Preserving HPT axis functions on cycle

[cucu]

There is heated debate on what is a viable option as an ancillary while on cycle, both for adverse side effect prevention and for easier recovery. Regarding recovery, most substances are used for their ability to salvage some function of an axis part, with the most prominenent and widely used being hCG . This hormone is used to preserve testicular function and form in the absence of LH, and FSH or its analog hMG have been proposed to support its spermatogenetic function.

But what about the other 2 parts of the axis? Granted, hypothalamus is a brain region with milllions and diverse inputs, both hormonal and neuronal. Lastly, is there anything we can do to preserve the third part of the HPTA, the pituitary?



The pituitary receives input from the hypothalamus via pulses of GnRH and from the testes via T and a few other hormones (namely activin and inhibin). It produces LH, which tells the testis to produce T, and FSH, which tells the testis to produce spermatozoa.

Regular pulses of GnRH promote the production of LH and FSH in the anterior pituitary, while prolonged and intense GnRH input blocks it. Most importantly, gonadal hormones like T and E reduce GnRH activity. Testosterone and estrogen on the other hand inhibit LH and FSH production. It is our body's way of telling that we have enough gonadal hormones and the testes do not need to produce more.

These tissues (the pituitary and the testes) undergo a process call sensitization.Put simply, if left for a long period without any excitation, even a small stimulus will produce great effect. The reverse is also true, if for a long period they are over-stimulated, a great stimulus will produce miniscule effect.

While on cycle, we provide the body with a supra-physiological amount of androgens. This leads eventually to a reduction in hypothalamic, pituitary and testicular activity. If there were a way to prevent GnRH and T/E sensitization of the pituitary, the recovery and the preserved function of it would be benefited.

Older studies (PMID: 3931502, 323393, 6781360, 3516082, sorry cant post links yet) suggest that is the case with a low dose of SERMs.

Specifically, there is a dose-dependent bell shaped curve where a low dose of tamoxifen will actually raise LH (and subsequently T) levels, and at the same time, sensitize the pituitary's input to GnRH. The dose studied was 20 mg / day. At higher doses of clomiphene or tamoxifen the reverse was true, as the pituitary was desensitized. There are specific limitations: these were mostly done in cell cultures, where GnRH input is absent by default; mainly female subjects were used; there was no supplementation.

In another study (PMID: 22946848) tamoxifen increased a marker of testicular function while on replacement therapy, indicating an increase in FSH activity. The replacement dose in this study was 120 mg / day of testorone undecanoate per os.

Other unecdotal evidence point to numerous steroid (ab)users to supplement their on cycle protocol with a low dose of SERM for the same reason.



On another substance, we have hMG. This is a hormone, analog in its action to both LH and FSH. It's sole role in the male is found in the testis, where it both increases T production and spermatogenesis. Its use has been documented reverse steroid-induce hypogonadism (PMID: 12801577). It is also supported by many that use of the substance up to the start of PCT helps recovery and preserves testicular function, as with hCG preserving another part of testicular function, T production.



Therefor, it would be interesting to assert whether there is the need for a low dose of tamoxifen and hMG during cycle, whether it would ease recovery and help preserve both pituitary and testicular function.

[XxAndreaxX]

Man, if there was a method to preserve LH and FSH, we would all be on TRT....
You can try to eat nolva and clomid and do BW during cycle, but I doubt it will work.
Find it out, we will thank you!

[Buster Brown]

Anecdotal at best in regards to serms on cycle for faster recovery....actually I would dub that the "everything but the kitchen sink" approach. At this point it isn't hotly debated and there is a lack of concrete study to show otherwise.

[cucu]

Anecdotal at best in regards to serms on cycle for faster recovery....actually I would dub that the "everything but the kitchen sink" approach. At this point it isn't hotly debated and there is a lack of concrete study to show otherwise.

You say that there might be anecdotal evidence, that is excellent! We only have anecdotal evidence of hCG during cycle, so that might be equally trusted. There is no study up to this point, to the best of my knowledge, that confirms that hCG administration during supra-physiological doses facilitates recovery. There are only personal observations (empirical or unecdotal evidence). A consensus in the steroid forum is not evidence (with all due respect).

So, I am saying that 1) It is a valid hypothesis that low doses of SERM facilitates recovery and 2) are there any personal evidence that it does?

[XxAndreaxX]

You say that there might be anecdotal evidence, that is excellent! We only have anecdotal evidence of hCG during cycle, so that might be equally trusted. There is no study up to this point, to the best of my knowledge, that confirms that hCG administration during supra-physiological doses facilitates recovery. There are only personal observations (empirical or unecdotal evidence). A consensus in the steroid forum is not evidence (with all due respect).

So, I am saying that 1) It is a valid hypothesis that low doses of SERM facilitates recovery and 2) are there any personal evidence that it does?

Hcg won’t help recovery. In fact, it will hinder recovery. HCG only helps against nuts shrinkage and shutdown, while on AAS.
Now, IMO, AI helps more for recovery than SERMS (if nuts are actually working due hcg)
Because AI will lower estrogens, and force your body to produce more test.
If you take SERMS, and have E2 skyhigh, you won’t really recover until you don’t lower your E2.
Its my personal experience eeh, there’s no evidence or study about this.
Now, you can do this experiment if you’re interested. Do a DHT only cycle, like Winstrol or something where E2 won’t be altered. Take along that, some SERMS like nolva and clomid, and check your blood weekly. If your test and E2 remains stable, your trick works.
Don't know if HMG could give additional benefits in this case...

