why can I say this with absolute confidence? Because I have treated with success males with AIH, testosterone replacement therapy (TRT), & hypogonadism. As above, this supposed problem is not seen in clinical care. Why do people continue to debate this point? This is a rumor that refuses to die. I wish to thank you for bringing this topic up since many who have been told this falsity will learn from the thread. Thanks.

 

[Primordial Performance]

actually no its not sufficient, why dont you ask some guys around here the difference between 250iu E4D and 750-1,000 a week..............I know you dont post here much but i do and i recieve feedback ALL the time.

I said efficient. Do you know what efficient means?

secondly you are saying im basing my argument on a single post post from scally but you dont even have a single post to back up your theory, not one, instead you have the audacity to tell me " common sense"...................gimme a break

Here, Ill post a single reference, again - http://www.steroidology.com/forum/2751687-post37.html

lastly thats not all im basing my argument on, I am basing my argument on the FACT (not assumption) that there are hundreds of studies on males using HCG for trt and moe than a handful on AAS users, and not 1 single study EVER reported HCG induced desensitization of the leydig cells..................not one.

Thats actually not true, but there are a bunch of studies on acute hCG treatment for hypogonadism and infertility, in an attempt to correct the disorder -- but this lends very little insight into the long-term desensitization caused by hCG -- which like I said, is seen in real world clinical practice when individuals mistakenly use hCG for TRT.

You do realise that although a study sets out to find one thing, it will report any other findings shown right?

So I dont understand why you dont dig deeper, im sure these guys claiming desensitiation are running all kinds of other shit.

Maybe its prolonged use of AAS that causes desensitization? I dont know but I know one thing for sure, its NOT HCG

Yes, prolonged AAS use causes desensitization as does over stimulation. This is true for LH, hCG, GHRH or any gonadotropin for that reason -- and there is a ton of research on down-regulation on these hormones to their target organs after over exposure. To assume that this doesnt apply to hCG and the testes would be silly.

-Eric

 

[THE-DET-OAK]

More from Scally.

I was hoping to obtain the full-text document, but no luck. If anyone has it, either post of forward. This article from 1982 does not show hCG desensitization. In fact, the article states, These data indicate that continuous long term hCG administration stimulated T levels in HH. The only note for partial desensitization is a delayed "kinetic" response to hCG administration from 24 to 48 hours! It is also of interest this was over 23 months, almost 2 years with a three times per week schedule. This is a long time, yet they state the above there continued to be T production. It would be nice to know what the hCG concentration is at this schedule after almost 2 years. The following abstract that used an every 6 day schedule over a year found a consistent T production. Moreover they note that maximal T production occurs 58 hours after injection.


D'Agata R, Vicari E, Aliffi A, Maugeri G, Mongiol A, Gulizia S. Testicular Responsiveness to Chronic Human Chorionic Gonadotropin Administration in Hypogonadotropic Hypogonadism. J Clin Endocrinol Metab 1982;55(1):76-80.

Steroidogenic responsiveness to long term hCG administration (1500 U three times a week for 23 months) was characterized in 8 males with hypogonadotropic hypogonadism (HH). During hCG treatment, testosterone (T), which was in the prepuberal range under basal conditions, rose considerably to the upper end of the normal range and remained at that level during the 23 months of observation. A 2.5-fold increase was observed in serum levels of 17{beta}-estradiol (E2) an increment less than seen with T. The increment in 17{alpha}-hydroxyprogesterone was also lower than that in T throughout the study; thus, the 17{alpha}-hydroxyprogesterone to T ratio, despite continuous hCG administration, remained low. Serum androstenedione was slightly increased during hCG therapy. No significant changes were observed in serum levels of dehydroepiandrosterone. These data indicate that continuous long term hCG administration stimulated T levels in HH, with a relatively small change in E2. The kinetics of the T and E2 responses to 2000 U hCG, evaluated after 23 months of therapy, indicated that the testicular response was markedly reduced. No increment in T levels was observed at 24 h; the maximal response occurred at 48 h. This pattern of T response supports the idea that partial testicular desensitization occurs in HH patients receiving chronic treatment with hCG.


Balducci R, Toscano V, Casilli D, Maroder M, Sciarra F, Boscherini B. Testicular responsiveness following chronic administration of hCG (1500 IU every six days) in untreated hypogonadotropic hypogonadism. Horm Metab Res 1987;19(5):216-21.

