A Criticism Of HCG

[wavelength123]

Disclaimer - y’all may or may not relate but I live in a huge metropolitan area and stressing less / leaving the city for a nice and quiet lifestyle far away from ambulance sirens, peak hour subways, and pollution is not an option.

So I’ve read a number of interesting biochem type studies where LH is shown to increase all types of enzymes involved in steroidogenesis. We know HCG tends to increase aromatase, I think 5a reductase also goes up, and I was nerding on 11b-HSD’s which LH also increase. It seems to me that all enzymes and thusly all hormones increase across the board. 11bHSD1 in particular increases cortisol.

My personal experience with HCG showed great T (total and free) and E2 improvements... but cortisol was borderline high.

Therefore I’m here guessing that if one has a high ish Cortisol / Test ratio naturally, be it because of personal stress or just a generally shitty fight or flight environment, HCG won’t cut it. Like what’s the benefit going from 400 ng/dL up to 700+ (with free T and E2 doubling up as well) if cortisol is nearly beyond normal range. Same goes for SERMS by the way, which also indiscriminately bump it all up. I know cortisol is extremely useful for normal human physiology but if it goes high there’s a reason for it and that is big bad stress. So I guess the point of my thread is to make sure that you guys on HCG monitor as many hormones as possible not just T/E2, and especially cortisol.

I’ve been fooling around with HCG only and then HCG+Trestolone but realistically I think that TRT is the only way we’ve got to totally turn around a bad T/C ratio.

I can share studies in here if this gets some traction. For now I’m only sharing skepticism about HCG

 

[Tristan Loscha]

Disclaimer - y’all may or may not relate but I live in a huge metropolitan area and stressing less / leaving the city for a nice and quiet lifestyle far away from ambulance sirens, peak hour subways, and pollution is not an option.

So I’ve read a number of interesting biochem type studies where LH is shown to increase all types of enzymes involved in steroidogenesis. We know HCG tends to increase aromatase, I think 5a reductase also goes up, and I was nerding on 11b-HSD’s which LH also increase. It seems to me that all enzymes and thusly all hormones increase across the board. 11bHSD1 in particular increases cortisol.

My personal experience with HCG showed great T (total and free) and E2 improvements... but cortisol was borderline high.

Therefore I’m here guessing that if one has a high ish Cortisol / Test ratio naturally, be it because of personal stress or just a generally shitty fight or flight environment, HCG won’t cut it. Like what’s the benefit going from 400 ng/dL up to 700+ (with free T and E2 doubling up as well) if cortisol is nearly beyond normal range. Same goes for SERMS by the way, which also indiscriminately bump it all up. I know cortisol is extremely useful for normal human physiology but if it goes high there’s a reason for it and that is big bad stress. So I guess the point of my thread is to make sure that you guys on HCG monitor as many hormones as possible not just T/E2, and especially cortisol.

I’ve been fooling around with HCG only and then HCG+Trestolone but realistically I think that TRT is the only way we’ve got to totally turn around a bad T/C ratio.

I can share studies in here if this gets some traction. For now I’m only sharing skepticism about HCG

what regimen did you take?did the results stick?morphological changes in your testes,did they prevail or reverted?

 

[sladerunner69]

Disclaimer - y’all may or may not relate but I live in a huge metropolitan area and stressing less / leaving the city for a nice and quiet lifestyle far away from ambulance sirens, peak hour subways, and pollution is not an option.

So I’ve read a number of interesting biochem type studies where LH is shown to increase all types of enzymes involved in steroidogenesis. We know HCG tends to increase aromatase, I think 5a reductase also goes up, and I was nerding on 11b-HSD’s which LH also increase. It seems to me that all enzymes and thusly all hormones increase across the board. 11bHSD1 in particular increases cortisol.

My personal experience with HCG showed great T (total and free) and E2 improvements... but cortisol was borderline high.

Therefore I’m here guessing that if one has a high ish Cortisol / Test ratio naturally, be it because of personal stress or just a generally shitty fight or flight environment, HCG won’t cut it. Like what’s the benefit going from 400 ng/dL up to 700+ (with free T and E2 doubling up as well) if cortisol is nearly beyond normal range. Same goes for SERMS by the way, which also indiscriminately bump it all up. I know cortisol is extremely useful for normal human physiology but if it goes high there’s a reason for it and that is big bad stress. So I guess the point of my thread is to make sure that you guys on HCG monitor as many hormones as possible not just T/E2, and especially cortisol.