[tobias 34]

Hcg won't help recovery. In fact, it will hinder recovery. HCG only helps against nuts shrinkage and shutdown, while on AAS. Now, IMO, AI helps more for recovery than SERMS (if nuts are actually working due hcg) Because AI will lower estrogens, and force your body to produce more test. If you take SERMS, and have E2 skyhigh, you won't really recover until you don't lower your E2. Its my personal experience eeh, there's no evidence or study about this. Now, you can do this experiment if you're interested. Do a DHT only cycle, like Winstrol or something where E2 won't be altered. Take along that, some SERMS like nolva and clomid, and check your blood weekly. If your test and E2 remains stable, your trick works. Don't know if HMG could give additional benefits in this case...

So your suggesting that There is no true benefit in using HCG on cycle but rather during pct along with AI and no serm?

[cucu]

So your suggesting that There is no true benefit in using HCG on cycle but rather during pct along with AI and no serm?

Well, this study (PMID: 24636400, Anabolic steroid -induced hypogonadism: diagnosis and treatment) clearly suggests that hCG is pseudoscience and that a low dose of clomiphene should be used on TRT-doses of T for testicular and pituitary function preservation.
It makes sense, because in ASIH (androgen steroid induced hypogonadism) it is the pituitary that fails, and not the testes that we address with hCG.

I understand it is only one study with limitations tho. It is a good read nonetheless, you should check it.

[XxAndreaxX]

Well, this study (PMID: 24636400, Anabolic steroid -induced hypogonadism: diagnosis and treatment) clearly suggests that hCG is pseudoscience and that a low dose of clomiphene should be used on TRT-doses of T for testicular and pituitary function preservation.
It makes sense, because in ASIH (androgen steroid induced hypogonadism) it is the pituitary that fails, and not the testes that we address with hCG.

I understand it is only one study with limitations tho. It is a good read nonetheless, you should check it.

HCG works wonders during cycle, I know it, because when my nuts starts to shrink, I feel much pain. When I start feeling pain in my nuts (usually at week 4) I start HCG, and pain goes away almost immediately.
But if your idea is to maintain full HPTA functionality during cycle, HCG shouldn’t be used.

[Docd187123]

You say that there might be anecdotal evidence, that is excellent! We only have anecdotal evidence of hCG during cycle, so that might be equally trusted. There is no study up to this point, to the best of my knowledge, that confirms that hCG administration during supra-physiological doses facilitates recovery. There are only personal observations (empirical or unecdotal evidence). A consensus in the steroid forum is not evidence (with all due respect).

So, I am saying that 1) It is a valid hypothesis that low doses of SERM facilitates recovery and 2) are there any personal evidence that it does?

You have more than anecdotal evidence supporting HCG. You have a study performed by Dr. Scally I beleive as well as labs from many endos/uros from people like Dr. Crisler.

[Docd187123]

Well, this study (PMID: 24636400, Anabolic steroid -induced hypogonadism: diagnosis and treatment) clearly suggests that hCG is pseudoscience and that a low dose of clomiphene should be used on TRT-doses of T for testicular and pituitary function preservation.
It makes sense, because in ASIH (androgen steroid induced hypogonadism) it is the pituitary that fails, and not the testes that we address with hCG.

I understand it is only one study with limitations tho. It is a good read nonetheless, you should check it.

I think you should actually read what you reference before referencing it. This is taken directly from the pubmed study:

RESULT(S): Symptomatic hypogonadism is a potential consequence of AAS use and may depend on dose, duration, and type of AAS used. Complete endocrine and metabolic assessment should be conducted. Management strategies for anabolic steroid-associated hypogonadism (ASIH) include judicious use of testosterone replacement therapy, hCG, and selective estrogen receptor modulators.

[kelkel]

clearly suggests that hCG is pseudoscience

And steroids don't build muscle either. If what your proposing "made sense" don't you think Crisler, Vergel, Scally, Morgantaler, Shippen and others would be all over this and it would be well known by now?

Cucu do you have hands on experience with cycling or is this just an area of interest for you?

[Buster Brown]

And steroids don't build muscle either. If what your proposing "made sense" don't you think Crisler, Vergel, Scally, Morgantaler, Shippen and others would be all over this and it would be well known by now?

Cucu do you have hands on experience with cycling or is this just an area of interest for you?

Amen!

[Lemonada8]

oh boy, another one of these threads love it! ill be short and to the point...

HCG on cycle has been shown to maintain ITT ( Intratesticular testosterone ) while under the effects of AAS-induced inhibition. (Low-dose human chorionic gonadotropin maintains intratesticular tes... - PubMed - NCBI) This linked study is paramount to using HCG while ON-cycle.

HMG is a FSH analoug. The reason we dont worry about FSH levels is that it has 2 routes of regulation compared to LH having one. So the drop in FSH isnt nearly as much as the drop in LH while on a cycle of AAS.

Well, this study (PMID: 24636400, Anabolic steroid -induced hypogonadism: diagnosis and treatment) clearly suggests that hCG is pseudoscience and that a low dose of clomiphene should be used on TRT-doses of T for testicular and pituitary function preservation.
It makes sense, because in ASIH (androgen steroid induced hypogonadism) it is the pituitary that fails, and not the testes that we address with hCG.

