HTPA Shutdown....

[Giants11]

Why a longer recovery? Tesicular atrophy would be worse and the body's ability to release FSH/LH would also undoubably be diminished. Same idea as trying to recover a muscle after surgery, the longer it has been imobilized the harder it is to get it back.

The size of one's testicles doesn't reflect that status f the HTPA. And yes while while muscle atrophy etc...would progress over weeks. In this instance when taking a compound that shuts you down, you would likely see the same testicular atrophy from both proposed cycles.

[Kratos]

What you see in the mirror when admiring your balls and what is going on biologically are very different things. Many people see no change in testicle size. What I'm most concerned about are not the balls themselves. The brain is a creature of habit and becomes set in it's ways. I am not saying long cycles can not be recoved from with propper pct, just that recovery will be more difficult.

[vitor]

The brain is a creature of habit and becomes set in it's ways. I am not saying long cycles can not be recoved from with propper pct, just that recovery will be more difficult.

Agreed,
The Whole HPTA system will basically sleep when you are ON, in a way that they dont have to produce hormones themselves...

I guess it can be compared to lying in a coma, wont the person who has been out for 4 week be more "clear" (mind-vise) that the guy who has been out for 4 years? Makes sense...

[Giants11]

Agreed,
The Whole HPTA system will basically sleep when you are ON, in a way that they dont have to produce hormones themselves...

I guess it can be compared to lying in a coma, wont the person who has been out for 4 week be more "clear" (mind-vise) that the guy who has been out for 4 years? Makes sense...

I would think they'd be just as ****ed up personally, but maybe that's why I started this thread

[BG]

20iu seems very very low considering some of the doses shown in this thread. What else are you taking?

Well I just bumped my test up to 300mgs and deca to 150, 2iu's of GH because Im low but it was at 8 iu's for awhile before, 50mcgs of t-4 and 50mgs of proviron.

EDIT: I dont like to publicy tell my AS usage, but for the sake of being honest for this conversation, Ive been on HRT dosage for a year but ran a 5month heavy cyle before , then went to hrt to perserve gains.

[BG]

As far as low dose, yes I agree, Ive been trying to get away from using high dosages anymore of anything. I want to see if I can get results from less, Ive read studies on hrt hcg dosage protocals being 200 iu's or less a week of hcg, but that was probably with guys that werent shut down yet, it snuck up on me, took awhile, I thought I wasnt going to completely shut down.

[Serotonin]

There's no evidence to really support HCG on a cycle, is there? I mean...real evidence?

Aside from a histological examination there really isn't any way of determining it, and I don't think many guys will be ok with their balls being cut off.

The reason the HCG probably does work, and I'm assuming it would even on cycle, is that it doesn't act on the hypothalamus or the pituitary, it acts on the testes. We know the testes will create testosterone in the presence of leutenizing hormone and HCG. So, it should be a pretty safe bet that using HCG during a cycle will keep the leydig cells active and not shutdown as severely as they are on a heavy cycle.

[Serotonin]

What you see in the mirror when admiring your balls and what is going on biologically are very different things. Many people see no change in testicle size. What I'm most concerned about are not the balls themselves. The brain is a creature of habit and becomes set in it's ways. I am not saying long cycles can not be recoved from with propper pct, just that recovery will be more difficult.

I would disagree in this instance. Most of the studies that are done using anabolics and HCG in male rats have their conclusions drawn after a histological examination. They sacrifice the rats to observe the physical differences in the testes to that of the control specimens.

Anyways, I haven't heard many people mentioning it but my concern isn't so much natural test levels but the quality of sperm. Its been known for a while heavy steroid use can impact a males sperm quality and production. Hell, I'm 25 and don't want kids till my mid 30's so if my test is off a bit after a cycle doesn't concern me as much as not being able to reproduce.

[Property of Steroid.com]

I agree. But are there other factors at work, besides leydig cells being unresponsive? Because thats the only conclusion I can come up with, caomparing a 4 year cycler to a 4 week cycler.

If they were to use the same compounds and shutdown GnRH/LH/FSH/T at the same time. Why does the 4 year cycler find it harder to recover?

Other than his/her leydig cells being out of whack?

But that's the only one you could come up with because it's the only one you read on the boards. There isn't even a study showing that to be a causative factor....usually it's idiopathic hypogonadism after steroid use, not "unresponsive leydig cells". If they were unresponsive, HCG wouldn't work at all.

[Swifto]

But that's the only one you could come up with because it's the only one you read on the boards. There isn't even a study showing that to be a causative factor....usually it's idiopathic hypogonadism after steroid use, not "unresponsive leydig cells". If they were unresponsive, HCG wouldn't work at all.

It pretty obvious in my eyes that leydig cells become unresponsive to LH over time, when they have layed dormant during a cycle for example.

"idiopathic hypogonadism" (Kallmann Syndrome), I'm guessing you talking about GnRH deficiany...Well you are actually.

Perhaps you'de like to explain more to everyone whos posted in thie thread why's thats a causative factor here.

Its fairly similar to secondary hypogonadism actually. Inhibition at the Hypothalamus and not testes.