I’ve been fooling around with HCG only and then HCG+Trestolone but realistically I think that TRT is the only way we’ve got to totally turn around a bad T/C ratio.

I can share studies in here if this gets some traction. For now I’m only sharing skepticism about HCG

Wow HCG increases 5-ar? Where did you learn that? I need to finally take the dive and try some of this stuff.

 

[wavelength123]

I learnt that in school 10 years ago, and was nerding again on steroidogenesis after putting 2 and 2 together with my own experience with HCG (500iu twice weekly @Tristan Loscha).

What’s the appeal of more 5a reductase anyway, especially with all of the other enzymes being up regulated as well?

This drug is best avoided is my conclusion... unless as a primary v secondary hypogonadal diagnosis tool, or for 5ar deficiency diagnosis, or other rare conditions. If secondary, HCG is not a proper band aid. In my case I know my issue is cortisol related and I will work on it. Testosterone is the primary male hormone for a reason and is excessively converted in its metabolites when sick.

 

[Tristan Loscha]

I learnt that in school 10 years ago, and was nerding again on steroidogenesis after putting 2 and 2 together with my own experience with HCG (500iu twice weekly @Tristan Loscha).

What’s the appeal of more 5a reductase anyway, especially with all of the other enzymes being up regulated as well?

This drug is best avoided is my conclusion... unless as a primary v secondary hypogonadal diagnosis tool, or for 5ar deficiency diagnosis, or other rare conditions. If secondary, HCG is not a proper band aid. In my case I know my issue is cortisol related and I will work on it. Testosterone is the primary male hormone for a reason and is excessively converted in its metabolites when sick.

interesting.thanks for the heads up.

 

[sladerunner69]

I learnt that in school 10 years ago, and was nerding again on steroidogenesis after putting 2 and 2 together with my own experience with HCG (500iu twice weekly @Tristan Loscha).

What’s the appeal of more 5a reductase anyway, especially with all of the other enzymes being up regulated as well?

This drug is best avoided is my conclusion... unless as a primary v secondary hypogonadal diagnosis tool, or for 5ar deficiency diagnosis, or other rare conditions. If secondary, HCG is not a proper band aid. In my case I know my issue is cortisol related and I will work on it. Testosterone is the primary male hormone for a reason and is excessively converted in its metabolites when sick.

I have post finasteride syndrome. I think it's basically lowerred 5ar resulting in lower DHT and allopregnenelone. It's horrible, I will stop at nothing to improve it.

 

[wavelength123]

I have post finasteride syndrome. I think it's basically lowerred 5ar resulting in lower DHT and allopregnenelone. It's horrible, I will stop at nothing to improve it.

you can use HCG to confirm your self diagnosis but PFS is just another internet induced way to blame a drug for hypogonadism. Studies have shown no difference VS placebo... in fact in one study the placebo group had worse “PFS”.

 

[Tristan Loscha]

you can use HCG to confirm your self diagnosis but PFS is just another internet induced way to blame a drug for hypogonadism. Studies have shown no difference VS placebo... in fact in one study the placebo group had worse “PFS”.

PFS is real,and indeed,drug induced hypogonadism.Mechanistic targets could be altered Geneexpression via imprinting of improper epigenetics.

Endocr Connect. 2019 Aug; 8(8): 1118–1125.
Published online 2019 Jul 4. doi: 10.1530/EC-19-0199
PMCID: PMC6652249
PMID: 31272082
Altered methylation pattern of the SRD5A2 gene in the cerebrospinal fluid of post-finasteride patients: a pilot study
Roberto Cosimo Melcangi,1 Livio Casarini,2,3 Marco Marino,2,3 Daniele Santi,2,4 Samantha Sperduti,2,3 Silvia Giatti,1 Silvia Diviccaro,1 Maria Grimoldi,5 Donatella Caruso,1 Guido Cavaletti,6 and Manuela Simoni2,3,4
Author information Article notes Copyright and License information Disclaimer
This article has been cited by other articles in PMC.
Go to:
Abstract
Context
Post-finasteride syndrome (PFS) occurs in patients with androgenic alopecia after suspension of the finasteride treatment, leading to a large variety of persistent side effects. Despite the severity of the clinical picture, the mechanism underlying the PFS symptoms onset and persistence is still unclear.

Objective
To study whether epigenetic modifications occur in PFS patients.

