HTPA Shutdown....

[Giants11]

Ok, so we know that certain steroids shut you down and do it very fast. Every compound you take will at the very least suppress you.

So if were are talking about cycles, short in duration or long....with compounds that shut you down, not just suppress...i.e 19-Nor's (Deca/Tren)


Most user's in here that I see (or at least myself) use a 19-Nor is just about every cycle. For me it's mainly Tren, but I know alot of people love Deca when bulking. So length of the cycle aside, when using any of the aforementioned drugs we are going to suffer from complete HTPA shutdown.

So the question then becomes....if we suffer complete HTPA shutdown within the first few days of using these harsh drugs, does it then matter how long we cycle for? This question was inspired by the yesterdays thread year long cycle. I began to think to myself, once one's HTPA is shutdown completely, does it matter how long it remains shutdown? Does the body somehow know the amount of time one is shutdown?

My thoughts would be that once you are shutdown you are shutdown and it will be equally as hard to restore HTPA function after a 8 week cycle or after a 8 month cycle. Anecdotally some users report that longer cycles take longer to recover from. That would lead to one conclusion, that the body does indeed sense the duration of shutdown and the longer one is shutdown the harder it is to restore HTPA function. My guess at the cause of this would be that during longer periods of shutdown perhaps eventually the body begins to forget how to produce endogenous hormones etc....?

I'd love to hear some thoughts and opinions on this matter.

[Serotonin]

I can only provide feedback on how the mechanism works as I've had to study it for many classes. The HPTA is nothing more than a negative-feedback cycle. Meaning that plasma levels of Testosterone are what tells your brain the body has enough testosterone, don't make more. So it doesn't send the chemical messengers that are used by the leydig cells in testicles to produce testosterone. Thus, the balls shutdown after an extended period and they shrink a tad as the leydig and sertoli cells kind of go dormant.

After saying all of that, my take on this is that it is OK to do an extended period of SOME anabolics. Clearly there are some that are harmful to the liver or hard on the prostate (DHT's). I made a post a while back on the cytotoxicity of trenbolone in cellular mitosis, which raised a big red flag in my head. Definitely not something I would do for a year.

In regards to the HPTA, I would have to do a bit more research on something that really isn't researched, but the testicles don't die. AIDS/Burn victims are put on steroids to combat body wasting for months to years. As long as you get cholesterol and BP checked regularly I don't see it being that bad. Utilizing HCG when you come off cycle would be paramount but with today's tools I think the recovery time is much exaggerated... but I think most of the stuff people just PARROT on these boards is exaggerated, like when people should start or what type of cycle to do first. It is all just speculation since each person is different. So, for me the bottom line is, I would do a year long cycle if I thought I would benefit from it.

[Giants11]

I can only provide feedback on how the mechanism works as I've had to study it for many classes. The HPTA is nothing more than a negative-feedback cycle. Meaning that plasma levels of Testosterone are what tells your brain the body has enough testosterone, don't make more. So it doesn't send the chemical messengers that are used by the leydig cells in testicles to produce testosterone. Thus, the balls shutdown after an extended period and they shrink a tad as the leydig and sertoli cells kind of go dormant.

After saying all of that, my take on this is that it is OK to do an extended period of SOME anabolics. Clearly there are some that are harmful to the liver or hard on the prostate (DHT's). I made a post a while back on the cytotoxicity of trenbolone in cellular mitosis, which raised a big red flag in my head. Definitely not something I would do for a year.

In regards to the HPTA, I would have to do a bit more research on something that really isn't researched, but the testicles don't die. AIDS/Burn victims are put on steroids to combat body wasting for months to years. As long as you get cholesterol and BP checked regularly I don't see it being that bad. Utilizing HCG when you come off cycle would be paramount but with today's tools I think the recovery time is much exaggerated... but I think most of the stuff people just PARROT on these boards is exaggerated, like when people should start or what type of cycle to do first. It is all just speculation since each person is different. So, for me the bottom line is, I would do a year long cycle if I thought I would benefit from it.

I agree with a lot of what you are saying. And I definitely agree with what compounds are run and for how long. For example I would never run Tren for months, as well as DHT derivatives or the Prostates sake as well.

It does seem however that you could cycle for long periods of time, while changing compounds and doses accordingly to prevent major side effects. And absolutely methylated androgens should not be take for weeks on end, I am focused more on injectables.

[Property of Steroid.com]

I was on a 3 year straight cycle, and my total testosterone levels were roughly 250ish (300 is the low end of normal) 3 weeks upon cessation. When I was 19, before ever using steroids, my test levels were 650ish. I doubt I would ever get back there, but I would bet that within a few more weeks, my test levels would be in the low/medium/normal range.

