How does 125IU of HCG ED affect hormones production while on TRT?

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Gianluca

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I have read the two case studies presented by Dr. Saya on HCG 150IU and 500IU, I understand how the two differ in terms of peak, and half life levels in the blood.

Do we have any data, perhaps anecdotal, of what can we expect in regards to Testosterone, Estrogen and Pregnenolone production, considering a small daily dose of HCG, vs a less frequent but higher dose? is perhaps a small daily dose, best for achieving higher Pregnenolone levels, and prevent testicles shrinkage only, when higher HCG dose may eventually boost Testosterone and Estrogen while on TRT? I understand this can be subjective as well as anything else
 
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I have read the two case studies presented by Dr. Saya on HCG 150IU and 500IU, I understand how the two differ in terms of peak, and half life levels in the blood.

Do we have any data, perhaps anecdotal, of what can we expect in regards to Testosterone, Estrogen and Pregnenolone production, considering a small daily dose of HCG, vs a less frequent but higher dose? is perhaps a small daily dose, best for achieving higher Pregnenolone levels, and prevent testicles shrinkage only, when higher HCG dose may eventually boost Testosterone and Estrogen while on TRT? I understand this can be subjective as well as anything else



Higher doses of hCG would have a greater impact on T, e2, and upstream hormones.





Dose-Dependant Increase in Intratesticulaar Testosterone by Very Low-Dose Human Chorionic Gonadotropin in Normal Men with Experimental Gonadotropin Deficiency

*Prior studies have shown that serum 17-hydroxyprogesterone, which is secreted by the testes in high concentrations, is a good correlate of IT-T (20, 21). However, in our study 17-hydroxyprogesterone was not significantly correlated with IT-T. This difference is likely due to the significantly lower IT-T concentrations induced in this study by the lower doses of hCG used.





------------------------------------------------------------------------------------------------------
Serum 17-hydroxyprogesterone strongly correlates with intratesticular testosterone in gonadotropinsuppressed normal men receiving various dosages of human chorionic gonadotropin (2008)



Previous work investigating the response of the testis to hCG has demonstrated that serum concentrations of T precursors such as 17-hydroxyprogesterone (17OH-P), androstenedione (A), and DHEA are increased by hCG administration (16). Therefore, we hypothesized that serum concentrations of these T precursors might correlate with ITT and potentially provide a serum biomarker of ITT and Leydig cell function.


Result(s): With T administration alone, serum 17OH-P decreased significantly and increased significantly when 500 IU hCG was administered. End-of-treatment ITT strongly correlated with serum 17OH-P. Moreover, serum 17OH-P, but not androstenedione or DHEA, was independently associated with end-of-treatment ITT by multivariate linear regression


DISCUSSION

In the present work, we demonstrated a significant association between serum concentrations of 17OH-P and ITT in men receiving TE and various dosages of hCG. Serum 17OH-P decreased by roughly 60% in men receiving placebo, whereas it increased by 70% in men at the highest dose (500 IU) of hCG. Although 17OH-P did not correlate with ITT at baseline, it was very strongly correlated with ITT on treatment, both when absolute concentration and when the change from baseline was taken into account. Moreover, end-of-treatment concentrations of serum 17OH-P were significantly associated with ITT after correction for other variables using linear regression. Although the overall correlation between ITT and serum 17OH-P was strong, in the lowest-dose hCG group the ITT increased much more than the serum 17OH-P. This implies that serum 17OH-P might not be as sensitive to changes in ITT mediated by lower levels of hCG stimulation as it is to the larger increases in ITT stimulated by higher doses of hCG.


Most of the circulating 17OH-P in men is likely of testicular and not adrenal origin. Orchiectomy reduces circulating levels of 17OH-P by approximately 70% (19, 20), a reduction very similar to that seen in our group of subjects receiving exogenous T and placebo (and therefore having little circulating LH activity). Therefore, roughly 30% of circulating 17OH-P is likely of nontesticular, presumably adrenal, origin. The testicular secretion of 17OH-P is known to be second only to that of T, with T accounting for 70% of steroid output and 17OH-P accounting for 20% (21).


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When I tried TRT with hCG at different doses, I found no benefit to 100iu every day. It had no effect on testicle size at all. Only 375iu-500iu hCG was able to restore testicular volume. 500iu twice a week caused too much estrogen conversion, so I settled on 375iu twice per week.
 
Higher doses of hCG would have a greater impact on T, e2, and upstream hormones.