Methods
Retrospective analysis of a multicentric, prospective, longitudinal, case–control clinical trial, enrolling 16 PFS patients, compared to 20 age-matched healthy men. Main outcomes were methylation pattern of SRD5A1 and SRD5A2 promoters and concentration of 11 neuroactive steroids, measured by liquid chromatography-tandem mass spectrometry, in blood and cerebrospinal fluid (CSF) samples.

Results
SRD5A1 and SRD5A2 methylation analysis was performed in all blood samples (n = 16 PFS patients and n = 20 controls), in 16 CSF samples from PFS patients and in 13 CSF samples from controls. The SRD5A2 promoter was more frequently methylated in CSF of PFS patients compared to controls (56.3 vs 7.7%). No promoter methylation was detected in blood samples in both groups. No methylation occurred in the SRD5A1 promoter of both groups. Unmethylated controls compared to unmethylated SRD5A2 patients showed higher pregnenolone, dihydrotestosterone and dihydroprogesterone, together with lower testosterone CSF levels. Andrological and neurological assessments did not differ between methylated and unmethylated subjects.

Conclusions
For the first time, we demonstrate a tissue-specific methylation pattern of SRD5A2 promoter in PFS patients. Although we cannot conclude whether this pattern is prenatally established or induced by finasteride treatment, it could represent an important mechanism of neuroactive steroid levels and behavioural disturbances previously described in PFS.

 

[wavelength123]

Lol, no....

Although we cannot conclude whether this pattern is prenatally established or induced by finasteride treatment,

...therefore your claim “PFS is real” is massively jumping to conclusions. This study isn’t suiting your bias sorry.

and I didn’t say “drug induced hypogonadism”. I said what’s correct: blaming a drug in lieu of realizing patient is hypogonadal.

Investigation of the Plausibility of 5-Alpha-Reductase Inhibitor Syndrome

The drug-related sexual adverse event profile for subjects who took finasteride was similar for subjects with or without a history of sexual dysfunction at baseline. A total of 4% of finasteride and 2% of placebo subjects discontinued the study due to sexual adverse events. A surprising finding in this study was that in these subjects who withdrew from the study due to sexual adverse events, 50% of finasteride users experienced continual sexual side effects after discontinuing finasteride, while 59% of placebo subjects noted continual sexual side effects. Thus, in this study persistent sexual side effects were reported more in placebo subjects than in patients treated with finasteride.

 

[Ashoka]

Lol, no....



...therefore your claim “PFS is real” is massively jumping to conclusions. This study isn’t suiting your bias sorry.

and I didn’t say “drug induced hypogonadism”. I said what’s correct: blaming a drug in lieu of realizing patient is hypogonadal.

Investigation of the Plausibility of 5-Alpha-Reductase Inhibitor Syndrome

So wave, what is the explanation to this constellation of symptoms that people with PFS, including me, are experiencing? I’m genuinely curious how you think this works. Also saying hypogonadal doesn’t really cut it, because our androgens normally look fine on tests. And of course, the vast majority were clearly enjoying full sexual health before treatment.

Really the only option is for you to say this is a nocebo effect. You honestly are willing to believe that? If that were true, wouldn’t you expect at least one of us to snap out of it? It’s telling there’s not a single such report of that. Also kind of a lot of mental hoops to jump through when we know it interferes with progesterone and DHT that are vital to mental and sexual health, can alter gut flora, and causes measurable nerve damage. haidut has made several posts on RPF about this.

I’m also somewhat amazed that nearly every single person involved in that study you mentioned has been connected to the drug manufacturer at some point in their career, as mentioned at the end of the paper. What a staggering conflict of interest on their part.

 

[mrchibbs]

I’m also somewhat amazed that nearly every single person involved in that study you mentioned has been connected to the drug manufacturer at some point in their career, as mentioned at the end of the paper. What a staggering conflict of interest on their part.

As Ray said in a recent interview, 90% of scientific articles are horseshit propaganda. (he didn't use those exact words) It's a bit disconcerting, but it highlights the effect of industrial interests/bias shaping discourse in academic literature. I've written a few papers myself, and read quite a few, and I've been profoundly disillusioned by the entire process.

There is subtle propaganda online on the most popular sites like medium.com with articles written by fake people criticizing research which raises doubt on conventional industrial practices, like use of carrageenan in food products. Follow the money, always.

 

[wavelength123]

I’d rather believe scientific articles over internet people, yeah, for sure.