Although I should mention that the last 6 months of my 3 year cycle, I was on HRT doses (100mgs of prop/EOD) which got my test levels to 950ish, which is still High/Normal.

[Swifto]

Ok, so we know that certain steroids shut you down and do it very fast. Every compound you take will at the very least suppress you.

So if were are talking about cycles, short in duration or long....with compounds that shut you down, not just suppress...i.e 19-Nor's (Deca/Tren)


Most user's in here that I see (or at least myself) use a 19-Nor is just about every cycle. For me it's mainly Tren, but I know alot of people love Deca when bulking. So length of the cycle aside, when using any of the aforementioned drugs we are going to suffer from complete HTPA shutdown.

So the question then becomes....if we suffer complete HTPA shutdown within the first few days of using these harsh drugs, does it then matter how long we cycle for? This question was inspired by the yesterdays thread year long cycle. I began to think to myself, once one's HTPA is shutdown completely, does it matter how long it remains shutdown? Does the body somehow know the amount of time one is shutdown?

My thoughts would be that once you are shutdown you are shutdown and it will be equally as hard to restore HTPA function after a 8 week cycle or after a 8 month cycle. Anecdotally some users report that longer cycles take longer to recover from. That would lead to one conclusion, that the body does indeed sense the duration of shutdown and the longer one is shutdown the harder it is to restore HTPA function. My guess at the cause of this would be that during longer periods of shutdown perhaps eventually the body begins to forget how to produce endogenous hormones etc....?

I'd love to hear some thoughts and opinions on this matter.

I think leydig cell desensitisation and them being unresponsive is a major factor. Once the leydig cells become unresponsive it doesnt matter what PCT meds you take, there not going to be producing testosterone anytime soon. Desensitisation of the leydig cells can take time and, I think, this is a major factor why someone thats cycled for 3 years will recover slower than someone for 3 months.

Primary hypogonadism is what you really want to avoid. This is when the testes become unresponsive to LH/FSH, also known as Klinefelter's syndrome (one example). As a note, overuse of HCG can cause this.

I'm not certain a bodybuilder can get this from staying shutdown or hypogondal for long peroids, but I suspect being shutdown for years leads to both primary and secondary hypogonadism.

[Giants11]

I was on a 3 year straight cycle, and my total testosterone levels were roughly 250ish (300 is the low end of normal) 3 weeks upon cessation. When I was 19, before ever using steroids, my test levels were 650ish. I doubt I would ever get back there, but I would bet that within a few more weeks, my test levels would be in the low/medium/normal range.

Although I should mention that the last 6 months of my 3 year cycle, I was on HRT doses (100mgs of prop/EOD) which got my test levels to 950ish, which is still High/Normal.

I would be willing to bet that over time, if you shutdown your HTPA, you will never see the same Test levels that you once had.

Granted I have no evidence to support this, just anecdotally, my bloodwork has shown that since my first or second cycle my Test has never fully gotten back to the levels that they once were when I was in my early 20's.....A price I pay gladly.

[goose]

The intricate solution that will revolutionize and deals with shutdown is Toremefine Citrate and Aromasin.Have been avoiding 19-nors for some time due to recovery,experimented last cycle using drol in a cutter (found it to be the best cutting tool too) Ran this PCT and its like the encrusted the tree of eden.Still going to keep cycles within 12 weeks range as your receptors get saturated and its hard to remain growing unless you mix and change compounds within the cycle.Its great as this means I can just use long esters (two) and an oral for the first 6-8 weeks.Great thread topic and we are going to crack this gaints...

[Giants11]

I think leydig cell desensitisation and them being unresponsive is a major factor. Once the leydig cells become unresponsive it doesnt matter what PCT meds you take, there not going to be producing testosterone anytime soon. Desensitisation of the leydig cells can take time and, I think, this is a major factor why someone thats cycled for 3 years will recover slower than someone for 3 months.

Primary hypogonadism is what you really want to avoid. This is when the testes become unresponsive to LH/FSH, also known as Klinefelter's syndrome (one example). As a note, overuse of HCG can cause this.

I'm not certain a bodybuilder can get this from staying shutdown or hypogondal for long peroids, but I suspect being shutdown for years leads to both primary and secondary hypogonadism.

Very good response. I would love to see some evidence on how long it takes fr Leydig cell desensitization and perhaps what drugs are worse than others...

[Swifto]

Very good response. I would love to see some evidence on how long it takes fr Leydig cell desensitization and perhaps what drugs are worse than others...

I'm not entirely sure. I'm having a little look now.