The observation that the testosterone (T) response to a single intramuscular injection of hCG is prolonged suggests that currently used regimens (2-3 injections per week) to stimulate endogenous androgen secretion in hypogonadotropic hypogonadism (HH) patients have to be reassessed. Moreover, during the last few years, Leydig cell steroidogenic desensitization has been found after massive doses of hCG. The aim of the present investigation, carried out in 6 HH patients who showed no signs of puberty, was to study the effect of 1500 IU hCG administered every six days over a period of one year to induce the onset of pubertal development. To evaluate the kinetics of the response of T, 17 alpha-hydroxyprogesterone (17 alpha-OHP) and 17 beta-oestradiol (E2), blood samples were taken basally and 1, 2, 4 and 6 days after drug injection. This dynamic study was performed after the first injection and after the 4th and 12th month of treatment. During this one year time period, a progressive increase in testicular size was observed. Comparing plasma T levels (mean +/- SE) before the first injection (11.2 +/- 4.7 ng/dl) with the corresponding values at the 4th (38.7 +/- 10.5 ng/dl) and 12th months (99.5 +/- 19.9 ng/dl) of therapy, a progressive and significant increase was observed. T reached a maximum elevation 58 hours after hCG injection at the 4th month (198.3 +/- 42 ng/dl; P less than 0.01) and at the 12th month (415.6 +/- 62.6 ng/dl; P less than 0.05), whereas it remained unchanged following the first hCG injection.(

 

[THE-DET-OAK]

More from Scally.

Another thread brought to mind a study on hCG and body composition (and other factors). [ Hypogonadism / Wanna do Steroids - PLEASE HELP! ] In that study, hCG was given at 5,000 IU twice weekly. In a similar doing study following, the T level increased. The dose of 5,000 IU is above what I recommend and what I see in use. I hope the myth of hCG desensitization can be laid to rest, but I know many will continue to hold onto this fairy tale.


Liu, PY, SM Wishart, DS Celermajer, et al., Do reproductive hormones modify insulin sensitivity and metabolism in older men? A randomized, placebo-controlled clinical trial of recombinant human chorionic gonadotropin. Eur J Endocrinol, 2003. 148(1): p. 55-66.

OBJECTIVE: In order to assess the hormonal determinants of insulin sensitivity and related components of the metabolic syndrome, we evaluated the effect of subcutaneous recombinant human chorionic gonadotropin (r-hCG; Ovidrel) on insulin sensitivity, vascular reactivity, leptin, insulin-like growth factor-I (IGF-I) and lipids in ambulant, community dwelling men >60 Years of age with serum testosterone <or= 15 nmol/l on two occasions. DESIGN: Forty eligible men were randomized to receive 250 microg (5000 IU) r-hCG subcutaneously twice each week (n=20) or placebo (n=20) injections for 3 Months, and all subjects (mean age 67 (range 60-85) Years) completed the study.

METHODS AND RESULTS: Groups were well matched for height, weight, anthropometry and insulin sensitivity. Insulin sensitivity was assessed by homeostasis model (HOMA) and euglycemic hyperinsulinemic clamp at baseline and at the end of the treatment period in the first 30 men who did not have diabetes mellitus. Insulin sensitivity (HOMA and euglycemic clamp) or beta cell function (HOMA) were not significantly changed by r-hCG despite a significant increase in lean body mass (approximately 2 kg, P<0.001) and reduced fat mass (approximately 1 kg, P<0.05). Subcutaneous fat (skinfold measurements), abdominal girth and serum leptin all decreased and IGF-I tended to increase, but these changes were not significant. Recombinant hCG significantly reduced total and low density lipoprotein cholesterol, and triglycerides, but did not significantly alter high density lipoprotein cholesterol. Endothelial function (vascular reactivity) was not significantly worsened. We conclude that three-Months of treatment with r-hCG demonstrates expected hormonal effects, improved lipids and did not worsen vascular endothelial function. Insulin sensitivity was not altered despite suggestive changes in body composition.

CONCLUSIONS: These findings suggest short-term metabolic and cardiovascular safety and argue against an important role for androgens in the hormonal control of insulin sensitivity in older men.

 

[THE-DET-OAK]

I said efficient. Do you know what efficient means?



Here, Ill post a single reference, again - http://www.steroidology.com/forum/2751687-post37.html



Thats actually not true, but there are a bunch of studies on acute hCG treatment for hypogonadism and infertility, in an attempt to correct the disorder -- but this lends very little insight into the long-term desensitization caused by hCG -- which like I said, is seen in real world clinical practice when individuals mistakenly use hCG for TRT.