I guess we are 2 different schools of thought clashing at this point. No need to keep going off topic any further.

 

[mrchibbs]

I’d rather believe scientific articles over internet people, yeah, for sure.

I guess we are 2 different schools of thought clashing at this point. No need to keep going off topic any further.

Confronting point of views is fine, as long as it's done respectfully, ultimately we both want the same thing.

 

[Ashoka]

I’d rather believe scientific articles over internet people, yeah, for sure.

I guess we are 2 different schools of thought clashing at this point. No need to keep going off topic any further.

That’s cool dude. Well, that paper you put forward clearly states it’s inconclusive, as well as cites an old pharma industry study as a gold standard. So it sounds like your position should be noncommittal at best, but instead you diminish people who have it without proposing an alternative explanation. That’s because any alternative explanation would clearly be unsatisfactory. You really betray the limitations of your “school of thought”. Also, we’re not internet people.

But by all means - back to HCG.

 

[Tristan Loscha]

Lol, no....



...therefore your claim “PFS is real” is massively jumping to conclusions. This study isn’t suiting your bias sorry.

and I didn’t say “drug induced hypogonadism”. I said what’s correct: blaming a drug in lieu of realizing patient is hypogonadal.

Investigation of the Plausibility of 5-Alpha-Reductase Inhibitor Syndrome

You didnt read the study you posted to refute my point:Gynecomastia is an accepted entity and doesnt vanish after discontinuation.Furthermore,the shift from Testosterone to Estradiol is itself gonadotoxic.

"In the survey conducted by Ganzer et al. [30] that involved subjects who complained of persistent side effects following finasteride use, approximately 69% (90/131) of survey respondents reported gynecomastia."

gynecomastia is a contemporary side effect,later on chronic, of Finasteride which can be symptom and sign of the chronification of T-Estradiol shifting induced gonadotoxicity,which would be drug induced hypogonadism.There is a mechanistic Rationale for PF Syndrome.





Physical Adverse Effects
Gynecomastia and Male Breast Carcinoma

Gynecomastia has been noted with finasteride (1 and 5 mg) and dutasteride (0.5 mg), while male breast cancer has been noted with finasteride (5 mg). Finasteride and dutasteride are potent inhibitors of type 2 5-alpha-reductase, inhibiting the conversion of testosterone to dihydrotestosterone (DHT) causing a decrease in formation of DHT. Inhibiting DHT synthesis may alter the estrogen to androgen ratio by shifting metabolism of testosterone to estradiol, thus increasing the risk of gynecomastia and male breast cancer [7,30,33]. Relative estrogen excess is associated with an increased risk of breast cancer in men [34].

Gynecomastia, an enlargement of breast tissue, is a reported side effect in males prescribed finasteride therapy. Results from the Prostate Cancer Prevention Trial (PCPT), a randomized, double-blind, placebo-controlled study showed that gynecomastia is among the more common side effects of finasteride therapy along with sexual dysfunction [35]. Men age 55 years and older were randomly assigned to treatment with finasteride (5 mg/day) or placebo for 7 years. At trial conclusion, gynecomastia was observed in 4.5% (426/9,423) of finasteride subjects and 2.8% (261/9,457) of placebo subjects [7,35]. In the survey conducted by Ganzer et al. [30] that involved subjects who complained of persistent side effects following finasteride use, approximately 69% (90/131) of survey respondents reported gynecomastia.

 

[sladerunner69]

PFS is real,and indeed,drug induced hypogonadism.Mechanistic targets could be altered Geneexpression via imprinting of improper epigenetics.

Endocr Connect. 2019 Aug; 8(8): 1118–1125.
Published online 2019 Jul 4. doi: 10.1530/EC-19-0199
PMCID: PMC6652249
PMID: 31272082
Altered methylation pattern of the SRD5A2 gene in the cerebrospinal fluid of post-finasteride patients: a pilot study
Roberto Cosimo Melcangi,1 Livio Casarini,2,3 Marco Marino,2,3 Daniele Santi,2,4 Samantha Sperduti,2,3 Silvia Giatti,1 Silvia Diviccaro,1 Maria Grimoldi,5 Donatella Caruso,1 Guido Cavaletti,6 and Manuela Simoni2,3,4
Author information Article notes Copyright and License information Disclaimer
This article has been cited by other articles in PMC.
Go to:
Abstract
Context
Post-finasteride syndrome (PFS) occurs in patients with androgenic alopecia after suspension of the finasteride treatment, leading to a large variety of persistent side effects. Despite the severity of the clinical picture, the mechanism underlying the PFS symptoms onset and persistence is still unclear.

