Long Term HCG Induced Testicular LH Desensitization

[NoRevolution]

Hi there,

Wanted to get some advice from those more knowledgeable in HPTA / testicular function. A quick background: Been cycling on and off for the last 5 years, with consistent HCG use of 300iu EOD to preserve fertility / prevent testicular atrophy. The reasoning behind this was two these two studies:

Low-dose human chorionic gonadotropin maintains intratesticular testosterone in normal men with testosterone-induced gonadotropin suppression ​

Therapy with human chorionic gonadotrophin alone induces spermatogenesis in men with isolated hypogonadotrophic hypogonadism--long-term follow-up ​

According to the first study, IF your are on testosterone sufficient to completely hinder LH production, 250iu/EOD HCG can preserve normal testicular testosterone production via stimulation of the LH receptor. This will prevent testicular atrophy and theoretically make recovery easier. And according to the second study, this also assists in sperm production although some may find it beneficial to add HMG.

I verified that this was indeed the case. On cycle, I added 250iu/EOD HCG, and my testosterone rose by around 700 ng/dl, thus indicating testes were producing testosterone. I also noticed no testicular atrophy during the 12 week long cycle (volume was measure at 25ml+ via orchidometer). Cycling off, I continued the 250iu/EOD HCG. After a steroids washout period of 8 weeks, testosterone came in at 900 ng/dl with 250iu/EOD HCG, thus indicating that HCG was continuing to stimulate the testes.

For the next 4 years, I continued to cycle. Despite cycling off AAS frequently, I never failed to take my 250iu/EOD HCG. And I noticed something: The first time I cycled off, HCG caused testes to produce 900 ng/dl. After another year or two, it was down to 300 ng/dl (same dose). Finally, I decided to take a 6 months break from AAS after 5 years of cycling. And total testosterone came back at just 63 ng/dl. This was despite 250iu/EOD HCG, and an LH level of 2.9 mIU/mL.

Initially, I doubted if the HCG I was using (Ovidac) was geniune. But a serum bHCG level was taken and came back elevated at 7 mIU/mL. Additionally, no testicular atrophy was ever observed, and testes remain at the same volume as 5 years ago. So, I am left with one simple conclusion: After years of HCG usage, it has desensitized the leydig cells in my testes such that they no longer respond to neither endogenous LH, or HCG. Based on the thread below, most of us here (including Scally) believe that HCG desensitization is a myth:

HCG and desensitization....​

I am correct here? I can provide all the necessary bloodwork if needed, would just like some second opinions of this!

Thanks

 

[GuerillaPete]

Did you try clomid/enclomiphene or nolva old school pct drugs?rFSH?Hmg?
Going on long cycles like this and coming of than back on sure did not help.
Interesting subject as many here me
Incuded use hcg on cycle !

 

[NoRevolution]

Did several conventional Power PCT's utilizing both clomid and nolvadex near the beginning of my 5-year long stint. They were all effective, with post-PCT test levels coming in between 900 and 1200 ng/dl. That is why, given the current situation, I am using the Power PCT now to recover.

But getting back to the main point of the thread: I'm confused as to why HCG stopped working. According to the second study and the above linked thread, there should be no risk of desensitization with long term low dose HCG usage.

 

[GuerillaPete]

Maybe your testicles are sick? How are your general bloods?
Im sure others will give they're 2 cents soon enough .
Interesting subject

 

[NoRevolution]

Here's my bloods from the three times I went off whilst using HCG 250iu/EOD:

11/2/2017: Total time on 6 mo. testes producing 900+ng/dl:

1/3/2019: Total time 2yrs. testes producing 228 ng/dl:

10/26/2021: Total time 4-5 yrs. testes producing just 63 ng/dl:


All bloods were taken on 250iu/EOD HCG, whilst cycling off of testosterone for at least 6 weeks so I could get an accurate reading of natural production

 

[testaholic]

Hi there,

Wanted to get some advice from those more knowledgeable in HPTA / testicular function. A quick background: Been cycling on and off for the last 5 years, with consistent HCG use of 300iu EOD to preserve fertility / prevent testicular atrophy. The reasoning behind this was two these two studies:

Low-dose human chorionic gonadotropin maintains intratesticular testosterone in normal men with testosterone-induced gonadotropin suppression ​

Therapy with human chorionic gonadotrophin alone induces spermatogenesis in men with isolated hypogonadotrophic hypogonadism--long-term follow-up ​

According to the first study, IF your are on testosterone sufficient to completely hinder LH production, 250iu/EOD HCG can preserve normal testicular testosterone production via stimulation of the LH receptor. This will prevent testicular atrophy and theoretically make recovery easier. And according to the second study, this also assists in sperm production although some may find it beneficial to add HMG.