The questions I have are:

Does the pituitary become unresponsive to GnRH over time, when its not supplied naturally?

Does it (pituitary) become desensitised to GnRH?

[Property of Steroid.com]

It pretty obvious in my eyes that leydig cells become unresponsive to LH over time, when they have layed dormant during a cycle for example.

"idiopathic hypogonadism" (Kallmann Syndrome), I'm guessing you talking about GnRH deficiany...Well you are actually.

Perhaps you'de like to explain more to everyone whos posted in thie thread why's thats a causative factor here.

Its fairly similar to secondary hypogonadism actually. Inhibition at the Hypothalamus and not testes.

The questions I have are:

Does the pituitary become unresponsive to GnRH over time, when its not supplied naturally?

Does it (pituitary) become desensitised to GnRH?

Why, in the absence of a stimuli, wouldn't they get more (not less responsive)? In many cases, that's they body's way of dealing with a lack of something. You don't have enough, so your body becomes more responsive to what you do have or can produce.

After a workout, when you're glycogen ***leted...your body becomes more sensitive to carbs right? Not less? Ok then....why are you making an assumption otherwise with your newfound Leydig Cell info?

FYI: idiopathic hypogonadism just means "we don't know why you're hypogonadal".

Answers to your questions:

1. Possibly
2. Under some circumstances

And we thought that HCG will keep you fertile (at least) during a cycle, but now, even that is not definate. In fact...it keeps you producing sperm, but the sperm that you produce are all ****ed up:

Int J Sports Med. 2004 May;25(4):257-63.
Concomitant abuse of anabolic androgenic steroids and human chorionic gonadotrophin impairs spermatogenesis in power athletes.

Karila T, Hovatta O, Seppälä T.
Laboratory of Substance Abuse, Helsinki, Finland. [email protected]
Abuse of anabolic androgenic steroids (AASs) may be an aetiological factor in male infertility among recreational power athletes. They try to avoid AAS-induced deterioration in spermatogenesis by combining doses of human chorionic gonadotrophin (HCG) and/or antiestrogens with their AAS abuse. Eighteen healthy male power athletes using massive doses of AASs were recruited for the study. Semen samples were collected during AAS abuse and 1.5 and 6 months after cessation of the abuse. They were also asked about their reproductive activity six years after the study. At the end of the AAS cycle, the sperm count was 33 +/- 49 x 10 (6) /ml (mean +/- SD), and only one subject had azoospermia. At 1.5 months after cessation of the AAS cycles, the mean sperm concentration was 30 +/- 42 x 10 (6) /ml, and after six months 77 +/- 70 x 10 (6) /ml. There were significant differences between the sample drawn six months after cessation of AAS abuse and both samples drawn during and 1.5 months after the abuse (p </= 0.05, repeated measures of ANOVA). There was a significant positive correlation between HCG dose during the cycle and the relative amount of morphologically abnormal spermatozoa (r = 0.60, p < 0.01). The concomitant abuse of HCG and supraphysiological AAS dose cause transient impairment on semen quality in males, although spermatogenesis is maintained with this regimen despite prolonged abuse of massive doses of AAS.
PMID: 15162244 [PubMed - indexed for MEDLINE]


Are we still sure HCG is doing what we want it to do? I'm not certain. The research isn't there, the main TRT doc we know to use it has clients rebelling against him, and I've never seen bloodwork proving it's usefulness. Ever since Duchaine talked about this use for HCG 2 decades ago, it's been "fact"...

I'm not saying 100% it doesn't work, I'm just saying I'd like to see more evidence.

[Swifto]

Why, in the absence of a stimuli, wouldn't they get more (not less responsive)? In many cases, that's they body's way of dealing with a lack of something. You don't have enough, so your body becomes more responsive to what you do have or can produce.

After a workout, when you're glycogen ***leted...your body becomes more sensitive to carbs right? Not less? Ok then....why are you making an assumption otherwise with your newfound Leydig Cell info?

FYI: idiopathic hypogonadism just means "we don't know why you're hypogonadal".

Answers to your questions:

1. Possibly
2. Under some circumstances

And we thought that HCG will keep you fertile (at least) during a cycle, but now, even that is not definate. In fact...it keeps you producing sperm, but the sperm that you produce are all ****ed up:

Int J Sports Med. 2004 May;25(4):257-63.
Concomitant abuse of anabolic androgenic steroids and human chorionic gonadotrophin impairs spermatogenesis in power athletes.