Dose-Dependant Increase in Intratesticulaar Testosterone by Very Low-Dose Human Chorionic Gonadotropin in Normal Men with Experimental Gonadotropin Deficiency

*Prior studies have shown that serum 17-hydroxyprogesterone, which is secreted by the testes in high concentrations, is a good correlate of IT-T (20, 21). However, in our study 17-hydroxyprogesterone was not significantly correlated with IT-T. This difference is likely due to the significantly lower IT-T concentrations induced in this study by the lower doses of hCG used.





------------------------------------------------------------------------------------------------------
Serum 17-hydroxyprogesterone strongly correlates with intratesticular testosterone in gonadotropinsuppressed normal men receiving various dosages of human chorionic gonadotropin (2008)



Previous work investigating the response of the testis to hCG has demonstrated that serum concentrations of T precursors such as 17-hydroxyprogesterone (17OH-P), androstenedione (A), and DHEA are increased by hCG administration (16). Therefore, we hypothesized that serum concentrations of these T precursors might correlate with ITT and potentially provide a serum biomarker of ITT and Leydig cell function.


Result(s): With T administration alone, serum 17OH-P decreased significantly and increased significantly when 500 IU hCG was administered. End-of-treatment ITT strongly correlated with serum 17OH-P. Moreover, serum 17OH-P, but not androstenedione or DHEA, was independently associated with end-of-treatment ITT by multivariate linear regression


DISCUSSION

In the present work, we demonstrated a significant association between serum concentrations of 17OH-P and ITT in men receiving TE and various dosages of hCG. Serum 17OH-P decreased by roughly 60% in men receiving placebo, whereas it increased by 70% in men at the highest dose (500 IU) of hCG. Although 17OH-P did not correlate with ITT at baseline, it was very strongly correlated with ITT on treatment, both when absolute concentration and when the change from baseline was taken into account. Moreover, end-of-treatment concentrations of serum 17OH-P were significantly associated with ITT after correction for other variables using linear regression. Although the overall correlation between ITT and serum 17OH-P was strong, in the lowest-dose hCG group the ITT increased much more than the serum 17OH-P. This implies that serum 17OH-P might not be as sensitive to changes in ITT mediated by lower levels of hCG stimulation as it is to the larger increases in ITT stimulated by higher doses of hCG.


Most of the circulating 17OH-P in men is likely of testicular and not adrenal origin. Orchiectomy reduces circulating levels of 17OH-P by approximately 70% (19, 20), a reduction very similar to that seen in our group of subjects receiving exogenous T and placebo (and therefore having little circulating LH activity). Therefore, roughly 30% of circulating 17OH-P is likely of nontesticular, presumably adrenal, origin. The testicular secretion of 17OH-P is known to be second only to that of T, with T accounting for 70% of steroid output and 17OH-P accounting for 20% (21).


View attachment 11094

thank you for the material!
 


Low-dose hCG can prevent sterility in men prescribed testosterone (2019)

The estimated male population in their reproductive years is about 52 million in the United States, with the age of first-time fathers rising, and about 2.5 million of those men are estimated to have low testosterone, Larry I. Lipshultz, MD, a professor of urology and chief of the division of male reproductive medicine and surgery at Baylor College of Medicine in Houston, said during a presentation. Intratesticular testosterone — typically 50 to 100 times higher than serum testosterone levels — is a prerequisite for normal sperm production in men; however, exogenous testosterone prescribed to men with hypogonadism suppresses the intratesticular testosterone level, impairing fertility.

“When one introduces exogenous testosterone, whether it is topical or injectable, what we see is [gonadotropin-releasing hormone] is turned off, gonadotropins decrease, and we see a corresponding decrease in testosterone within the testes and an associated turnoff of sperm production,” Lipshultz said. “A lot of what we know about this phenomenon comes from previous studies in male contraception using testosterone.”




In a study published in 2005 in The Journal of Clinical Endocrinology & Metabolism, Andrea D. Coviello, MD, a reproductive endocrinologist and practicing clinician and researcher at Boston University School of Medicine, and colleagues analyzed data from 29 men with normal reproductive physiology randomly assigned to 200 mg testosterone enanthate weekly in combination with saline placebo or 125 IU, 250 IU or 500 IU hCG every other day for 3 weeks. The researchers found that intratesticular testosterone increased linearly with increasing hCG dose, demonstrating that a relatively low dose of hCG maintains intratesticular testosterone within the normal range in healthy men with gonadotropin suppression,
Lipshultz said.