I verified that this was indeed the case. On cycle, I added 250iu/EOD HCG, and my testosterone rose by around 700 ng/dl, thus indicating testes were producing testosterone. I also noticed no testicular atrophy during the 12 week long cycle (volume was measure at 25ml+ via orchidometer). Cycling off, I continued the 250iu/EOD HCG. After a steroids washout period of 8 weeks, testosterone came in at 900 ng/dl with 250iu/EOD HCG, thus indicating that HCG was continuing to stimulate the testes.

For the next 4 years, I continued to cycle. Despite cycling off AAS frequently, I never failed to take my 250iu/EOD HCG. And I noticed something: The first time I cycled off, HCG caused testes to produce 900 ng/dl. After another year or two, it was down to 300 ng/dl (same dose). Finally, I decided to take a 6 months break from AAS after 5 years of cycling. And total testosterone came back at just 63 ng/dl. This was despite 250iu/EOD HCG, and an LH level of 2.9 mIU/mL.

Initially, I doubted if the HCG I was using (Ovidac) was geniune. But a serum bHCG level was taken and came back elevated at 7 mIU/mL. Additionally, no testicular atrophy was ever observed, and testes remain at the same volume as 5 years ago. So, I am left with one simple conclusion: After years of HCG usage, it has desensitized the leydig cells in my testes such that they no longer respond to neither endogenous LH, or HCG. Based on the thread below, most of us here (including Scally) believe that HCG desensitization is a myth:

HCG and desensitization....​

I am correct here? I can provide all the necessary bloodwork if needed, would just like some second opinions of this!

Thanks

What compounds were you taking? Test only? Or were there others also

 

[NoRevolution]

What compounds were you taking? Test only? Or were there others also

During the on periods, a variety of compounds were used (deca, tren, orals), with a minimum of 600mg test as a base. These obviously varied whether or not I was close to competition. When the above blood tests were taken, no compounds were being used as I cycled off.

However, according to the first study, it shouldn't matter whether or not you are taking 300mg test or a whole host of other compounds - LH will be completely suppressed in either case. This is why we supplement with HCG, to prevent testicular atrophy and the corresponding primary hypogonadism that ensues.

In my case of using 250iu/EOD HCG, testicular atrophy was prevented but primary hypogonadism was not (testes became desensitized to LH).

 

[VenomYo]

No offense, but what comes to my mind is, that you can become desensitized to everything. Even superdrol will feel like sugarpills if you do it for long enough

you religiously ran HCG for 5 years straight right?

Ive seen a pretty reputable doctor on muscleinsider talk about a conference he went to where he talked to the leading expert on fertility, who said hcg desensitization
was a myth. Also if Ovidac is a bayer brand, then you didnt have legit hcg the whole 5 years unless you ran doctor prescribed Ovidac the entire time, bayer will always be swamped with fakes

 

[testaholic]

During the on periods, a variety of compounds were used (deca, tren, orals), with a minimum of 600mg test as a base. These obviously varied whether or not I was close to competition. When the above blood tests were taken, no compounds were being used as I cycled off.

However, according to the first study, it shouldn't matter whether or not you are taking 300mg test or a whole host of other compounds - LH will be completely suppressed in either case. This is why we supplement with HCG, to prevent testicular atrophy and the corresponding primary hypogonadism that ensues.

In my case of using 250iu/EOD HCG, testicular atrophy was prevented but primary hypogonadism was not (testes became desensitized to LH).

I didn't read the first study, but my hunch is one of 2 things:

- did you give enough time for the 19nors to clear your system before testing? There's speculation that 19nor metabolites can remain in your system for 18 months following cessation of use, so if you tested within said window, your results could be influenced by that.

- there's speculation that all the HCG in the world won't prevent atrophy when harsher compounds are present. Aka tren and deca

In other words, I'd suspect its not so much an issue of HCG desensitization, but rather a complication resulting from the use of tren / deca.

