HPTA recovery: Time off or PCT?

^ this is not me being snarky, btw (only a little tongue-in-cheek). I'm trying to provoke a discussion and don't want to do all the study finding myself :)

I've never outright dismissed the potential of various PCT strategies (including stuff like prolactin suppression, triptorelin etc) to possibly help some guys (and for various reasons, maybe even just mood enhancement).

My issue is and always has been the way they're dispensed on forums like magic cures for AAS-induced HPG-axis damage without much reliable evidence - even anecdotal (far from it, as those various population studies demonstrating failure to recover from AAS clearly capture).

This gives guys a false sense of security and belief they'll recover. Which encourages them to be reckless, insensible, and start practices like b'n'c without really thinking things through consequences like: "do I want children in a few years" or "do I want to spend my life on TRT."
 
^No I totally understand and respect that. I researched AAS for a solid 3 or 4 months before getting on JUST for the aspect of potentially having kids/fertility, long term implications, etc and will share my thoughts and findings but also ALWAYS tell guys to don?t their own research and not to just take my word for it. Part of that is letting them know that once they start use, it?s going to likely mean being on for life at some point for all of these reasons.

That said, from the research I did (a while ago, like 5-6 years) and from the many doctors I sought thoughts from, my impression was that HCG (if used appropriately throughout any cycle) would maintain leydig cell function the best of any means we have available. Not to say that it?s 100% foolproof but definitely the best option out there.

That said, it?s been a while since I researched and am always open to having my opinions changed if presented with new information.

Actually have 4 fucking tests coming up in the next 2 weeks along with some travel for work so I haven?t had the time to go sift through studies yet but would like to when I have some time for my own knowledge as well. Would love to see anything you do have on the topic though as I?m always interested to learn!
 
This is also really random but not sure if the apostrophes in my posts appear as question marks to anyone else but if they do, I was wondering if anyone knew what was causing that? Guessing it was maybe because Im on mobile
 
Swim15 said:
That said, it?s been a while since I researched and am always open to having my opinions changed if presented with new information.
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Nothing stands still in science I'm afraid, there has been much advancement in our knowledge regards the importance of mitochondrial health, and their contribution towards oxidative stress within the cellular environment... We have already discussed means of reducing or negating oxidative stress, but that is only one mechanism.. Overworking mitochondria without sufficient time to rest on a daily basis can trigger a negative cascade of mitochondrial stress response and/or death.. Overworking sertoli/leydig cell mitochondria via the use of exogenous hormones or LH mimetics, without the advantage of pulsatile release, plus off time present with natural hormones, might induce mitochondrial and subsequent cell dysfunction or death..
 
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Swim15 said:
This is also really random but not sure if the apostrophes in my posts appear as question marks to anyone else but if they do, I was wondering if anyone knew what was causing that? Guessing it was maybe because Im on mobile
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You post from an iPhone don't you?
 
Genetic Freak said:
Nothing stands still in science I'm afraid, there has been much advancement in our knowledge regards the importance of mitochondrial health, and their contribution towards oxidative stress within the cellular environment... We have already discussed means of reducing or negating oxidative stress, but that is only one mechanism.. Overworking mitochondria without sufficient time to rest on a daily basis can trigger a negative cascade of mitochondrial stress response and/or death.. Overworking sertoli/leydig cell mitochondria via the use of exogenous hormones or LH mimetics, without the advantage of pulsatile release, plus off time present with natural hormones, might induce mitochondrial and subsequent cell dysfunction or death..
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I'm curious if dnp in low doses can be used to counteract the mitochondria issues as its been shown to boost the count of mitochondria in cells.
 
Swim15 said:
The endocrinologist I've seen, have said that HCG is the most effective protector against damage to leydig cells induced by exogenous hormone administration since it keeps them active by mimicking LH signaling.
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Which endocrinologist advise hCG in conjunction with exogenous hormones, unless part of TRT (is that what you are referring to)..?

Remember most endos are concerned with fertility in the short term for childless couples, not decades of exogenous hormone use to which we are discussing.. hCG should mostly work in this regard (in the short term) if secondary hypogonadism is the problem, it wont do anything for primary hypogonadism if the testes are damaged through decades of abuse..