True in ASIH the pituitary gland doesnt produce LH like it normally should, however the pituitary gland is very quick at adapting and is not the focus of using HCG on cycle. THe problem with cycling is that the testes essentially shrivel up and stop producing testosterone and that is what takes so long to recover. THe HCG helps prevent the testes from shutting down by keeping them functioning and keeping the ITT to near normal levels. So when PCT comes, clomid n nolva act upon the pituitary gland to increase the frequency of LH pulses and increase the amount of LH released during these pulses. SO that is addressing the pituitary aspect of the AAS induced suppression. THe HCG is maintaining the testes functionablity to produce Testosterone so when the pit begins to make LH again (with the help of clomid/nolva) they can properly respond via making testosterone.

At higher doses of clomiphene or tamoxifen the reverse was true, as the pituitary was desensitized.

THis is inaccurate slightly. for desensitization It doesnt matter the dosage of the drug what matters is the duration of it. True, at long durations of clomid studies have shown a desensitization of the pituitary gland to LHRH but in that aspect it was over longer periods of time ( much longer than a pct), and those studies were done with a much higher dose of clomid also.
Tamox/nolva has been shown to increase the sensitivity of the pit to LHRH. THis was done at the dosages that are used during a PCT.


FYI the pct protocol i def suggest which im basin the above mentions of PCT is:
Clomid 100/75/50/50
Nolva 40/40/20/20/20/20

[Buster Brown]

Nice job Lemonada......

[NACH3]

oh boy, another one of these threads love it! ill be short and to the point...

HCG on cycle has been shown to maintain ITT ( Intratesticular testosterone ) while under the effects of AAS-induced inhibition. (Low-dose human chorionic gonadotropin maintains intratesticular tes... - PubMed - NCBI) This linked study is paramount to using HCG while ON-cycle.

HMG is a FSH analoug. The reason we dont worry about FSH levels is that it has 2 routes of regulation compared to LH having one. So the drop in FSH isnt nearly as much as the drop in LH while on a cycle of AAS.





True in ASIH the pituitary gland doesnt produce LH like it normally should, however the pituitary gland is very quick at adapting and is not the focus of using HCG on cycle. THe problem with cycling is that the testes essentially shrivel up and stop producing testosterone and that is what takes so long to recover. THe HCG helps prevent the testes from shutting down by keeping them functioning and keeping the ITT to near normal levels. So when PCT comes, clomid n nolva act upon the pituitary gland to increase the frequency of LH pulses and increase the amount of LH released during these pulses. SO that is addressing the pituitary aspect of the AAS induced suppression. THe HCG is maintaining the testes functionablity to produce Testosterone so when the pit begins to make LH again (with the help of clomid/nolva) they can properly respond via making testosterone.




THis is inaccurate slightly. for desensitization It doesnt matter the dosage of the drug what matters is the duration of it. True, at long durations of clomid studies have shown a desensitization of the pituitary gland to LHRH but in that aspect it was over longer periods of time ( much longer than a pct), and those studies were done with a much higher dose of clomid also.
Tamox/nolva has been shown to increase the sensitivity of the pit to LHRH. THis was done at the dosages that are used during a PCT.


FYI the pct protocol i def suggest which im basin the above mentions of PCT is:
Clomid 100/75/50/50
Nolva 40/40/20/20/20/20

Why Clomid only 4 wks and Nolva 6 wks... Is it due to what you referenced in your post about long term clomid use?(was thinking long term is 3 months or so?) So Is it not essential to run a 6 wk clomid protocol w/a 19nor(NPP)...

I ask b/c my cycle prop 600mgs wkly/NPP 400mgs wkly/winny oral 50mg last 4 wks or mast prop 400mg from wks5-12(&T3 5-12 upping my cals from 2700 in 1-5 to 3200 so my muscle tissue isn't getting eatin up... Lol

PCT clomid - 100/75/50/50/50/25
Nolvadex - 40/40/20/20/20/10

[Lemonada8]

^^ you are correct w/ long term usage being much longer, but since clomid mainly increases the LH pulse size and not the frequency, doing 4 weeks of it will be enough. Also some users complain of side effects so I feel that 4 weeks is plenty of time for clomid. The clomid is great to increase the amount of LH released, but can possibly have a rebound effect after stopping due to the decrease in pulse size. Thats where the nolva going 2 weeks longer helps prevent any of those issues.

as with every PCT, the nolva should be ran 2 weeks longer due to its effect on the increased LH pulse frequency and the increased sensitization of the pit to LHRH is better to finish on. It will negate any desensitization done ( if any) from the clomid. Also it will help take any gyno on cycle to decrease in size. Nolva can be continued longer if gyno is still present at the 20mg dosage.

[Mr.BB]

^^Thanks for this^

Starting PCT in a few days (test p + NPP) so im increasing the nolva duration based on your info.

[NACH3]

^^^ thanks for clarifying that Lemonada... Does make sense... I personally have not taken clomid for 6 wks but thought I should hit it a lil harder do to the NPP... But will incorporate the Nolva as I had w/maybe even keeping my last wk(6th) at 20mg also!

So clomid at 100/75/50/50 would be sufficient enough then?

[Lemonada8]

yes that should be sufficient.

[NACH3]

yes that should be sufficient.

Thanks again for the info! Much appreciated!

[austinite]

Well I missed all the fun.

[cucu]

Well I missed all the fun.

OK, I'll try to address the points I feel need clarification. So, aus, you are still welcome to jump in.

First of all, Lemonada you are 100%. Apart from 1 thing. That the pituitary is the easy part. Virtually all cases of hypogonadism due to steroids are hypogonadotropic, secondary. That means that the pituitary fails first, and then the testes, if they fail at all. So, everyone, yes, hCG works! But does it work at preserving pituitary function? NO!