“Without any hCG replacement ... there was literally no intratesticular testosterone, and then as hCG was given in a stepwise fashion, once it reached about 500 U, you were back to baseline [level],” Lipshultz said. “Using this data, and realizing that despite very high doses of testosterone, there were high levels of intratesticular testosterone maintained with low-dose hCG, we then asked whether this low-dose maintenance could also protect spermatogenesis during testosterone treatment.”




If the man desires a future pregnancy, the clinician should prescribe hCG concurrent with testosterone therapy, typically at 500 U subcutaneous three times per week or 1,500 U once weekly if the patient wishes only to prevent testicular atrophy.
The patient should cycle off of testosterone twice yearly, at a rate of 3,000 U three times per week for 4 weeks, adding 25 mg daily clomiphene therapy during that period, Lipshultz said. However, for men desiring a pregnancy, 3,000 U hCG three times per week should be prescribed in addition to clomiphene therapy. Clinicians should check the patient’s follicle-stimulating hormone (FSH) level and conduct a semen analysis after 4 months for men desiring pregnancy; if the FSH level is not sufficiently elevated, the clinician should discontinue clomiphene and instead introduce FSH concurrent with the hCG, he said.
 



Low-dose hCG can prevent sterility in men prescribed testosterone (2019)


The estimated male population in their reproductive years is about 52 million in the United States, with the age of first-time fathers rising, and about 2.5 million of those men are estimated to have low testosterone, Larry I. Lipshultz, MD, a professor of urology and chief of the division of male reproductive medicine and surgery at Baylor College of Medicine in Houston, said during a presentation. Intratesticular testosterone — typically 50 to 100 times higher than serum testosterone levels — is a prerequisite for normal sperm production in men; however, exogenous testosterone prescribed to men with hypogonadism suppresses the intratesticular testosterone level, impairing fertility.

“When one introduces exogenous testosterone, whether it is topical or injectable, what we see is [gonadotropin-releasing hormone] is turned off, gonadotropins decrease, and we see a corresponding decrease in testosterone within the testes and an associated turnoff of sperm production,”
Lipshultz said. “A lot of what we know about this phenomenon comes from previous studies in male contraception using testosterone.”



In a study published in 2005 in The Journal of Clinical Endocrinology & Metabolism, Andrea D. Coviello, MD, a reproductive endocrinologist and practicing clinician and researcher at Boston University School of Medicine, and colleagues analyzed data from 29 men with normal reproductive physiology randomly assigned to 200 mg testosterone enanthate weekly in combination with saline placebo or 125 IU, 250 IU or 500 IU hCG every other day for 3 weeks. The researchers found that intratesticular testosterone increased linearly with increasing hCG dose, demonstrating that a relatively low dose of hCG maintains intratesticular testosterone within the normal range in healthy men with gonadotropin suppression, Lipshultz said.

“Without any hCG replacement ... there was literally no intratesticular testosterone, and then as hCG was given in a stepwise fashion, once it reached about 500 U, you were back to baseline [level],” Lipshultz said. “Using this data, and realizing that despite very high doses of testosterone, there were high levels of intratesticular testosterone maintained with low-dose hCG, we then asked whether this low-dose maintenance could also protect spermatogenesis during testosterone treatment.”




If the man desires a future pregnancy, the clinician should prescribe hCG concurrent with testosterone therapy, typically at 500 U subcutaneous three times per week or 1,500 U once weekly if the patient wishes only to prevent testicular atrophy. The patient should cycle off of testosterone twice yearly, at a rate of 3,000 U three times per week for 4 weeks, adding 25 mg daily clomiphene therapy during that period, Lipshultz said. However, for men desiring a pregnancy, 3,000 U hCG three times per week should be prescribed in addition to clomiphene therapy. Clinicians should check the patient’s follicle-stimulating hormone (FSH) level and conduct a semen analysis after 4 months for men desiring pregnancy; if the FSH level is not sufficiently elevated, the clinician should discontinue clomiphene and instead introduce FSH concurrent with the hCG, he said.

excellent, I stopped HCG about a year an half ago, and I'm resuming a 125IU daily, see how that goes now
 
125 IU daily will not accomplish much. No upstream hormone increases, no 17-OH progesterone increase enough to normalize sperm, no testicular volume improvement. Not my opinion but that is what everyone on this thread is trying to convey.
hCG has a long half life (3 days) and higher doses are needed for all of the above benefits. 350-500 IU twice per week is minimum.
 
125 IU daily will not accomplish much. No upstream hormone increases, no 17-OH progesterone increase enough to normalize sperm, no testicular volume improvement. Not my opinion but that is what everyone on this thread is trying to convey.
hCG has a long half life (3 days) and higher doses are needed for all of the above benefits. 350-500 IU twice per week is minimum.