Surely common sense should prevail in that damage via R.O.S should be countered or negated (whilst it is happening, on-cycle) with the use of antioxidants, do you really need research papers to confirm this..??
 
Genetic Freak said:
Which endocrinologist advise hCG in conjunction with exogenous hormones, unless part of TRT (is that what you are referring to)..?

Remember most endos are concerned with fertility in the short term for childless couples, not decades of exogenous hormone use to which we are discussing.. hCG should mostly work in this regard (in the short term) if secondary hypogonadism is the problem, it wont do anything for primary hypogonadism if the testes are damaged through decades of abuse..

Surely common sense should prevail in that damage via R.O.S should be countered or negated (whilst it is happening, on-cycle) with the use of antioxidants, do you really need research papers to confirm this..??
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Yes I was referring to TRT in that scenario.

And yes, the only way that this would work is low dose HCG used continuously throughout a cycle. Not enough to overwork cellular functions but enough to keep leydig cells sensitized to LH signaling, this seems to fall safely around 250iu 2-3 tines per week from studies (ie use, not abuse). Additionally, there wouldnt be any need for HCG if someone was blasting a cruising for life, just for someone who wanted to cycle, in which case there would be plenty of times that person would return to homeostatic function.

And I really have not looked at the issue extensively from that angle although I have read some. Thats primarily due to the fact that I havent seen any human studies reguarding antioxidants although there are probably some out there. That said, Ive said it would be optimal to use both routes of protection so the best protocol for harm reduction would be HCG in conjunction with taurine and royal jelly from what Ive seen and your previous comments.
 
Swim15 said:
^I believe I see what you are saying but the goal isn?t to overwork them, just to keep things at or near baseline.

It?ll probably take god knows how long to go back and find a lot of the data that I?ve seen but I did find these that I had saved and didn?t have to look for which I thought were at least helpful/interesting reads

http://www.allthingsmale.com/commun...lacy-of-hcg-desensitization.13095/#post-79885

https://www.ncbi.nlm.nih.gov/m/pubmed/15713727/
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Thanks for finding the paper on maintaining ITT levels. I remember discussing it when it first came out, back on CEM I think, which is where the idea of using about 125iu/day originally came from.

The issue we identified at the time is that hCG can cause active Leydig cells to release test in a dose-dependent fashion, and rather like a bleed, unlike the pulsatile way the body does. Which means even if you only have, say, 30% functional Leydig cells left, enough LH can still cause them to release above average levels of test. Which gives the outward appearance of having maintained testicular function, but doesn't protect the cells from on-cycle damage. So it's like squeezing more juice out of fewer active 'testosterone factories' (it also doesn't protect Sertoli cells).

It's only when you cut off that artificial LH tap and hormonal bleed, that you get to see what damage you've actually caused.
 
Serotonin101 said:
Seems to be an issue with the iPhone. At least they fixed the other issues that would put some weird characters in place of letters.
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Yeah it's to do with Apple's adoption of a new character set/thingy. Should be getting fixed when the site gets an upgrade! :)
 
Swim15 said:
I havent seen any human studies reguarding antioxidants although there are probably some out there. That said, Ive said it would be optimal to use both routes of protection so the best protocol for harm reduction would be HCG in conjunction with taurine and royal jelly from what Ive seen and your previous comments.
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Unfortunately, like I said in the earlier post, we're not likely to see many human studies.

It's expensive to do that, and caters for a very small population of what they consider to be 'drug abusers'.

They don't really care about ameliorating side effects from AAS use, since the focus for most research will either be (a) helping post-cycle recovery from long-term AAS abuse or (b) preventing men from using AAS in the first place.

I live in hope though. But until then, we have to make the best of what theory we can string together. Which, to be fair, is how most bodybuilding practice has evolved anyway, with science usually following behind in our wake.
 
CFC said:
Thanks for finding the paper on maintaining ITT levels. I remember discussing it when it first came out, back on CEM I think, which is where the idea of using about 125iu/day originally came from.