 

[VenomYo]

I didn't read the first study, but my hunch is one of 2 things:

- did you give enough time for the 19nors to clear your system before testing? There's speculation that 19nor metabolites can remain in your system for 18 months following cessation of use, so if you tested within said window, your results could be influenced by that.

- there's speculation that all the HCG in the world won't prevent atrophy when harsher compounds are present. Aka tren and deca

In other words, I'd suspect its not so much an issue of HCG desensitization, but rather a complication resulting from the use of tren / deca.

good thinking, he didnt even mention what stuff he ran

 

[NoRevolution]

I didn't read the first study, but my hunch is one of 2 things:

- did you give enough time for the 19nors to clear your system before testing? There's speculation that 19nor metabolites can remain in your system for 18 months following cessation of use, so if you tested within said window, your results could be influenced by that.

- there's speculation that all the HCG in the world won't prevent atrophy when harsher compounds are present. Aka tren and deca

In other words, I'd suspect its not so much an issue of HCG desensitization, but rather a complication resulting from the use of tren / deca.

What about 19-nors directly affects leydig cell function? I would assume that, if HCG is still stimulating the LH receptor of the leydig cells, it theoretically shouldn't matter what compounds are present.

 

[GuerillaPete]

What about 19-nors directly affects leydig cell function? I would assume that, if HCG is still stimulating the LH receptor of the leydig cells, it theoretically shouldn't matter what compounds are present.

Yeah true but in practice the soldiers get way smaller on Tren than anything else!
Personally i add clomid to the hcg while on tren for this reason

 

[NoRevolution]

Yeah true but in practice the soldiers get way smaller on Tren than anything else!
Personally i add clomid to the hcg while on tren for this reason

Definitely concur with that! The 19-nors (deca/tren) shut me down harder even at low doses than any other compounds I have taken. Thing is, I'd expect the shutdown to occur at the Hypothalamus part of the HPTA. This is indeed the case - looking at my 3rd bloodwork FSH is near zero and LH is low, even after 8 months!

But I'm still confused as to what caused the longer term appearance of primary hypogonadism. The only studies I could find on 19-nors inducing testicular damage was this one done on rats: Taurine protects steroids users' testes. The question there remains - did the damage occur because of the lack of LH stimulation, or the steroid itself? Does anyone else have some insight into this?

 

[GuerillaPete]

Definitely concur with that! The 19-nors (deca/tren) shut me down harder even at low doses than any other compounds I have taken. Thing is, I'd expect the shutdown to occur at the Hypothalamus part of the HPTA. This is indeed the case - looking at my 3rd bloodwork FSH is near zero and LH is low, even after 8 months!

But I'm still confused as to what caused the longer term appearance of primary hypogonadism. The only studies I could find on 19-nors inducing testicular damage was this one done on rats: Taurine protects steroids users' testes. The question there remains - did the damage occur because of the lack of LH stimulation, or the steroid itself? Does anyone else have some insight into this?

I heard on the Leo Longevity channel something on the subject!
Looks like the more time you are shut down and the testicles atrophied the less chance of them coming back and it can cause fibrosis !
I don't know the exact mechanism tho maybe others can shed some light on the subject!
Maybe @PeterBond can tell us something on why this happens!?!?

 

[ManK]

Hi there,

Wanted to get some advice from those more knowledgeable in HPTA / testicular function. A quick background: Been cycling on and off for the last 5 years, with consistent HCG use of 300iu EOD to preserve fertility / prevent testicular atrophy. The reasoning behind this was two these two studies:

Low-dose human chorionic gonadotropin maintains intratesticular testosterone in normal men with testosterone-induced gonadotropin suppression ​

Therapy with human chorionic gonadotrophin alone induces spermatogenesis in men with isolated hypogonadotrophic hypogonadism--long-term follow-up ​

According to the first study, IF your are on testosterone sufficient to completely hinder LH production, 250iu/EOD HCG can preserve normal testicular testosterone production via stimulation of the LH receptor. This will prevent testicular atrophy and theoretically make recovery easier. And according to the second study, this also assists in sperm production although some may find it beneficial to add HMG.