Also, I have failed to find that study referring to dosage vs duration in SERM's. Would you be kind enough to share a link? If I am wrong I'llbe happy to accept it.

Docd, I think that you should read past the abstract, especially when you care to demean. The actual study (you know, the paper) says that hCG is reserved for irreversible cases of established ASIH and that it can (with or without hMG) promote spermatogenesis. It says nothing about a prophylactic nature for ASIH.

kelkel, Scally? Really? When was it the last time you proposed the "20000 iu's of hCG in PCT" to a fellow steroid user? Please give me a break from alleged authorities and stop patronising. You sound like Rich Piana: Look at me, Im big, so you should take hCG in PCT. Science advances. Things change. Protocols of the past can and will be altered or scrapped of. Who would you trust on steroid advice, a champion from the 70's or a contemporary gym rat? Please answer with honesty.

To make it all clear. hCG helps testes functioning on cycle. That's that, and that's all. We dont know if it prevents ASIH. Is there a study that says it does? NO. Is there a/some duplications of that study? NO.
Is there a study for Serm's doing that? No. No duplications either. Does it makes sense that it prevents ASIH? YES!

BTW, I am not saying "drop the hCG". I am saying maybe adjust it to the least amount needed and add a SERM. There was a time when no PCT was used. Now we do. Maybe we can move forward. It is a pity seeing so much negativity to progress.

[Docd187123]

One of the most detailed views of what a post-cycle crash probably looks like comes from an investigation into testosterone enanthate .354 It involves a group of men that were given weekly injections (250 mg) for 21 weeks, a dose that admittedly does go beyond normal HRT use. Various hormones were measured each week during the study, and for more than 4 months after the medication was discontinued. A review of the data shows that at the start of the study, “LH levels were suppressed in direct relation to the rise in testosterone (see Figure I). Once the steroid was withdrawn, however, there was a delay between the return towards normal LH production (which began to correct by the 3rd week) and testosterone (which took more than 10 weeks before noticeable correction).

The above study suggests that one of the first things to happen after steroid cessation is that the brain recognizes testosterone levels are low again. This will cause GnRH and LH levels begin correcting fairly quickly. The substantial delay between this and an increase in testosterone levels is caused largely by “testicular unresponsiveness to luteinizing hormone. After months of receiving extremely weak stimulation, they will have lost a substantial amount of mass (atrophied). This is a well-documented side effect of anabolic steroid use, even if a size difference may not be immediately visible in all cases. When LH levels begin surging back, the testes will initially be unable to handle the workload. This is expected to correct itself in time, but it may take many weeks for the testes to slowly restore to their original mass. With a good portion of the post-cycle recovery period actually being characterized by normal (even high) levels of LH, we must address recovery broadly if we expect it to be effective

Excerpt From: Llewellyn, William. “Anabolics.” iBooks.

Sorry I can't get a better copy of the pictures




The above data would indicate that it's not the pituitary that's the problem with recovery but rather the response to the pituitary by the testicles.

Nobody has said HCG preserves pituitary function. It maintains testicular volume which is a fundamental roadblock in the recovery process. Nobody has claimed that HCG prevents ASIH but rather that it CAN HELP in recovering from it.

Wasn't Dr. Scally the one who pushed and lobbied for government and medicine to recognize ASIH and coined the term? If so it's ironic you use Scally's own term then demonized him right after.

Comparing Piana to Scally is ludicrous. One is an idiot and the other has he educational and clinical background to speak from experience. Nobody is saying hey listen to this one doctor, but when many of the top doctors around the world agree on this and is based on the research out there it's hard not to lend them some credibility. Especially when they years and years of blood work from thousands of patients to use as data points.

Last time I recommended "20,000IU of HCG in PCT" to someone was the last time I recommended Scally's Power PCT to someone, was just last month in January if I'm not mistaken.

[cucu]

The above data would indicate that it's not the pituitary that's the problem with recovery but rather the response to the pituitary by the testicles.

Well, I am glad we are talking with more sense and calmly now.



But, ASIH is hypogonadotropic hypogonadism. Otherwise known as secondary hypogonadism. What does that mean? That the pituitary fails, not the testes. And if they fail, they fail after the pituitary does. In other terms, the rise of the first graph is guaranteed (more or less) but the rise of LH is not. The rise in the second graph is not always there for the rise in T to be, even if strenuous.

What you are trying maybe to say is that the testes are reduced in size and hence the lag in response. They have to "get bigger before they can react". That is true potentially.

Apart from that, I dont know Scally or anyone else. But please bear with me when I say hCG does not prevent ASIH. We just don't have the data that support that notion.

It may facilitate (or most prolly just speed up) recovery, but if you are to get ASIH, hCG wont help you. I hope that makes sense to all of you by now. And I was trying to say that maybe, we can tinker with those chances by providing a signal to the pituitary and not let it "fall off" due to not being used.



I understand this is only a hypothesis, but please leave out the authorities. Piana says hCG is good for ASIH or Scally does (I am not comparing them but they both say use hCG for PCT) so good it is. It simply does not work like that.

What I honestly think would be an advancement in this thread would be if someone had data or a study on long-term SERM usage (the duration vs dosage being important). That would be a deal-breaker if what was said above by Lemonada holds true.