The issue we identified at the time is that hCG can cause active Leydig cells to release test in a dose-dependent fashion, and rather like a bleed, unlike the pulsatile way the body does. Which means even if you only have, say, 30% functional Leydig cells left, enough LH can still cause them to release above average levels of test. Which gives the outward appearance of having maintained testicular function, but doesn't protect the cells from on-cycle damage. So it's like squeezing more juice out of fewer active 'testosterone factories' (it also doesn't protect Sertoli cells).

It's only when you cut off that artificial LH tap and hormonal bleed, that you get to see what damage you've actually caused.
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Ah, interesting but makes sense. So hCG wouldn?t be optimal from a ?wishful? perspective but sounds like low doses to maintain some sensitization would be better than nothing [Mod-edit No it would not, do you not listen to anything] since damage is more than likely going to occur on cycle regardless, just via a different mechanism. Just isn?t going to be comprehensively protective, although combined with antioxidants it sounds like the best protection since it?s minimizing two different types of risk?
 
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Ideally I'm looking for some case studies of effective hCG use - ie where recovery from damage was proven, to help balance out a couple I have which show hCG merely disguising recovery or actually appearing to prevent recovery.

I will do a search eventually, but I figured you guys probably still read more popular boards and they probably have some recovery stickies and the like easily at hand ;)
 
Swim15 said:
Ah, interesting but makes sense. So hCG wouldn?t be optimal from a ?wishful? perspective but sounds like low doses to maintain some sensitization would be better than nothing since damage is more than likely going to occur on cycle regardless, just via a different mechanism. Just isn?t going to be comprehensively protective, although combined with antioxidants it sounds like the best protection since it?s minimizing two different types of risk?
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Yeah I'm not pretending like I have an answer - nobody does. Low dose hCG does anecdotally seem to help guys on cycle from a number of perspectives like mood, libido etc. It may keep cells more sensitised so that when you come off cycle and natural LH/FSH comes on tap, there's a chance test might start at a slightly higher level. But tbh the idea of 'sensitisation' seems pretty bunk.

In this study, for example: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2360778 all hCG did is inhibit genuine recovery. It caused a transient increase in test output back to normal physiological levels while using hCG, then as soon as that was stopped test dropped back lower than where they started and only slowly recovered naturally thereafter. Which implies hCG didn't sensitise in any way, and if anything caused the opposite.

That could be down to the dose of hCG used, or a number of other factors.
 
^Oh yeah that?s exactly what I would expect it to do in that scenario. The only way it?s going to ?work? is if it is always used on cycle, otherwise it won?t do anything more than nolva or clomid besides speed up the restart process. Definitely isnt going to repair damage in retrospect.

I can?t see the full study but I think the doses they used were too high or too prolonged although the summary says that normal hormone levels were maintained after the discontinuation of AAS and, subsequently, HCG.
 
There's no mechanism that I'm aware of for an LH-mimetic to protect testes cells (or the hypothalamus) from AAS harms. As I said, superficially maintaining ITT doesn't mean it's doing anything to protect either, merely forcing the release of test from surviving cells.

As for the paper, yeah it's sneakily worded. They give their subject hCG and when stopped he does worse that before he started lol. Normal hormone levels are eventually achieved afterwards, but not as a result of the hCG. And therefore a more reliable interpretation is that it hindered recovery.

Anyway the point for bringing it up was that if it can't turn things around when someone's off a cycle, it would be even less logical to think it would do so while they're on one.
 
Oh I do get that and also thanks for the clarification.

My understanding is that a lot of the potential damage can come from leydig cells shutting down during a cycle and becoming desensitized to LH signals since the hard part of recovery isn?t LH coming back online but the leydig cells responding to the LH. The HCG keeps them responsive and therefore prevents their shutdown.

I?ll have to dig out my copy of 10th Anabolics but there are tons of studies in there iirc that list the recovery times from cycles in the 6-12 months range due to the non-response to LH signaling as LH achieves normal levels post cycle rather quickly.

I may need to update some of my thinking but that was the basics of my understanding
 
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