I know LH is the major regulator of Leydig cell differentiation and steroidogenic function. This is why HCG is so important to a bodybuilder.

FSH is mainly for spermantageous production.

If bodybuilders or those who have been on TRT/HRT for lengthy peroids, find it hard to have kids (fertility), that would suggest they suffer particially from primary hypogondism, aswell as secondary IMHO. As the testes are unresponsive to both LH/FSH.

[Swifto]

I think you really need an endriconologist to answer how long it takes for the leydig cells to become desensitised/unresponsive.

I'd also suspect different compounds act differently. As not all compounds cause shutdown via the same action. Testosterone and 19-Nors for example.

[Property of Steroid.com]

I'm not entirely sure. I'm having a little look now.

I know LH is the major regulator of Leydig cell differentiation and steroidogenic function. This is why HCG is so important to a bodybuilder.

FSH is mainly for spermantageous production.

If bodybuilders or those who have been on TRT/HRT for lengthy peroids, find it hard to have kids (fertility), that would suggest they suffer particially from primary hypogondism, aswell as secondary IMHO. As the testes are unresponsive to both LH/FSH.

FSH is actually important to keep high, because increased FSH leads to an increase in LH receptors.

I would love to see some evidence on how long it takes fr Leydig cell desensitization and perhaps what drugs are worse than others...

It would seem that length of time (IMHO) is not as important as dose, for Leydig Cell issues. As an example, we know that estrogen is one of the primary culprits in this issue, but that a single high dose of estrogen is worse for the leydig cells than a bunch of lower doses.

[Swifto]

FSH is actually important to keep high, because increased FSH leads to an increase in LH receptors.


It would seem that length of time (IMHO) is not as important as dose, for Leydig Cell issues. As an example, we know that estrogen is one of the primary culprits in this issue, but that a single high dose of estrogen is worse for the leydig cells than a bunch of lower doses.

Is there an difinitive way of preventing the leydig cells from becoming desensitised, other than use HCG?

And I guess avoiding aromotasables and keeping estrogen in normal/low ranges.

[Serotonin]

The intricate solution that will revolutionize and deals with shutdown is Toremefine Citrate and Aromasin.Have been avoiding 19-nors for some time due to recovery,experimented last cycle using drol in a cutter (found it to be the best cutting tool too) Ran this PCT and its like the encrusted the tree of eden.Still going to keep cycles within 12 weeks range as your receptors get saturated and its hard to remain growing unless you mix and change compounds within the cycle.Its great as this means I can just use long esters (two) and an oral for the first 6-8 weeks.Great thread topic and we are going to crack this gaints...

Check this out goose...

Idiopathic hypogonadotropic hypogonadism in a male runner is reversed by clomiphene citrate

Burge, Mark R.; Lanzi, Richard A.; Skarda, Shayne T.; Eaton, R. Philip

Objective: To assess the efficacy of estrogen antagonist therapy on the function of the hypothalamic-pituitary-testicular axis in a young male runner with significant morbidity attributable to idiopathic hypogonadotropic hypogonadism.

Design: An uncontrolled case study.

Setting: The outpatient endocrinology clinic of a university tertiary referral center.

Patient(s): A 29-year-old male who has run 50 to 90 miles per week since 15 years of age and who presented with a pelvic stress fracture, markedly decreased bone mineral density, and symptomatic hypogonadotropic hypogonadism.

Intervention(s): Clomiphene citrate (CC) at doses up to 50 mg two times per day over a 5-month period.

Main Outcome Measure(s): Serum concentrations of LH, FSH, and T before and after CC therapy, as well as clinical indicators of gonadal function.

Result(s): Barely detectable levels of LH and FSH associated with hypogonadal levels of T were restored to the normal range with CC therapy. The patient experienced improved erectile function, increased testicular size and sexual hair growth, and an improved sense of well being.

Conclusion(s): Exercise-induced hypogonadotropic hypogonadism exists as a clinical entity among male endurance athletes, and CC may provide a safe and effective treatment option for males with debilitating hypogonadism related to endurance exercise.

I know this is old news Clomid, but it is interesting none the less. So with clomid and HCG, what are your guys test level differences after your first cycles? On average?

[Property of Steroid.com]

We really don't know enough about HCG, honestly. We don't even know, though it's unlikely, that doses typically used in this arena would desensitize the Leydigs. Additionally, there is a disparate effect with HCG in normal vs/ hypogonadic subjects, and we don't know if this is due to the presence of LH or testosterone or FSH or whatever. Trained athletes also have a disparate response to HCG...

There's too many variables, but in my estimation, the chance of desensitizing your leydig cells from HCG is almost nothing.