[cucu]

And since you mentioned Llewelyn:

[...] Researchers were also conducting GnRH stimulation tests before and after various points of treatment with Nolvadex and clomid, and the two compounds had markedly different results. These tests involved infusing patients with 100mcg of GnRH and measuring the output of pituitary lh - leutenizing hormone - in response. The focus of this test is to see how sensitive the pituitary is to Gonadotropin Releasing Hormone. The more sensitive the pituitary, the more lh - leutenizing hormone - will be released. The tests showed that after ten days of treatment with Nolvadex, pituitary sensitivity to GnRH increased slightly compared to pre-treated values. This is contrast to 10 days of treatment with 150mg clomid, which was shown to consistently DECREASE pituitary sensitivity to GnRH (more lh - leutenizing hormone - was released before treatment). As the study with Nolvadex progresses to 6 weeks, pituitary sensitivity to GnRH was significantly higher than pre-treated or 10-day levels. At this point the same 20mg dosage was also raising testosterone and lh - leutenizing hormone - levels to an average of 183% and 172% of base values, respectively, which again is measurably higher than what was noted 10 days into therapy. Within 10 days of treatment clomid is already exerting an effect that is causing the pituitary to become slightly desensitized to GnRH, while prolonged use of Nolvadex serves only to increase pituitary sensitivity to this hormone.[...]

Nolvadex vs Clomid, by Bill Llewelyn

[Docd187123]

Well, I am glad we are talking with more sense and calmly now.

I wasn't not calm before.

But, ASIH is hypogonadotropic hypogonadism. Otherwise known as secondary hypogonadism. What does that mean? That the pituitary fails, not the testes. And if they fail, they fail after the pituitary does. In other terms, the rise of the first graph is guaranteed (more or less) but the rise of LH is not. The rise in the second graph is not always there for the rise in T to be, even if strenuous.

Hypogonadotropic hypogonadism is not necessarily a problem with the pituitary. It can also be with the hypothalamus. The rise of the either graph is not guaranteed. They're doing some research now on mixed hypogonadism I need to look it up to recall the details but basically you can have reduced sensitivity to LH and also not produce enough LH and get a combination of both.

What you are trying maybe to say is that the testes are reduced in size and hence the lag in response. They have to "get bigger before they can react". That is true potentially.

I believe that is what the author is saying correct.

Apart from that, I dont know Scally or anyone else. But please bear with me when I say hCG does not prevent ASIH. We just don't have the data that support that notion.

Can you point me to somewhere where someone has claimed HCG prevents ASIH?

It may facilitate (or most prolly just speed up) recovery, but if you are to get ASIH, hCG wont help you. I hope that makes sense to all of you by now. And I was trying to say that maybe, we can tinker with those chances by providing a signal to the pituitary and not let it "fall off" due to not being used.





I understand this is only a hypothesis, but please leave out the authorities. Piana says hCG is good for ASIH or Scally does (I am not comparing them but they both say use hCG for PCT) so good it is. It simply does not work like that.

What I honestly think would be an advancement in this thread would be if someone had data or a study on long-term SERM usage (the duration vs dosage being important). That would be a deal-breaker if what was said above by Lemonada holds true.

[cucu]

Hypogonadotropic hypogonadism is not necessarily a problem with the pituitary. It can also be with the hypothalamus.

That is true. But that is why I posted just above that that low doses of tamoxifen (nolva) actually sensitize the pituitary to GnRH. But most of the times it is secondary (pituitary) and not tertiary (hypothalamus). Tertiary hormonal deficiency is rare throughout the hormonal spectrum and mainly accounted for by tumors, whereas primary and secondary are not.

Can you point me to somewhere where someone has claimed HCG prevents ASIH?

Perfect. So you may be agreeing that A) hCG does not prevent ASIH and helps one aspect of recovery (the testicular part) and B) SERM's may be beneficial for preventing/reducing risk for ASIH and help another aspect of recovery (the pituitary part)? Both A and B being on cycle.

[kelkel]

kelkel, Scally? Really? When was it the last time you proposed the "20000 iu's of hCG in PCT" to a fellow steroid user? Please give me a break from alleged authorities and stop patronising. You sound like Rich Piana: Look at me, Im big, so you should take hCG in PCT. Science advances. Things change. Protocols of the past can and will be altered or scrapped of. Who would you trust on steroid advice, a champion from the 70's or a contemporary gym rat? Please answer with honesty.

Yes, really. I'd propose the power pct protocol to anyone coming off a cycle where they did not use hcg . Where's the fault in that? And btw, they are well educated men who are trusted in this arena. Sorry, we don't know you. You've been here for a whole 25 posts but apparently you are "the authority" on the subject matter. And no, I'm not a fan of Piana, but no doubt he is much bigger than you and I.

Tell us, what experience do you have when it comes to cycling?

[Docd187123]

That is true. But that is why I posted just above that that low doses of tamoxifen (nolva) actually sensitize the pituitary to GnRH. But most of the times it is secondary (pituitary) and not tertiary (hypothalamus). Tertiary hormonal deficiency is rare throughout the hormonal spectrum and mainly accounted for by tumors, whereas primary and secondary are not.



Perfect. So you may be agreeing that A) hCG does not prevent ASIH and helps one aspect of recovery (the testicular part) and B) SERM's may be beneficial for preventing/reducing risk for ASIH and help another aspect of recovery (the pituitary part)? Both A and B being on cycle.

I've not seen enough evidence to conclude one way or another whether SERMs may be beneficial to preventing ASIH. I quickly glanced through a couple of the studies you mentioned and they seemed to be talking more about sperm production but again that was only a quick glance.