Karila T, Hovatta O, Seppälä T.
Laboratory of Substance Abuse, Helsinki, Finland. [email protected]
Abuse of anabolic androgenic steroids (AASs) may be an aetiological factor in male infertility among recreational power athletes. They try to avoid AAS-induced deterioration in spermatogenesis by combining doses of human chorionic gonadotrophin (HCG) and/or antiestrogens with their AAS abuse. Eighteen healthy male power athletes using massive doses of AASs were recruited for the study. Semen samples were collected during AAS abuse and 1.5 and 6 months after cessation of the abuse. They were also asked about their reproductive activity six years after the study. At the end of the AAS cycle, the sperm count was 33 +/- 49 x 10 (6) /ml (mean +/- SD), and only one subject had azoospermia. At 1.5 months after cessation of the AAS cycles, the mean sperm concentration was 30 +/- 42 x 10 (6) /ml, and after six months 77 +/- 70 x 10 (6) /ml. There were significant differences between the sample drawn six months after cessation of AAS abuse and both samples drawn during and 1.5 months after the abuse (p </= 0.05, repeated measures of ANOVA). There was a significant positive correlation between HCG dose during the cycle and the relative amount of morphologically abnormal spermatozoa (r = 0.60, p < 0.01). The concomitant abuse of HCG and supraphysiological AAS dose cause transient impairment on semen quality in males, although spermatogenesis is maintained with this regimen despite prolonged abuse of massive doses of AAS.
PMID: 15162244 [PubMed - indexed for MEDLINE]


Are we still sure HCG is doing what we want it to do? I'm not certain. The research isn't there, the main TRT doc we know to use it has clients rebelling against him, and I've never seen bloodwork proving it's usefulness. Ever since Duchaine talked about this use for HCG 2 decades ago, it's been "fact"...

I'm not saying 100% it doesn't work, I'm just saying I'd like to see more evidence.

So your saying leydig cells dont become unresponsive when not stimulated?

Then why are cycles of longer duration harder to recover from, than short cycles?

If your the one with all the answers, as you so well put in each and every post, as your "at the top of the industry" whats your take on it?

Rather than trying to shoot down everyones post, offering a theory why it takes longer, why not contribute a little more positively? Huh?

[Property of Steroid.com]

I'm saying you don't know. That's what I'm saying. You're making assumption upon assumption, with nothing to back it up.

I'm barely even making statements, I'm really just asking questions about the validity of others statements. And in this light, they seem quite lacking in substantiation.

[Swifto]

Well...

If leydig cell's being unresponsive isnt a factor, what is then?

Because I dont think you have a solid answer either.

A qualified Endo states HCG is good to use when cycling, for testicular size and function. Yet you attack his credibility when he's (Swale) been through years of medical school and an expert in the field, yet you have NO qualifications in the field AT ALL. One in english and another (I forget) which means **** all in this subject.

Your responses are so negative I'm no longer going to respond to them.

Again, rather than shooting others theory's down, offer your own. Or are you going to charge $200 per hour?

[Property of Steroid.com]

I'm saying you got this piece of information, and now it's the answer to the question at hand, but honestly, it's the answer because you don't know much about anything else, and don't even know much about the answer you think you have. I'm saying it's unsubstantiated, but it's all you've got, so you are dogmatically clinging to it, and the word of a quack doctor is enough to prove it to you.

I'm saying in short, all you have in your toolbox is a hammer, so everything looks like a nail to you.

The conclusions and assumptions you are making are without a shred of evidence, and I'm questioning them, and asking for proof. That's all I'm doing. I'm pointing out the fundamental flaw in your assertions.

[Giants11]

I'm saying you got this piece of information, and now it's the answer to the question at hand, but honestly, it's the answer because you don't know much about anything else, and don't even know much about the answer you think you have. I'm saying it's unsubstantiated, but it's all you've got, so you are dogmatically clinging to it, and the word of a quack doctor is enough to prove it to you.

I'm saying in short, all you have in your toolbox is a hammer, so everything looks like a nail to you.

The conclusions and assumptions you are making are without a shred of evidence, and I'm questioning them, and asking for proof. That's all I'm doing. I'm pointing out the fundamental flaw in your assertions.

Well then in-line with Swito's comments.

I believe you stated this in the beginning of the thread but just for clarification. Providing one does a properly structured PCT (in your case I believe that would involve Aromasin/Nolva), does it take one longer to recover when shut down for longer? In your opinoin of course.

[Giants11]

Again, I can state that for me personally, I have been just fine recovering from longer cycles. But my PCT is a bit different from most people's in that fact that I do not believe that the "Standard" 4 Week PCT protocol I see most advise is correct in terms of length. Blood work should be the ultimate factor in PCT length, even then, I still like to extend the run of an AI, to help keep test levels elevated well beyond the 4 week mark.

[Serotonin]

Typically, what Roberts is saying is right. Cells tend to saturate themselves in receptors when "starved" of a messenger they use to fulfill their function.

I've spent a decent amount of time reading on pituitary sensitivity, spermatogenesis, and even reviewing the exact process from messenger to excretion of how testosterone is synthesized... and aside from expert medical opinion it seems like this to me: All of the tiny processes, from the droplets of cholesterol in leydig cytoplasm, to the gene transcription and translation leading to the formation of test... it seems pretty reasonable to me that if you were to shut down the HPTA for a long time and all these microscopic mechanisms lay dormant, that it will take longer for them to pick the pace back up. Because hell, for all we know this could affect EVERYTHING from the concentration of LDL receptors on leydig cells to the concentration of GNRH receptors on the pituitary. Perhaps the leydig cells stop the uptake of cholesterol, stop creating the kinases and GMP required for this signal transduction to take place... If the cell has to make all of its hardware again after that long of a time of not working then yes it will take much longer.