[Swifto]

We really don't know enough about HCG, honestly. We don't even know, though it's unlikely, that doses typically used in this arena would desensitize the Leydigs. Additionally, there is a disparate effect with HCG in normal vs/ hypogonadic subjects, and we don't know if this is due to the presence of LH or testosterone or FSH or whatever. Trained athletes also have a disparate response to HCG...

There's too many variables, but in my estimation, the chance of desensitizing your leydig cells from HCG is almost nothing.

So could one stay shutdown and use HCG regularly to maintain leydig cells dont fully desensitise then? So recovery is still possible?

I'm guessing no...

Because natural testosterone levels cannot be maintained while hypogondal artificially (the use of anndrogens). Well, studies dont state it anyway.

[Serotonin]

You know where you could make a ton of money? Finding something that could somehow inhibit the negative feedback cycle that leads to the hypogonadism associated with AAS use. Except I know nothing of the receptors on the hypothalamus... you could very well block the skeletal muscle receptors as well.

It would be quite the endeavor though and one hell of a breakthrough if it is ever discovered.

[Swifto]

You know where you could make a ton of money? Finding something that could somehow inhibit the negative feedback cycle that leads to the hypogonadism associated with AAS use. Except I know nothing of the receptors on the hypothalamus... you could very well block the skeletal muscle receptors as well.

It would be quite the endeavor though and one hell of a breakthrough if it is ever discovered.

Ahem...

SARM's with no effect on the HPTA.

Or a special injectable GnRH for bodybuilders.

[vitor]

I think exessive ammount of Estrogen will inhibit Leydig Cell development, growth and function, resulting in permenant supression of androgen production.

(In rodent with "high" aromatase), I read a study(some time ago) that aromatase is expressed in both Leydic cells and Sertoil cells in the rodents fetal testis. Which resulted in declined androgen levels and infertelity in some cases.

I have noticed from my own cycling that using AI on results in much better recovery aswell, not to mention that my T-levels are signifently higher(between cycles) when I have used letro or aromasin.

It seems like the hypotalmus will decide what info to send down to Leydig cells, ***ending on how much estrogen it senses.

[vitor]

my bloodwork has shown that since my first or second cycle my Test has never fully gotten back to the levels that they once were when I was in my early 20's.....A price I pay gladly.

That is to be expected if cycling or not.

T-levels will be on a all time high in late teens, b/f they slowly start decreasing a little bit every year for the rest of your live.

[Serotonin]

That is to be expected if cycling or not.

T-levels will be on a all time high in late teens, b/f they slowly start decreasing a little bit every year for the rest of your live.

Yea, not sure how many people know this but many men go through andropause and don't even know about it in their mid to late stages of life. Test levels get so low it affects mood (sense of well being), bone density, lean body mass, and a slew of other things.

[Giants11]

You know where you could make a ton of money? Finding something that could somehow inhibit the negative feedback cycle that leads to the hypogonadism associated with AAS use. Except I know nothing of the receptors on the hypothalamus... you could very well block the skeletal muscle receptors as well.

It would be quite the endeavor though and one hell of a breakthrough if it is ever discovered.

I believe SARM's are close to being produced. I know GTXi Inc, is developing one.

This would proportedly block the negative feedback loop.

It has be theorized that ATD could also accomplish this, as it has been shown in rat models. This is something that Author L Rea suggested, however I have a real hard time taking anything he says seriously. However, there are some interesting abstracts around that I posted about a year ago, I'll dig it up.

[kfrost06]

Or a special injectable GnRH for bodybuilders.

I don't think GnRH will work because GnRH has a very short half-life in the blood (approximately 2 to 5 minutes). The pituitary gland is therefore exposed to high levels of GnRH in hypophyseal-portal blood for brief periods of time.

[Property of Steroid.com]

I believe SARM's are close to being produced. I know GTXi Inc, is developing one.

This would proportedly block the negative feedback loop.

It technically wouldn't even involve the loop. It's a non-hormonal stimulation of the AR.

So could one stay shutdown and use HCG regularly to maintain leydig cells dont fully desensitise then? So recovery is still possible?

I'm not sure what you're asking...

[kfrost06]

For those that are reading this but feel a little lost, there are three main components to the hormonal axis in men, 1.)the Hypothalamus, 2.) the Pituitary gland, and 3.) the Testis hence the H, P, T, and the A for axis. This axis functions in a tightly regulated manner to produce concentrations of circulating steroids (testosterone). When doing steroids you negatively disrupt the axis which then results in a decrease in your production of testosterone and in some cases stops your production of testosterone altogether. The million dollar question, does the amount of time your system is suppressed or shut down effect how long it takes your axis (HPTA) to "get back to normal"?