Objective
To study whether epigenetic modifications occur in PFS patients.

Methods
Retrospective analysis of a multicentric, prospective, longitudinal, case–control clinical trial, enrolling 16 PFS patients, compared to 20 age-matched healthy men. Main outcomes were methylation pattern of SRD5A1 and SRD5A2 promoters and concentration of 11 neuroactive steroids, measured by liquid chromatography-tandem mass spectrometry, in blood and cerebrospinal fluid (CSF) samples.

Results
SRD5A1 and SRD5A2 methylation analysis was performed in all blood samples (n = 16 PFS patients and n = 20 controls), in 16 CSF samples from PFS patients and in 13 CSF samples from controls. The SRD5A2 promoter was more frequently methylated in CSF of PFS patients compared to controls (56.3 vs 7.7%). No promoter methylation was detected in blood samples in both groups. No methylation occurred in the SRD5A1 promoter of both groups. Unmethylated controls compared to unmethylated SRD5A2 patients showed higher pregnenolone, dihydrotestosterone and dihydroprogesterone, together with lower testosterone CSF levels. Andrological and neurological assessments did not differ between methylated and unmethylated subjects.

Conclusions
For the first time, we demonstrate a tissue-specific methylation pattern of SRD5A2 promoter in PFS patients. Although we cannot conclude whether this pattern is prenatally established or induced by finasteride treatment, it could represent an important mechanism of neuroactive steroid levels and behavioural disturbances previously described in PFS.

Wow an actual professional abstract that mentions PFS!

I am having trouble understanding the implications of what is written. I ahve never heard of SRD5A2 gene before. I suspect that my pfs is caused by chronically lowerred 5-ar levels, although there is probably more to it than this. Hypogonadism is certainly part of it - I have tested very low for both testosterone and DHT levels. However, I also suffer very bad neruological issues such as brain fog, headaches, numbness throughout my body, etc even when I take things like Androsterone or Testosterone. Therefore I suspect that low allopregnenlone and progesterone are also part of it.

 

[sladerunner69]

Lol, no....



...therefore your claim “PFS is real” is massively jumping to conclusions. This study isn’t suiting your bias sorry.

and I didn’t say “drug induced hypogonadism”. I said what’s correct: blaming a drug in lieu of realizing patient is hypogonadal.

Investigation of the Plausibility of 5-Alpha-Reductase Inhibitor Syndrome

It's much worse than hypogonadism- it includes a littany of nuerological problems which on their own are worse than the low libido seen in hypogonadism. Most of us PFS guys would be fine with having low libido if our cognitive states weren't so impaired. I have had constant headaches and pressures, numbness, difficulty concentrating and thinking, no emotions, for many years now even after taking testosterone and DHT. These help but don't solve the issue because 5-ar does more than create DHT. It also creates thdoc, allopregnenlone, and probably does other things that are important for nerve health.

 

[sladerunner69]

you can use HCG to confirm your self diagnosis but PFS is just another internet induced way to blame a drug for hypogonadism. Studies have shown no difference VS placebo... in fact in one study the placebo group had worse “PFS”.

I am skeptical but would be very interested to see this study...

 

[wavelength123]

I am skeptical but would be very interested to see this study...

well I quoted it in my other post that you quoted.

I have absolutely zero interest in debating PFS with you guys. If bad stuff happens permanently in 2% if finasteride users then that’s still a lot of people who will go online and complain about side effects, that’s fine.

All I’m saying is when I posted this thread I wanted to discuss that HCG increases ALL enzymes across the board. If one is a high cortisol mess, HCG will yield *some* DHT and lots of E2 and more cortisol. So be careful when using HCG.

 

[sladerunner69]

well I quoted it in my other post that you quoted.

I have absolutely zero interest in debating PFS with you guys. If bad stuff happens permanently in 2% if finasteride users then that’s still a lot of people who will go online and complain about side effects, that’s fine.

All I’m saying is when I posted this thread I wanted to discuss that HCG increases ALL enzymes across the board. If one is a high cortisol mess, HCG will yield *some* DHT and lots of E2 and more cortisol. So be careful when using HCG.

Actually a lot of fellow PFS guys have told me that they feel improved when taking things that increase cortisol or that increase estrogen. I do not know why this is, it si coutnerintuitive.