[Giants11]

Typically, what Roberts is saying is right. Cells tend to saturate themselves in receptors when "starved" of a messenger they use to fulfill their function.

I've spent a decent amount of time reading on pituitary sensitivity, spermatogenesis, and even reviewing the exact process from messenger to excretion of how testosterone is synthesized... and aside from expert medical opinion it seems like this to me: All of the tiny processes, from the droplets of cholesterol in leydig cytoplasm, to the gene transcription and translation leading to the formation of test... it seems pretty reasonable to me that if you were to shut down the HPTA for a long time and all these microscopic mechanisms lay dormant, that it will take longer for them to pick the pace back up. Because hell, for all we know this could affect EVERYTHING from the concentration of LDL receptors on leydig cells to the concentration of GNRH receptors on the pituitary. Perhaps the leydig cells stop the uptake of cholesterol, stop creating the kinases and GMP required for this signal transduction to take place... If the cell has to make all of its hardware again after that long of a time of not working then yes it will take much longer.

Point well, taken. The question becomes more analytical for me at least.

What I would want to do is determine gains vs gains lost and recovery time for different length cycles. If one can stay on longer and gain more and keep the more gains % wise, then for me perhaps it's worth it to stay on longer. Also who doesn't love to have high Test.

However we are neglecting a lot of other factors as well, Prostate health, Lipids etc...But for the sake of conversation I will assume that one will take the proper precautions etc...

As for AR's comment, I think it does make sense when you withhold something from your body, it responds by becoming MORE sensitive not LESS. That is certainly true in many aspects of the human body.

[Giants11]

By the way....Saw this on another board earlier and found it very interesting and relevant here, considering we were talking about both Prolactin issues as well as LH:

Zinc may have a physiological role in regulating pituitary prolactin secretion.
Login IS, Thorner MO, MacLeod RM.

We studied the in vitro influence of physiologically relevant zinc concentrations on the pituitary synthesis and secretion of prolactin (Prl). Zinc in concentrations between 1 and 10 microM reduced Prl secretion and, to a milder extent, synthesis, but not basal or stimulated growth hormone (GH) or LH release. At a supraphysiological concentration of 100 microM, zinc markedly decreased Prl synthesis and secretion, but increased LH secretion. The ability of a physiological zinc concentration to influence Prl secretion suggests that this trace element may have a role in the in vivo regulation of Prl release.

PMID: 6646348 [PubMed - indexed for MEDLINE]

[hackskii]

First post here.
I am an older man 47 that has done a few cycles and found I myself shutdown more than anyone I ever have known.
I suffer from massive testicular atrophy really bad.

For the record Leydig cells become more sensitive during cycle due to less stimulation.
Hence the concern for over doing it with the HCG and becoming less sensitive (desensitize).

I have ran many protocols myself, one by Mr. Roberts, one buy Swale, one by Scally.
During this time I was on TRT due to very low androgens 75 and just above a womans test level.
After 10 months on TRT I felt worse and decided to do a PCT.
I followed Mr. Roberts protocol to the letter and I failed.
I contacted a Dr by the name of Scally and had fantastic success.

Here is what “I” know about HCG coming from my personal practice and have no other studies other than the desentization issues being covered with the use of nolvadex during HCG administration.
Here is what I know.
You can run HCG during the cycle to keep and maintain full testicular function, or you can run it at the end to restore testicular function.
Again my nuts get the size of smashed grapes on cycles and I never cycle more than 10 weeks.

I notice HCG works best if shot in late afternoon.
If the dose is too high It interferes with my sleep.
I notice HCG works better if not shot ED, instead I shoot EOD during recovery phase and just twice a week if during the cycle starting week 3.
Trying to restore testicular function is a bit tricky with me as 1,000iu for the most part ED barely does anything. 2,500 EOD does a hell of a lot.
At this time during recovery I take an AI as HCG aromatizes quite heavily and many AI’s will lower blood plasma levels of a SERM. My selection is Aromasin during the high dose of HCG.
I do 2500iu HCG EOD for 8 shots (16 days).
At this time I run clomid and nolva together.
For me nothing works like nolva and clomid together.
I run the clomid @ 100mg a day (split between two doses) for 30 days and run the nolva @ 20mg for 45 days.

I do not like the idea of running the AI during PCT, I don’t think it is necessary and although both clomid and nolva are agonists and antagonists for estrogen id rather leave things alone as estrogen wont be a factor anyway due to running the AI during the use of HCG, that and low test levels wont aromatize too heavily so estrogen wont be a factor.
That and the possibility of compromised lipid profile and bone loss seems risky, especially as lipid profiles will be a bit compromised anyway after a cycle.
First hand experience with the use of nolva lowers my cholesterol really nice too.