I noticed in your OP you talked about sensitization and said

"Put simply, if left for a long period without any excitation, even a small stimulus will produce great effect."

^^^ how does this apply to the testes or pituitary for example? You are saying on one hand that the lack of stimulus will produce a greater effect when the stimulus is reintroduced and on the other hand you say the pituitary needs help restoring homeostasis bc it's been suppressed on cycle. Those seem like contradictory statements to me.

[cucu]

Yes, really. I'd propose the power pct protocol to anyone coming off a cycle where they did not use hcg . Where's the fault in that? And btw, they are well educated men who are trusted in this arena. Sorry, we don't know you. You've been here for a whole 25 posts but apparently you are "the authority" on the subject matter. And no, I'm not a fan of Piana, but no doubt he is much bigger than you and I.

Tell us, what experience do you have when it comes to cycling?

You do not have to trust me. In fact, I urge you to question me. Think for yourself, question authorities. I have been very kind all along and I expect the same courtesy on your behalf.

You do not seem to like my statement. I can go with that. But still, you have not proven wrong that "hCG does not prevent ASIH, it simply kick-starts or preserves testicular function".

I can understand people being reluctant to change. But I am willing to try to rationally convince you without demeaning until one of us is proven wrong, without relying on authorities without proof. The people on TRT on these forums following these pieces of advice are enough (and more out there not following any advice, like PCT, granted). We can do better. I am not saying it is someones fault. All I am saying is that there is room for development. Maybe the exact opposite way from the one I propose? Maybe. But there is room.

Docd, what I was describing is a very well-known physiological process. If a stimulus is given in too much of an intensity, receptors downregulate so that a higher absolute signal accounts for the same amount of response. For example, if a man is working well at 500 pulses of GnRH, and you give him 1000 of GnRH, then double the receptors will be occupied (I am simplifying to the extent of over-simplifying). At a point later in time, he will have less receptors because the gonadotropic cell understands that it is over-activated, say dropping them to half of the original. So, in a large enough time frame, double the pulses will equal the same response in LH. If you give the first guy a pulse, he will output 100% of LH. If you give the second one a pulse, a 50% will be output. Again, over-simplified.
This is desensitization by downregulation. The opposite holds true as well.

[kelkel]

Cucu your quest or theory here is without a doubt, noble. Whether it's demonstrable is another matter. It's one reason I keep asking if you cycle or actually use AAS, to which you keep ignoring.

[cucu]

Cucu your quest or theory here is without a doubt, noble. Whether it's demonstrable is another matter. It's one reason I keep asking if you cycle or actually use AAS, to which you keep ignoring.

Yes, the testability is crucial for any theory to be regarded scientific. But if you go that way, nothing has been scientifically proven in the non-prescribed AAS (ab)use - cycling apart from the main part - that steroids work. Just recently (2012) the New England Journal of Medicine (the most prominent medical journal) published a paper that showed that steroids increase mass!... That's where science's at, all the rest are pseudoscience in cycling if you follow that strict definition.

Secondly, I bet you have more cycles under your belt than I do. But I wouldn't trust my urologist based on how many prostate cancers he has been diagnosed with. Unless you don't wanna regard us as "scientists" and we are simply users, in which case yes, personal experience would come first. In that case, I'd rather go with Rich Piana and not you, humbly and in all honesty. After all, he is bigger than you and me.

Doing a little "research" on other forums, there are a few people who have been trying to experiment with SERM's on cycle, so I guess I was not the only one to think about that, and certainly not the first. There are a few users at the UK who actually cycle without hCG and use Clomid eod (you can search their boards, the most prominent member there is ausbuilt, I am not linking). Maybe there is more information, and we are reluctant to share it or evaluate it as it has been shown in this thread.

Anyway, I guess there isn't any response by Lemonada as to that theory he mentioned about dose vs duration, is it? I'd like to read that and I haven't found it.

[NACH3]

Yes, the testability is crucial for any theory to be regarded scientific. But if you go that way, nothing has been scientifically proven in the non-prescribed AAS (ab)use - cycling apart from the main part - that steroids work. Just recently (2012) the New England Journal of Medicine (the most prominent medical journal) published a paper that showed that steroids increase mass!... That's where science's at, all the rest are pseudoscience in cycling if you follow that strict definition.

Secondly, I bet you have more cycles under your belt than I do. But I wouldn't trust my urologist based on how many prostate cancers he has been diagnosed with. Unless you don't wanna regard us as "scientists" and we are simply users, in which case yes, personal experience would come first. In that case, I'd rather go with Rich Piana and not you, humbly and in all honesty. After all, he is bigger than you and me.

Doing a little "research" on other forums, there are a few people who have been trying to experiment with SERM's on cycle, so I guess I was not the only one to think about that, and certainly not the first. There are a few users at the UK who actually cycle without hCG and use Clomid eod (you can search their boards, the most prominent member there is ausbuilt, I am not linking). Maybe there is more information, and we are reluctant to share it or evaluate it as it has been shown in this thread.

Anyway, I guess there isn't any response by Lemonada as to that theory he mentioned about dose vs duration, is it? I'd like to read that and I haven't found it.