I verified that this was indeed the case. On cycle, I added 250iu/EOD HCG, and my testosterone rose by around 700 ng/dl, thus indicating testes were producing testosterone. I also noticed no testicular atrophy during the 12 week long cycle (volume was measure at 25ml+ via orchidometer). Cycling off, I continued the 250iu/EOD HCG. After a steroids washout period of 8 weeks, testosterone came in at 900 ng/dl with 250iu/EOD HCG, thus indicating that HCG was continuing to stimulate the testes.

For the next 4 years, I continued to cycle. Despite cycling off AAS frequently, I never failed to take my 250iu/EOD HCG. And I noticed something: The first time I cycled off, HCG caused testes to produce 900 ng/dl. After another year or two, it was down to 300 ng/dl (same dose). Finally, I decided to take a 6 months break from AAS after 5 years of cycling. And total testosterone came back at just 63 ng/dl. This was despite 250iu/EOD HCG, and an LH level of 2.9 mIU/mL.

Initially, I doubted if the HCG I was using (Ovidac) was geniune. But a serum bHCG level was taken and came back elevated at 7 mIU/mL. Additionally, no testicular atrophy was ever observed, and testes remain at the same volume as 5 years ago. So, I am left with one simple conclusion: After years of HCG usage, it has desensitized the leydig cells in my testes such that they no longer respond to neither endogenous LH, or HCG. Based on the thread below, most of us here (including Scally) believe that HCG desensitization is a myth:

HCG and desensitization....​

I am correct here? I can provide all the necessary bloodwork if needed, would just like some second opinions of this!

Thanks

i am in my 8° years and didn't happened....

 

[PeterBond]

I heard on the Leo Longevity channel something on the subject!
Looks like the more time you are shut down and the testicles atrophied the less chance of them coming back and it can cause fibrosis !
I don't know the exact mechanism tho maybe others can shed some light on the subject!
Maybe @PeterBond can tell us something on why this happens!?!?

There appears to be a diminished response of the testes to LH and FSH after prolonged suppression thereof. Effectively inducing primary hypogonadism to one degree or another. This usually appears to resolve quite quickly (matter of weeks) when LH & FSH levels are increased again after coming off. There's no reliable data on this in regard to long-term AAS use. I've seen some autopsy reports indicate fibrosis of the testes in (ex) AAS users, but this is a far cry from a causal link.

Desensitization as proposed in OP doesn't occur in response to hCG, even with years of use. The drug has been prescribed for ages in treatment of (congenital) secondary hypogonadism.

 

[GuerillaPete]

There appears to be a diminished response of the testes to LH and FSH after prolonged suppression thereof. Effectively inducing primary hypogonadism to one degree or another. This usually appears to resolve quite quickly (matter of weeks) when LH & FSH levels are increased again after coming off. There's no reliable data on this in regard to long-term AAS use. I've seen some autopsy reports indicate fibrosis of the testes in (ex) AAS users, but this is a far cry from a causal link.

Desensitization as proposed in OP doesn't occur in response to hCG, even with years of use. The drug has been prescribed for ages in treatment of (congenital) secondary hypogonadism.

Thanks for clearing this up!

 

[ManK]

Here's my bloods from the three times I went off whilst using HCG 250iu/EOD:

11/2/2017: Total time on 6 mo. testes producing 900+ng/dl:
View attachment 157126
1/3/2019: Total time 2yrs. testes producing 228 ng/dl:
View attachment 157127
10/26/2021: Total time 4-5 yrs. testes producing just 63 ng/dl:
View attachment 157128

All bloods were taken on 250iu/EOD HCG, whilst cycling off of testosterone for at least 6 weeks so I could get an accurate reading of natural production

Looking your last blood test i read lh 2.9.
In my personal experience usually to return to normal levels of T i need to force lh until 5-5.5, then T begin to increase to my normal levels (4.5ng) and lh slowly go down @ 3.
So maybe you need to force lh to grow to higher levels...
I specify that to return @ normal Tlevel after 2 years of suppression, i had to use clomid for 14 weeks... not usual few week used by people that suppressed just for the time of 1 single cycle.

 

[ManK]

just a question, you talk about hcg desinsitation:
what about your testes size?

 

[ManK]

Another data is strange and i think that maybe here is the error:
700 or 900 ng dl of T from just 875 ui hcg week (250 eod is 875 mg week) is a lot...
Usually is difficult obtain more then 400/500 at that dosage.
If so a lot of peole could stay on trt with just 250 ui eod of hcg....