I don’t think using an AI to raise test levels is a good idea.
Coming from an older mans perspective it is the aromatase that seems to be the problem. Older men have a higher amount of fat and primarily belly fat. Belly fat seems to raise aromatase enzyme considerably. This means more estrogen, more estrogen would equal less testosterone (if high) and less testosterone and more estrogen will probably give you more belly fat and the whole thing would be a vicious circle.
Hell, alcohol raises estrogen.
So, in the light of that, besides diet, belly fat, lifestyle, using an AI to lower estrogen would work providing estrogen is high.
If both test and estrogen are within normal levels it seems pointless to use an AI to elevate test levels.
Minor lifestyle changes and diet will lower estrogen especially if cruciferous vegetables are added.

On the issue of HCG I will never start a PCT without it. My nuts are very stubborn and either keeping them full function and or bringing them back to life prior to starting PCT will aid and speed recovery.

I also don’t think lowering prolactin would be a good thing, this compromises immune function and also puts the LH receptors at risk, at this point that would be counterproductive and it is not prolactin that is the culprit using deca, it is progesterone.

My success for PCT is nolva, clomid and HCG.

[Swifto]

First post here.
I am an older man 47 that has done a few cycles and found I myself shutdown more than anyone I ever have known.
I suffer from massive testicular atrophy really bad.

For the record Leydig cells become more sensitive during cycle due to less stimulation.
Hence the concern for over doing it with the HCG and becoming less sensitive (desensitize).

I have ran many protocols myself, one by Mr. Roberts, one buy Swale, one by Scally.
During this time I was on TRT due to very low androgens 75 and just above a womans test level.
After 10 months on TRT I felt worse and decided to do a PCT.
I followed Mr. Roberts protocol to the letter and I failed.
I contacted a Dr by the name of Scally and had fantastic success.

Here is what “I” know about HCG coming from my personal practice and have no other studies other than the desentization issues being covered with the use of nolvadex during HCG administration.
Here is what I know.
You can run HCG during the cycle to keep and maintain full testicular function, or you can run it at the end to restore testicular function.
Again my nuts get the size of smashed grapes on cycles and I never cycle more than 10 weeks.

I notice HCG works best if shot in late afternoon.
If the dose is too high It interferes with my sleep.
I notice HCG works better if not shot ED, instead I shoot EOD during recovery phase and just twice a week if during the cycle starting week 3.
Trying to restore testicular function is a bit tricky with me as 1,000iu for the most part ED barely does anything. 2,500 EOD does a hell of a lot.
At this time during recovery I take an AI as HCG aromatizes quite heavily and many AI’s will lower blood plasma levels of a SERM. My selection is Aromasin during the high dose of HCG.
I do 2500iu HCG EOD for 8 shots (16 days).
At this time I run clomid and nolva together.
For me nothing works like nolva and clomid together.
I run the clomid @ 100mg a day (split between two doses) for 30 days and run the nolva @ 20mg for 45 days.

I do not like the idea of running the AI during PCT, I don’t think it is necessary and although both clomid and nolva are agonists and antagonists for estrogen id rather leave things alone as estrogen wont be a factor anyway due to running the AI during the use of HCG, that and low test levels wont aromatize too heavily so estrogen wont be a factor.
That and the possibility of compromised lipid profile and bone loss seems risky, especially as lipid profiles will be a bit compromised anyway after a cycle.
First hand experience with the use of nolva lowers my cholesterol really nice too.

I don’t think using an AI to raise test levels is a good idea.
Coming from an older mans perspective it is the aromatase that seems to be the problem. Older men have a higher amount of fat and primarily belly fat. Belly fat seems to raise aromatase enzyme considerably. This means more estrogen, more estrogen would equal less testosterone (if high) and less testosterone and more estrogen will probably give you more belly fat and the whole thing would be a vicious circle.
Hell, alcohol raises estrogen.
So, in the light of that, besides diet, belly fat, lifestyle, using an AI to lower estrogen would work providing estrogen is high.
If both test and estrogen are within normal levels it seems pointless to use an AI to elevate test levels.
Minor lifestyle changes and diet will lower estrogen especially if cruciferous vegetables are added.

On the issue of HCG I will never start a PCT without it. My nuts are very stubborn and either keeping them full function and or bringing them back to life prior to starting PCT will aid and speed recovery.

I also don’t think lowering prolactin would be a good thing, this compromises immune function and also puts the LH receptors at risk, at this point that would be counterproductive and it is not prolactin that is the culprit using deca, it is progesterone.

My success for PCT is nolva, clomid and HCG.

Thank you very much for posting this.

If one uses HCG during the cycle, what advantage does one have over someone that doesnt? Thats if leydig cells dont become unresponsive, but more sensitive.

You state you use it to kind of jump start the testes, ready for PCT. But what do you mean specifically?

If the leydigs arnt unresponsive and more sensitive to LH, why is HCG needed?

[Kratos]

I don’t think using an AI to raise test levels is a good idea.
Coming from an older mans perspective it is the aromatase that seems to be the problem. Older men have a higher amount of fat and primarily belly fat. Belly fat seems to raise aromatase enzyme considerably. This means more estrogen, more estrogen would equal less testosterone (if high) and less testosterone and more estrogen will probably give you more belly fat and the whole thing would be a vicious circle.