Why do you think Crisler recommended 100iu hCG per day?
 
Why do you think Crisler recommended 100iu hCG per day?
Crisler was wrong. He assumed that hCG is the same as LH. He forgot that once you introduce TRT and consider hCG’s longer half life, higher & less frequent doses are needed. If you read the two small studies that measured 17-OH progesterone you will understand. Crisler equated LH production in the absence of TRT as 100 IU of hCG.
Crisler was right about one thing that no one saw before him: that hCG can reactivate upstream hormone production. I give him full credit for that. He also really was one of the first that advocated for subcutaneous injections.
i miss him since we were able to argue about a topic and still be friends. Very hard to find someone like him anymore.
 
I've been speculating similarly about testosterone: What if peak levels of LH are important, independent of average levels? This would explain why such relatively high doses of hCG are needed to get the effects we want, which in turn increase the risk of side effects. Very crudely, at least, the numbers may reconcile. It's claimed that on a per-IU basis, hCG is six to eight times more potent than LH. Dr. Saya's case study on hCG suggests a response area-under-the-curve (AUC) of ~6 mIU/mL*days for a 500 IU injection. One study showed normal intratesticular testosterone would be achieved with injections of 300 IU every other day. This would translate to average serum levels of 1.8 mIU/mL. Applying a factor of six or so is supposed to give an LH equivalent—10.8 mIU/mL. And this figure corresponds pretty well with peak LH values reported in this work. It's pretty tenuous evidence, and much more would be needed to say if the idea really has merit.
 
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125 IU daily will not accomplish much. No upstream hormone increases, no 17-OH progesterone increase enough to normalize sperm, no testicular volume improvement. Not my opinion but that is what everyone on this thread is trying to convey.
hCG has a long half life (3 days) and higher doses are needed for all of the above benefits. 350-500 IU twice per week is minimum.

if I understand well the studies, 125IU of HCG still do a little something though, much less then 500IU, and I'm realizing probably not enough. My personal anecdotal throughout the years, is that I do remember when I was on 350IU HCG 3 x week, I had full and better then before testicle fullness, better erections, sensitivity and maybe mood, but quiet unstable because of it, not sure about 17-OH Progesterone then. I also tried the 125IU daily HCG with Dr Crisler, and I don't think it fully worked to restore testicles sides, maybe a little, not quiet remember then what 125IU daily was doing for me. But for sure, I remember testing 17-OH Progesterone, and that was low. Because of that test result, I have attributed HCG not useful to restore Upstream hormones, and decided to think about Pregnenolone supplementation, which worked well.

I guess you guys are right, it looks like lower doses of HCG may not be worth. still, I want to give two weeks trial of 125IU daily again, this time paying more attention to what happens
 
been prescribed HCG 300 IU x 3 a week from early beginning

since starting always had either back acne or back redness

stopped HCG completely thinking it would reduce E2 and inflammation would go away

inflammation disappeared eventually

took 500 HCG once, back started getting some tiny non-red pimples within couple days

funny thing, after a year without HCG the E2 levels didn't drop (35), but inflammation is gone

I'm thinking to reintroduce HCG, 2020 without HCG I felt kinda depressed all the time, slow, daytime sleepy even after two weeks away from caffeine. Although my test cyp intake was only 34mg x 3 a week. All higher levels (44mg, 40mg) were done only along with HCG.
 
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been prescribed HCG 300 IU x 3 a week from early beginning

since starting always had either back acne or back redness

stopped HCG completely thinking it would reduce E2 and inflammation would go away

inflammation disappeared eventually

took 500 HCG once, back started getting some tiny non-red pimples within couple days

funny thing, after a year without HCG the E2 levels didn't drop (35), but inflammation is gone

I'm thinking to reintroduce HCG, 2020 without HCG I felt kinda depressed all the time, slow, daytime sleepy even after two weeks away from caffeine. Although my test cyp intake was only 34mg x 3 a week. All higher levels (44mg, 40mg) were done only along with HCG.

how do you determine inflammation? did you run some inflammation marker test, or you assuming the skin redness is inflammation?
 
how do you determine inflammation? did you run some inflammation marker test, or you assuming the skin redness is inflammation?

before TRT I had perfect back skin all my life I believe, never much facial acne.