Yes, prolonged AAS use causes desensitization as does over stimulation. This is true for LH, hCG, GHRH or any gonadotropin for that reason -- and there is a ton of research on down-regulation on these hormones to their target organs after over exposure. To assume that this doesnt apply to hCG and the testes would be silly.

-Eric

Hey man your little study is on of the studies Scally has debunked, I posted it in this thread for you............................................................try again please............................

 

[THE-DET-OAK]

Thats actually not true, but there are a bunch of studies on acute hCG treatment for hypogonadism and infertility, in an attempt to correct the disorder -- but this lends very little insight into the long-term desensitization caused by hCG -- which like I said, is seen in real world clinical practice when individuals mistakenly use hCG for TRT.



-Eric

Dear sir I have posted every single study you could possibly be blindly referencing in this thread, Scally has debunkd every single one of them.....................................thanks

 

[Primordial Performance]

There are many errors in the above analysis. It is far too lengthy to put them in a post. One will demonstrate: a hCG dose of 300 IU will not normalize T serum T. If you are taking this from the ITT article, you are misinterpreting the article.

If i understand the post, the rational for the hCG two days in a row on Friday and Saturday before the Sunday injection is to assist in the lowest part of the week. If you read the literature on hCG effects, they come about 48-72 hours after injection. This schedule dosing is nonsense. I have a better question: produce literature that supports the use in this manner! Instead, we have theoretical and hypothetical baloney. And even that is based on imagined science.

For all practical purposes, hCG Leydig Cell desensitization does not exist within the clinical framework .

Why can I say this with absolute confidence? Because I have treated with success males with AIH, testosterone replacement therapy (TRT), & hypogonadism. As above, this supposed problem is not seen in clinical care. Why do people continue to debate this point? This is a rumor that refuses to die. I wish to thank you for bringing this topic up since many who have been told this falsity will learn from the thread. Thanks.

Im not sure if these posts are your words or Scally's or what... but I think this "no desensitizing theory" is a one man theory here... It just doesnt agree with common endocrinology no matter how much you continue to repeat it.

-Eric

 

[THE-DET-OAK]

I said efficient. Do you know what efficient means?

-Eric

a hCG dose of 300 IU will not normalize T serum T. If you are taking this from the ITT article, you are misinterpreting the article..

I wanted to highlight this for you since you are getting the information of your dosing protocol from the reference he is refering to here.......................................

 

[THE-DET-OAK]

Im not sure if these posts are your words or Scally's or what... but I think this "no desensitizing theory" is a one man theory here... It just doesnt agree with common endocrinology no matter how much you continue to repeat it.

-Eric

They are his words just like i put in the title.............you keep making up excuses but for some reason every explaination you give has been thouroughly debunked by this man....................so please give it a rest.

every study you have cited to back up yor theory is in this thread and is completely torn to shreds by this man, maybe you should read his explaination of why your references are full of falsehoods before you respond.......................

 

[Primordial Performance]

I was hoping to obtain the full-text document, but no luck. If anyone has it, either post of forward. This article from 1982 does not show hCG desensitization. In fact, the article states, ***8221;These data indicate that continuous long term hCG administration stimulated T levels in HH.***8221; The only note for ***8220;partial desensitization***8221; is a delayed "kinetic" response to hCG administration from 24 to 48 hours! It is also of interest this was over 23 months, almost 2 years with a three times per week schedule. This is a long time, yet they state the above ***8211; there continued to be T production. It would be nice to know what the hCG concentration is at this schedule after almost 2 years. The following abstract that used an every 6 day schedule over a year found a consistent T production. Moreover they note that maximal T production occurs 58 hours after injection.


D'Agata R, Vicari E, Aliffi A, Maugeri G, Mongiol A, Gulizia S. Testicular Responsiveness to Chronic Human Chorionic Gonadotropin Administration in Hypogonadotropic Hypogonadism. J Clin Endocrinol Metab 1982;55(1):76-80.