Sounds like ass-backword thinking

[Giants11]

I don’t think using an AI to raise test levels is a good idea.
Coming from an older mans perspective it is the aromatase that seems to be the problem. Older men have a higher amount of fat and primarily belly fat. Belly fat seems to raise aromatase enzyme considerably. This means more estrogen, more estrogen would equal less testosterone (if high) and less testosterone and more estrogen will probably give you more belly fat and the whole thing would be a vicious circle.


Sounds like ass-backword thinking

Yeah I didn't get that part either. Lower estrogen, raise Test. That is one of the basic principals of the Negative Feedback loop.

[vitor]

Yeah I didn't get that part either. Lower estrogen, raise Test. That is one of the basic principals of the Negative Feedback loop.

I think what he meant/thought was that older men have more bodyfat(diet is the key here lol), Estrogens aromatazion in fat-cells is the problem, not testosterones aromatazion to Estrogen which an AI is used for.

But he is wrong...

Letro will penetrate aromatazion in fat-cells quite effectively, and from whetever the Estrogen cames from, it will inhibit the hypotalamus in a way that it will produce less LH.

[hackskii]

Ok, older men have more aromitization going on then younger men in general.
That would mean higher estrogen and lower testosterone. Testosterone declines in men along with other hormones.
This changes the testosterone to estrogen ratio for the worse.
So, yes blocking estrogen that is high will yield a more favorable test to estrogen ratio and also higher test levels.

But only one TRT doc that I know of Dr. Shippen treats this form of low testosterone in men.
It can be done pretty effectivly with diet and lifestyle changes.

Lets use soy products for example.
Due to it being a phytoestrogen men that are lean with no estrogen problems would not use soy products.
Men that have more aromatase activity and higher than normal estrogen should use soy as it acts as a very mild estrogen similar to a SERM.

My point is this.
Using an AI for the sake of raising testosterone levels in a man with normal base levels of estrogen and testosterone is just stupid.
You will not get any more gains than leaving estrogen alone.
Estrogen has some envolvement in gains too.
Dropping estrogen at the risk of compromising lipid profiles and bone loss in the attempt for some gains wont happen.

[hackskii]

Thank you very much for posting this.

If one uses HCG during the cycle, what advantage does one have over someone that doesnt? Thats if leydig cells dont become unresponsive, but more sensitive.

You state you use it to kind of jump start the testes, ready for PCT. But what do you mean specifically?

If the leydigs arnt unresponsive and more sensitive to LH, why is HCG needed?

If someone uses HCG during the cycle they will maintain full testicular function.
The benefits of this is when the cycle is done and a SERM is used recovery will be quicker, as the testicles do not have to come back to life.

Think of an arm in a cast, it is not being used (6 weeks), the cast comes off (cycle stops) the arm will take time comming back to normal. Think of your balls like this, if the arm did not atrophy in the cast then once the cast came off the arm would come back quicker.

HCG is an LH analog, it acts just like the pituitary sending the chemical signal LH to the testicles. The nuts do not know the diffrence from LH and the stimulation from LH to the leydig cells and HCG's stimulation of the leydig cells.
It is the same.
So, it makes sense keeping the nuts alive and non atrophied then handing them off to a SERM which will prime the hypothalamus and pituitary to product GnRH, FSH, LH.
Now the nuts are functioning and able to produce testosterone due to the stimulation from the SERMs raising LH and FSH.

Once the nuts go south, they take forever on clomid and nolva to come back to life.
There is a study somewhere on the net where thy put guys on 250 test a week for 6 months.
LH and FSH came back in around 2 weeks or so, the nuts didnt start producting testosterone for 10 weeks and even at week 10 they were below base normal ranges.

So, if the nuts are the sticky part of the equation in recovery would not it make the most sense to have them ready, willing, and able to start production of testosterone so gains are not lost?

You guys seem to demonize estrogen, but estrogen is necessary and should be kept in normal base ranges for good health, even on cycle you block too much estrogen and you will lose some gains, as well as libido.
During a cycle I use very mild doses of an AI just for estrogen management.

The statements lower estrogen = raise testosterone means nothing in regards to lean muscle gains.
You do know that lowering estrogen also lowers IGF-1 right?
The knife cuts both ways here, everything in moderation.

[kfrost06]

Yeah I didn't get that part either. Lower estrogen, raise Test. That is one of the basic principals of the Negative Feedback loop.

Actually he accidentally made a factual statement, clinical test have shone AIs do not work in older men to increase testosterone. It has nothing to do with body fat and everything to do with reduced hypothalamic GnRH stimulus strength.

"Age did not influence the ability of anastrozole to ***ress (24-h pooled) estradiol concentrations by 50% (compared with placebo) and elevate mean LH concentrations by 2-fold. Nonetheless, under pharmacologically equivalent estrogen withdrawal, older subjects failed to achieve normal young adult augmentation of total testosterone concentrations or molar testosterone to SHBG ratios"

Short-Term Aromatase-Enzyme Blockade Unmasks Impaired Feedback Adaptations in Luteinizing Hormone and Testosterone Secretion in Older Men
Johannes D. Veldhuis and Ali Iranmanesh

Note: older is defined as 60+ and younger is 25-33

[Giants11]

HRT.................That's all I can say,

Good post.