In reference to Rich Piana: from "Austinites Database":




Why You Should Not Use hCG Post Cycle:

Let's establish what we are trying to accomplish here. You just got done with your cycle and you've been suppressed for however many weeks. We want to bring our natural HPTA back to life, can we all agree on that? If you said no, please ask Mom if she dropped you on your head when you were a baby. Moving on...

hCG is suppressive! Since we know that hCG mimics LH, then we know that in the presence of exogenous LH, the pituitary gland will not produce LH. Hang on a minute! You see that word in blue above? It says "natural". So which one is natural? The one I just induced by using hCG, or the one coming from the pituitary? Doh! The pituitary of course! So why? Why on earth would you want to suppress your pituitary with hCG when you're trying to recover?! "Ain't nobody got time for dat!" Are we clear on this one, folks? If you said no, you know what to do...

So next time you meet Rich Piana. Tell him that he is a dingdong, and he's hurting a lot of people with his statements. Please, Rich. stop hurting people. (Jon Stewart voice)

SERMS! Clomid and Nolva are not suppressive. In fact, they work on your brain to help the pea sized gland pump out your precious LH. That is all you should be using for PCT. Otherwise, it would be like walking into a closed door and never being able to get inside. Would you constantly walk into a door without being able to get inside? Wait... that's doing the wrong thing over and over again. I'm pretty sure that's referred to as insane. Ok, enough comedy. Lame, I know. Sorry, I'm not kelkel.

[NACH3]

^^^ very dumbed down for peops... But we're in a situation where science will advance in this area(we are just the current lab rats)... I get and respect your theory but this is the most proven and safest way as of now! But later down the road is it possible to have more scientific breakthroughs... But now Piana's theory is and will hurt people... hCG should be taken as low a dose throughout cycle as possible(trying not to exceed 500iu in a wk, or like you stated desensitization will occur! Just my .02... Seems you have a great backroung in Endo/IB?!

[Lemonada8]

Anyway, I guess there isn't any response by Lemonada as to that theory he mentioned about dose vs duration, is it? I'd like to read that and I haven't found it.

I had to get my SD card out so i could get the articles. but here u go.


DIFFERENTIAL DEPLETION OF CYTOPLASMIC HIGH AFFINITY OESTROGEN RECEPTORS AFTER THE in vivo ADMINISTRATION OF THE ANTIOESTROGENS, CLOMIPHENE, MER-25 AND TAMOXIFEN

In summary the results demonstrate that the antioestrogens, clomiphene, MER-25 and tamoxifen produce long term cytosol HAR depletion in the CNS and pituitary, similar to that found for the uterus. It has also been shown that in vivo, higher doses of the drugs are required to produce depletion of the HAR when compared to the peripheral tissues.

Granted yes it is in a female rat, but the principles are generally the same with males ( with differing stimulation of males vs females) but nevertheless it describes desensitization. The dosage of the clomid was 5mg/kg so for 100kg male the dosage would be 500mg of clomid, which is way more than used in a PCT setting.

Clomiphene Citrate Effects on Testosterone /Estrogen Ratio in Male Hypogonadism

After initiating therapy with 25 mg of oral clomiphene citrate once a day, patients were reevaluated approximately 4–6 weeks later.

Clomiphene citrate effectively induces endogenous testosterone production via competitive inhibition of the hypothalamic estrogen receptor. Clomiphene citrate was able to increase serum testosterone and improve the testosterone/estrogen ratio. Clomiphene citrate was well toleratedand may be an alternative in the treatment of secondary hypogonadism in the aging male.

THis study describes the T/E ratio in males which is very important esp during exogenous testosterone injection aka AAS. Estrogen really increases during a cycle ( hence using a AI during cycle). This is key to maintain/recover from the exogenous suppression brought on by AAS, and this study was done in hypogonadic males.

Pituitary-Testicular Responsiveness in Male Hypogonadotropic Hypogonadism

The low levels of serum LH (< 1 mIU/ml) observed in this study were reflected by prepubertal levels of plasma testosterone. However, the plasma concentrations of the weekly androgenic 17-ketosteroids, androstenedione, and dehydroepiandrosterone, which are derived almost entirely from the adrenal gland, were within the range of values observed in normal adult males. Thus, it appears unlikely that the presence of LH is necessary, acting synergistically with ACTH, to initiate adrenal 17-ketosteroid secretion.

THis article describes the function of the testes responding to LH is the biggest problem, and not the adrenal glands. Yet another reason to use HCG on cycle, to maintain testicular function via keeping ITT levels high.

Clomiphene citrate: a correlation of its effect on sperm concentration and morphology, total gonadotropins, ICSH, estrogen and testosterone excretion and testicular cytology in normal men

Sperm concentration was dosage related: low dosages of clomiphene (50 mg/day) caused an increase; intermediate dosages (100 and 200 mg/day) caused an increase, decrease, or no change; and high doses caused precipitous decreases.

Spermatogenesis is a good indicator for testicular function because it is the main function of the testes.


the effect of clomiphene citrate on the 24 hour LH secretory pattern in normal men

The results show that clomiphene causes a consistent, significant increase in the 24 hr mean LH concentration

THis was done w/ a trial of 100mg clomid for 1 week. Also known as a clomiphene stimulation test to endocrinologists. LH is supposed to double in that time frame w/ the dosage provided. THis is a key reason i suggest 100mg clomid for the first week, then decrease it in the following weeks.
This paper also shows that the increase in LH is due to larger LH puleses and not increased pulse frequency. Thats where the nolva/tamox comes in to increase pulse frequency.

Clomiphene increases free testosterone levels in men with both secondary hypogonadism and erectile dysfunction: who does and does not benefit?

Of the 272 men with hypogonadotropic hypogonadism and ED, 228 (83.8%) completed a 4-month course of clomiphene citrate, 50mg orally on Monday, Wednesday, and Friday.

significant increases in luteinizing hormone (Po0.001) and free testosterone (Po0.001) occurred in all patients.