I only ever had CRP, which was within normal range. Yes, was assuming skin redness which was never on my back before was due to elevated estrogen (elevated due to HCG or high total t / free t). Looks like it's HCG related, E2 still elevated (E2 = 35, I started TRT because of low E2 <5) after a year of no TRT and low dose test cyp: 34mg x TIW or 51mg twice a week
 
before TRT I had perfect back skin all my life I believe, never much facial acne.

I only ever had CRP, which was within normal range. Yes, was assuming skin redness which was never on my back before was due to elevated estrogen (elevated due to HCG or high total t / free t). Looks like it's HCG related, E2 still elevated (E2 = 35, I started TRT because of low E2 <5) after a year of no TRT and low dose test cyp: 34mg x TIW or 51mg twice a week

got it, possibly some extra DHT being produced or just a reaction to it
 
Good evening my friends, greetings from Brazil.
I have been doing research on HCG for a week and it is very difficult to find anything concrete. Dosages differ widely.
My biggest concern is keeping the cascade of hormones, produced by lh, active (pregnenolone, dhea and etc.)
I read several reports of well being and etc and I really want to feel it
I am currently using TRT cypio 150mg 2x week (75mg per application)
Reading Dr. Crysler's protocol, there is guidance and applying HCG two days before the application of testosterone, therefore, I am thinking of making two applications of 250UI of HCG, always one day before the application of testosterone.
I read many reports about HCG increasing total testosterone, is that really true? If so, I will be required to decrease the dose of my testo injection.
Could you help me with some suggestions?
Thank you.
 
Good evening my friends, greetings from Brazil.
I have been doing research on HCG for a week and it is very difficult to find anything concrete. Dosages differ widely.
My biggest concern is keeping the cascade of hormones, produced by lh, active (pregnenolone, dhea and etc.)
I read several reports of well being and etc and I really want to feel it
I am currently using TRT cypio 150mg 2x week (75mg per application)
Reading Dr. Crysler's protocol, there is guidance and applying HCG two days before the application of testosterone, therefore, I am thinking of making two applications of 250UI of HCG, always one day before the application of testosterone.
I read many reports about HCG increasing total testosterone, is that really true? If so, I will be required to decrease the dose of my testo injection.
Could you help me with some suggestions?
Thank you.
There's a lot of individual variation in response to hCG, so you will need to do some experimenting. Generally guys are adding from 500-1,500 IU per week to a TRT protocol. Your proposed starting point of 250 IU twice weekly is fine. Don't worry about the particular days—as long as they are spread out and at least twice a week; if it's convenient to inject it with your testosterone then do so.

If you are younger then you have a better chance of seeing improvements in hormones such as progesterone that are otherwise suppressed by TRT. But many men, and especially older ones, may not see any bump in these and should consider direct supplementation. Be prepared to monitor the hormone levels. This general rule applies to testosterone as well. Some men do see significant endogenous production even at lower hCG doses. But more typical would be 100 ng/dL of extra testosterone or less.
 
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There's a lot of individual variation in response to hCG, so you will need to do some experimenting. Generally guys are adding from 500-1,500 IU per week to a TRT protocol. Your proposed starting point of 250 IU twice weekly is fine. Don't worry about the particular days—as long as they are spread out and at least twice a week; if it's convenient to inject it with your testosterone then do so.

If you are younger then you have a better chance of seeing improvements in hormones such as progesterone that are otherwise suppressed by TRT. But many men, and especially older ones, may not see any bump in these and should consider direct supplementation. Be prepared to monitor the hormone levels. This general rule applies to testosterone as well. Some men do see significant endogenous production even at lower hCG doses. But more typical would be an extra 100 ng/dL of extra testosterone or less.
I thank you for your attention in answering my post.
I thought that exogenous production would go up a lot but I could see that it goes up very little. I will keep my testo twice a week.
I've always had an easy time accumulating fat in my hips and I heard some doctors comment on this relationship between hip fat and estradiol
My estradiol is currently at 40 but I would love to lower it to 20 to see how I feel. Do you have any suggestions?
 
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I thank you for your attention in answering my post.
I thought that exogenous production would go up a lot but I could see that it goes up very little. I will keep my testo twice a week.
I've always had an easy time accumulating fat in my hips and I heard some doctors comment on this relationship between hip fat and estradiol
My estradiol is currently at 40 but I would love to lower it to 20 to see how I feel. Do you have any suggestions?
Lowering the TRT dose is best. What is your total testosterone level? When was it tested relative to your TRT injections? Do you know your SHBG?

Unfortunately a common side effect of hCG is higher estradiol. In my case hCG increases estradiol by nearly 20 pg/mL even at only 500 IU total per week.
 
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