[Serotonin]

I'm almost certain estrogen and testosterone serve the same role in bone density, but clearly in men it is the testosterone that plays the larger role. Unless of course you just meant in older males, kind of like, taking what you can get to keep bone density.

[vitor]

hackscii-When I was using letro as a stand-alone between cycles, my IGF levels doubled(according to BW).

"Lower estrogen=raise testosterone means nothing in regards to lean muscle gains"...Please explain?

Isnt testosterone anabolic?
Wont higher levels of testosterone be more anabolic than lower levels?

And how could I(and several others) make gains between cycles when I was using letro as a stand-alone, if normal levels of estrogen is needed for muscle grow

[hackskii]

I think we got off track here somewhat.

We are talking about recovery here and how to bring the HPTA back online as soon as possible.

There are other factors here that have not even been addressed in recovery.
But a snip from Swale on the benefits of the use of HCG:
But there’s another metabolic reason to employ this protocol. The P450 Side Chain Cleavage enzyme, which converts CHOL into pregnenolone at the initiation of all three metabolic pathways CHOL serves as precursor (the sex hormones, glucocorticoids and mineralcorticoids), is actively stimulated, or ***ressed, by LH concentrations. It is intuitively consistent that during conditions of lowered testosterone levels, commensurate increases in LH production would serve to stimulate this conversion from CHOL into these pathways, thereby feeding more raw material for increased hormone production. And vice versa. Thus the addition of HCG (which also stimulates the P450scc enzyme) helps restore a more natural balance of the hormones within this pathway in patients who are entirely, or even partially, HPTA-suppressed.


One of the other problems with recovery during shutdown is excessive Cortisol and adrenal burnout.

[plzr8]

hackscii-When I was using letro as a stand-alone between cycles, my IGF levels doubled(according to BW).

"Lower estrogen=raise testosterone means nothing in regards to lean muscle gains"...Please explain?

Isnt testosterone anabolic?
Wont higher levels of testosterone be more anabolic than lower levels?

And how could I(and several others) make gains between cycles when I was using letro as a stand-alone, if normal levels of estrogen is needed for muscle grow

vitor...curious how you combatted sides (such as libido issues) when running letro as a standalone...did you incoporate a low dose proviron or anything of that nature?

[Swifto]

If someone uses HCG during the cycle they will maintain full testicular function.
The benefits of this is when the cycle is done and a SERM is used recovery will be quicker, as the testicles do not have to come back to life.

Think of an arm in a cast, it is not being used (6 weeks), the cast comes off (cycle stops) the arm will take time comming back to normal. Think of your balls like this, if the arm did not atrophy in the cast then once the cast came off the arm would come back quicker.

HCG is an LH analog, it acts just like the pituitary sending the chemical signal LH to the testicles. The nuts do not know the diffrence from LH and the stimulation from LH to the leydig cells and HCG's stimulation of the leydig cells.
It is the same.
So, it makes sense keeping the nuts alive and non atrophied then handing them off to a SERM which will prime the hypothalamus and pituitary to product GnRH, FSH, LH.
Now the nuts are functioning and able to produce testosterone due to the stimulation from the SERMs raising LH and FSH.

Once the nuts go south, they take forever on clomid and nolva to come back to life.
There is a study somewhere on the net where thy put guys on 250 test a week for 6 months.
LH and FSH came back in around 2 weeks or so, the nuts didnt start producting testosterone for 10 weeks and even at week 10 they were below base normal ranges.

So, if the nuts are the sticky part of the equation in recovery would not it make the most sense to have them ready, willing, and able to start production of testosterone so gains are not lost?

You guys seem to demonize estrogen, but estrogen is necessary and should be kept in normal base ranges for good health, even on cycle you block too much estrogen and you will lose some gains, as well as libido.
During a cycle I use very mild doses of an AI just for estrogen management.

The statements lower estrogen = raise testosterone means nothing in regards to lean muscle gains.
You do know that lowering estrogen also lowers IGF-1 right?
The knife cuts both ways here, everything in moderation.

Exactly. This is also what Swale said.

This would suggest the leydig cells are still responsive as their stimulated from the HCG, mimicing LH.

Which is an advantage leading to PCT, which is what I've been argueing all along.

Yet a certain member wants scientific proof, studies, this, that...

But your also saying the leydigs become MORE responsive when their not stimulated. Then why is PCT harder to somone cycling 2 years, than someone cycling 2 months using the same compounds? It doesnt make sense.

Thanks for your responses by the way. Their appreciated.

[hackskii]

Leydig cells are more responsive to LH when LH has been absent for a while. This like using an AI making the estrogen receptors more responsive once the AI has stopped and estrogen rebounding can occur.