Steroidogenic responsiveness to long term hCG administration (1500 U three times a week for 23 months) was characterized in 8 males with hypogonadotropic hypogonadism (HH). During hCG treatment, testosterone (T), which was in the prepuberal range under basal conditions, rose considerably to the upper end of the normal range and remained at that level during the 23 months of observation. A 2.5-fold increase was observed in serum levels of 17{beta}-estradiol (E2) an increment less than seen with T. The increment in 17{alpha}-hydroxyprogesterone was also lower than that in T throughout the study; thus, the 17{alpha}-hydroxyprogesterone to T ratio, despite continuous hCG administration, remained low. Serum androstenedione was slightly increased during hCG therapy. No significant changes were observed in serum levels of dehydroepiandrosterone. These data indicate that continuous long term hCG administration stimulated T levels in HH, with a relatively small change in E2. The kinetics of the T and E2 responses to 2000 U hCG, evaluated after 23 months of therapy, indicated that the testicular response was markedly reduced. No increment in T levels was observed at 24 h; the maximal response occurred at 48 h. This pattern of T response supports the idea that partial testicular desensitization occurs in HH patients receiving chronic treatment with hCG.


Balducci R, Toscano V, Casilli D, Maroder M, Sciarra F, Boscherini B. Testicular responsiveness following chronic administration of hCG (1500 IU every six days) in untreated hypogonadotropic hypogonadism. Horm Metab Res 1987;19(5):216-21.

The observation that the testosterone (T) response to a single intramuscular injection of hCG is prolonged suggests that currently used regimens (2-3 injections per week) to stimulate endogenous androgen secretion in hypogonadotropic hypogonadism (HH) patients have to be reassessed. Moreover, during the last few years, Leydig cell steroidogenic desensitization has been found after massive doses of hCG. The aim of the present investigation, carried out in 6 HH patients who showed no signs of puberty, was to study the effect of 1500 IU hCG administered every six days over a period of one year to induce the onset of pubertal development. To evaluate the kinetics of the response of T, 17 alpha-hydroxyprogesterone (17 alpha-OHP) and 17 beta-oestradiol (E2), blood samples were taken basally and 1, 2, 4 and 6 days after drug injection. This dynamic study was performed after the first injection and after the 4th and 12th month of treatment. During this one year time period, a progressive increase in testicular size was observed. Comparing plasma T levels (mean +/- SE) before the first injection (11.2 +/- 4.7 ng/dl) with the corresponding values at the 4th (38.7 +/- 10.5 ng/dl) and 12th months (99.5 +/- 19.9 ng/dl) of therapy, a progressive and significant increase was observed. T reached a maximum elevation 58 hours after hCG injection at the 4th month (198.3 +/- 42 ng/dl; P less than 0.01) and at the 12th month (415.6 +/- 62.6 ng/dl; P less than 0.05), whereas it remained unchanged following the first hCG injection.(

oh boy... here come the hoards of copy n pastes... what a compelling argument.

Good luck on this guys...

 

[THE-DET-OAK]

In fact, the article states, These data indicate that continuous long term hCG administration stimulated T levels in HH. The only note for partial desensitization is a delayed "kinetic" response to hCG administration from 24 to 48 hours!(

thought you might find this highlighted nugget of interest, since it comletely goes against every single thing you are claiming. the study to back the statement up is in the original post.......................

 

[THE-DET-OAK]

yes sir i will copy/paste it all here for you, since you are obviously too lazy to look it up yourself, like i have already done numerous times................................

 

[Primordial Performance]

They are his words just like i put in the title.............you keep making up excuses but for some reason every explaination you give has been thouroughly debunked by this man....................so please give it a rest.

every study you have cited to back up yor theory is in this thread and is completely torn to shreds by this man, maybe you should read his explaination of why your references are full of falsehoods before you respond.......................

dude, you just ruined this thread...

ugh...

 

[THE-DET-OAK]

im just sick of arguing with someone who is trying to pull a fast one. I dont know hat your motives are but i have posted ample eveidence to call bullshit.

Im sorry im not as smart as Scally, I dont pretend to be. I have read these posting so many times i could prolly repeat them myself, and no matter how hard i tried he was right. I argued with him for a week over this shit......................it doesnt happen. its a myth.

 

[Primordial Performance]

Its official...

THE DET OAK wins by posting enough erroneous copy n paste shit to dilute out all sound reasoning and debate.

See you all later...

 

[THE-DET-OAK]

You can say I ruined the thread, there is so much valuble info in here its not even funny. His interpretations of the citations are way more important than the study itself. I think thats where your wrong, your interpretations are incorrect.

Not just valubale info either, studies and arguments proving you wrong.....................