This is showing the non desensitization occuring at the PCT dosages i suggest.

These are only excerpts from the studies that i have that correlate to the disscussion at hand. Ive been meaning to write a PCT protocol paper with alot of these studies but ive been to busy with other things to fully finish it. I have, however, read most of the studies that i have regarding this topic ( 30+) and go off of that. One of these days when i have time i will write the whole paper and then plan on having it reviewed by some of the medical professionals in the field of endocrinology and AAS ( ie Dr Scally) and get their opinion of it.

FYI what is ur education level? Like where did this discussion come from? you just tryin to research this as a 'bro' or do you have indepth medical knowledge and wondering about this aspect of medicine?

[NACH3]

^^^ Very in depth... Thanks for sharing and goin thru what you had to in order to get it! lol

[cucu]

Thanks a lot Lemonada! It will take some time to sort out what is most useful for PCT and what would be important for my question. In the meantime, please do arrange your proposed protocol for PCT, it will certainly be helpful to present it.

Yes I have medical education (not an endocrinologist though), but I am here as a "bro" as you say it. You know this is an "illegal" steroid forum, so everything we say is not medical advice, just us trying to find our way through dark fields (my disclaimer..)


Apart from that, to the point:

1) The first study describes a reduction in cytosolic AR, a downregulation. It is a desensitization, similar to the one described with high doses of SERM's. What do we learn from that? Do not use high dosages, and certainly not for long.
2) Clomiphene increases testosterone after 4-6 weeks. The T/E ratio is decreased in hypogonadic males and when normogonadism is achieved then the ratio returns to normal too. We learn that clomid works after a 4-6 wk dosage scheme.
3) You say "THis article describes the function of the testes responding to LH is the biggest problem, and not the adrenal glands." Did you mean the pituitary? If so that is not the case, LH is low so even a functioning testis would not produce T. In fact, the low LH means that the pituitary is deficient for a fact.
4) Here as well we learn that low dosages of clomid work best.
5) Yeah, this is a known study that suggests all that you say there.
6) This is a very interesting one. It suggests that a very conservative scheme (50 mg x 3/wk) works after 4 months in elevating LH (and subsequently T). We don't know what would happen to a patient (us) that does not have hypogonadotropic gonadism per se, but is using suppressive doses of AAS, but it seems like the result would be the same. This is very supporting of what I was trying to corroborate, thanks a lot!

Keep up the good work Lemonada and keep us posted on your progress.

I am currently looking into this discussion in some other forums that debate the SERM usage while on cycle to preserve pituitary function, will let you know if anything comes up.

[XxAndreaxX]

yeah, These are all studies for PCT recovery but... the topic here is to keep up LH and FSH while on high doses of AAS.

[Lemonada8]

yeah, These are all studies for PCT recovery but... the topic here is to keep up LH and FSH while on high doses of AAS.

Ok.... and...? this is where the topic veered off towards i was replying to the above mentions. Sorry for your spectating views we veered off topic.

Thanks a lot Lemonada! It will take some time to sort out what is most useful for PCT and what would be important for my question. In the meantime, please do arrange your proposed protocol for PCT, it will certainly be helpful to present it.

Yes I have medical education (not an endocrinologist though), but I am here as a "bro" as you say it. You know this is an "illegal" steroid forum, so everything we say is not medical advice, just us trying to find our way through dark fields (my disclaimer..)


Apart from that, to the point:

1) The first study describes a reduction in cytosolic AR, a downregulation. It is a desensitization, similar to the one described with high doses of SERM's. What do we learn from that? Do not use high dosages, and certainly not for long.
2) Clomiphene increases testosterone after 4-6 weeks. The T/E ratio is decreased in hypogonadic males and when normogonadism is achieved then the ratio returns to normal too. We learn that clomid works after a 4-6 wk dosage scheme.
3) You say "THis article describes the function of the testes responding to LH is the biggest problem, and not the adrenal glands." Did you mean the pituitary? If so that is not the case, LH is low so even a functioning testis would not produce T. In fact, the low LH means that the pituitary is deficient for a fact.
4) Here as well we learn that low dosages of clomid work best.
5) Yeah, this is a known study that suggests all that you say there.
6) This is a very interesting one. It suggests that a very conservative scheme (50 mg x 3/wk) works after 4 months in elevating LH (and subsequently T). We don't know what would happen to a patient (us) that does not have hypogonadotropic gonadism per se, but is using suppressive doses of AAS, but it seems like the result would be the same. This is very supporting of what I was trying to corroborate, thanks a lot!

Keep up the good work Lemonada and keep us posted on your progress.

I am currently looking into this discussion in some other forums that debate the SERM usage while on cycle to preserve pituitary function, will let you know if anything comes up.

The only way i could postulate mainting pit function while on a cycle is to control estrogen levels b/c estrogen is the main regulatory factor with regards to the pituitary gland. However there is a long feed back look with really high androgen levels that deals w/ the hypothalamus which regulates it by increasing prolactin levels. prolactin inhibits the pituitary gland from producing gonadotropes. THis problem comes into play with either really really high test usage or tren usage (because tren is so potent) hence the usage of caber/bromo to keep those levels at bay.

I still keep my original views of that the main issue w/ recovery is the testes and not the pituitary gland, where the pit is faster recovery compared to the testes. I have yet to see any info regarding loss of basophilic gonadotropes in the pituitary due to excess testosterone usage.