What is really going on here is that the leydig cells are more repsonsive in the absense of LH but the leydig cells are also not very efficient or lazy if you will in the production of testosterone.
Once they have atrophied they need time to recover to manufacture testosterone.
This is why HCG is used during to maintain full testicular function, not to keep them more responsive. They maybe more responsive to produce testosterone but LH is mearly the signal to the nuts to go to work.
Atrophied nuts are lazy nuts, they are not very efficent at going to work.

So, the nuts are the sticky part of recovery in regards to the HPTA.

In one study I have seen cited countless times (1), normal men were given a fairly light 12 week cycle of a combo of testosterone ( 150 mg/wk), nadrolone (150 mg/wk),Methandrostenolone (15 mg/day), winstrol (5 mg/day). Baseline LH was 6.8 U/L. It fell to a nadir of 4.1 U/L. One month after quitting it had risen to 5.2 U/L. However, 12 weeks after the cycle testosterone was still ***ressed (14nmol/l vs. a baseline of 21.8 nmol/L), but LH had risen above baseline to 8.0 U/L.


(1) Am J Sports Med 1987 Jul-Aug;15(4):357-61

[hackskii]

hackscii-When I was using letro as a stand-alone between cycles, my IGF levels doubled(according to BW).

"Lower estrogen=raise testosterone means nothing in regards to lean muscle gains"...Please explain?

Isnt testosterone anabolic?
Wont higher levels of testosterone be more anabolic than lower levels?

And how could I(and several others) make gains between cycles when I was using letro as a stand-alone, if normal levels of estrogen is needed for muscle grow

Of course testosterone is anabolic just like cortisol is catabolic.
Dude estrogen is critical for a healthy mind, De-pression can result in lowering estrogen too low among a ton of other things.

You suggested your IGF-1 doubled, was that doubled above base levels or when?
Aromatase inhibitors lower IGF-1 and so does nolva.

As far as your gains being made between cycles could be a varying degree of factors like, your gear had long acting esters and even up to 6 weeks later deconate and undeconate esters still will be releasing gear into your system.
You probably thought that the gear was out of your system and it still was in your system.

Your gear might have been bogus and the gains came from letro lowering above base values of estrogen.

You are not any near your genetic potential and jumped into a cycle when you would have made great gains without gear due to new muscle growth and not at your genetic potential.

Who knows, using peptides during PCT can cause gains outside of a cycle, more food intake can cause anabolism.
Water loss due to aromitization and looking leaner might be happening.

If you are making gains on letro then why cycle steroids

I made gains during PCT but was on IGF-1LR3 too.


Getting back to the HCG issue:
I am sure you are well aware of the recent study where 250 EOD IU of hCG inducted Tosterone production within 7 percent of baseline in HPTA supressed adult males. This study tells me all I need to know.

[Swifto]

Of course testosterone is anabolic just like cortisol is catabolic.
Dude estrogen is critical for a healthy mind, De-pression can result in lowering estrogen too low among a ton of other things.

You suggested your IGF-1 doubled, was that doubled above base levels or when?
Aromatase inhibitors lower IGF-1 and so does nolva.

As far as your gains being made between cycles could be a varying degree of factors like, your gear had long acting esters and even up to 6 weeks later deconate and undeconate esters still will be releasing gear into your system.
You probably thought that the gear was out of your system and it still was in your system.

Your gear might have been bogus and the gains came from letro lowering above base values of estrogen.

You are not any near your genetic potential and jumped into a cycle when you would have made great gains without gear due to new muscle growth and not at your genetic potential.

Who knows, using peptides during PCT can cause gains outside of a cycle, more food intake can cause anabolism.
Water loss due to aromitization and looking leaner might be happening.

If you are making gains on letro then why cycle steroids

I made gains during PCT but was on IGF-1LR3 too.


Getting back to the HCG issue:
I am sure you are well aware of the recent study where 250 EOD IU of hCG inducted Tosterone production within 7 percent of baseline in HPTA supressed adult males. This study tells me all I need to know.

Is that suppressed from androgens?

Also, what exactly does ITT (intrtesticular testosterone) do?

[vitor]

But your also saying the leydigs become MORE responsive when their not stimulated. Then why is PCT harder to somone cycling 2 years, than someone cycling 2 months using the same compounds? It doesnt make sense.

According to Bill roberts, the problem with recovering from long cycles, might have to do with change in the "clock" that regulates the pulse of LHRH secretion.

[Swifto]

According to Bill roberts, the problem with recovering from long cycles, might have to do with change in the "clock" that regulates the pulse of LHRH secretion.

Thats intresting. The GnRH pulse generator. A kind of GnRH deficiency or amount or possibly frequency of pulses. Like idiopathic hypogonadism.

Anthony expanding on idiopathic hypogonadism may be useful I guess?

[vitor]

hackskii-My igf levels doubled from what they where pre-cycle. (If you want to se the exact numbers I can put them up later.)

(I have never had bogus gear, and I use short esters.)

I got the idea of doing this(between cycles) b/c someone I know had an endocrine problem which resulted in low testosterone levels. He was given letro(by hes doc) hes T-levels went 3x up, and IGF increased signifently aswell. He started making greate gains on using nothing but letro, as he had low T-levels to start with.