[Giants11]

It technically wouldn't even involve the loop. It's a non-hormonal stimulation of the AR.



I'm not sure what you're asking...

I see, so SARM's will not play a role in keeping one's HTPA alive on cycle?

[Giants11]

Here is some data that could suggest ATD could block the negative feedback loop:

Effects of ATD on male sexual behavior and androgen receptor binding: a reexamination of the aromatization hypothesis.

Kaplan ME, McGinnis MY.

***artment of Anatomy, Mount Sinai School of Medicine, CUNY, New York 10029.

The aromatization hypothesis asserts that testosterone (T) must be aromatized to estradiol (E2) to activate copulatory behavior in the male rat. In support of this hypothesis, the aromatization inhibitor, ATD, has been found to suppress male sexual behavior in T-treated rats. In our experiment, we first replicated this finding by peripherally injecting ATD (15 mg/day) or propylene glycol into T-treated (two 10-mm Silastic capsules) or control castrated male rats. In a second experiment, we bilaterally implanted either ATD-filled or blank cannulae into the medial preoptic area (MPOA) of either T-treated or control castrated male rats. With this more local distribution of ATD, a lesser decline in sexual behavior was found, suggesting that other brain areas are involved in the neurohormonal activation of copulatory behavior in the male rat.To determine whether in vivo ATD interacts with androgen or estrogen receptors, we conducted cell nuclear androgen and estrogen receptor binding assays of hypothalamus, preoptic area, amygdala, and septum following treatment with the combinations of systemic T alone.ATD plus T, ATD alone, and blank control. In all four brain areas binding of T to androgen receptors was significantly decreased in the presence of ATD, suggesting that ATD may act both as an androgen receptor blocker and as an aromatization inhibitor. Competitive binding studies indicated that ATD competes in vitro for cytosol androgen receptors, thus substantiating the in vivo antiandrogenic effects of ATD. Cell nuclear estrogen receptor binding was not significantly increased by exposure to T in the physiological range. No agonistic properties of ATD were observed either behaviorally or biochemically. Thus, an alternative explanation for the inhibitory effects of ATD on male sexual behavior is that ATD prevents T from binding to androgen receptors.


Effect of an inhibitor of aromatization, 1,4,6 androstatriene-3,17-dione (ATD) on LH release and steroid binding in hypothalamus of adult female rats.

Slama A, Gogan F, Sarrieau A, Vial M, Rostene W, Kordon C.
Exp Brain Res. 1986;64(3):407-10.

Prevention of testosterone aromatization in the female rat pups by perinatal treatment with 1,4,6 androstatriene-3,17-dione (ATD) induces an important defeminization as shown by a reduction of fluctuations of LH release after castration and estradiol implantation. The fact that, under our in vitro experimental conditions, ATD is able to displace testosterone binding in the hypothalamus whereas estradiol does not, confirms the hypothesis that ATD acts on aromatase. The most attractive explanation for the defeminization effect of ATD is then an estrogen-like action of ATD.

[Property of Steroid.com]

Dude....that study says that ATD is preventing androgens from binding to the androgen receptor and that it has estrogen like action.

[Swifto]

It technically wouldn't even involve the loop. It's a non-hormonal stimulation of the AR.



I'm not sure what you're asking...

Can HCG be used to keep the leydig cells responsive when shutdown from androgens? Or when LH/FSH arnt being naturally produced ie, shutdown?

If, yes. Then wouldnt PCT be easier as the leydig cells are still responsive?

Isnt it a wise idea to use low amounts of HCG during a cycle then?

[Giants11]

Dude....that study says that ATD is preventing androgens from binding to the androgen receptor and that it has estrogen like action.

I believe it states that it blocks the AR in the Brain, no?

And it clearly states that ATD is a aromatse inhibitor.

"in support of this hypothesis, the aromatization inhibitor, ATD..."

"In all four brain areas binding of T to androgen receptors was significantly decreased in the presence of ATD, suggesting that ATD may act both as an androgen receptor blocker and as an aromatization inhibitor."

[vitor]

I believe it states that it blocks the AR in the Brain, no?

Yes, but it didnt state clearly if the AR in the muscle would be blocked aswell which would make AAS uselesss basically?

[Giants11]

Yes, but it didnt state clearly if the AR in the muscle would be blocked aswell which would make AAS uselesss basically?

Absolutely, i just figured I'd throw those out there. Considering its the only thing I've seen thus far that "could" have the ability to block the AR in the Hypothalamus.

[kfrost06]

Or a special injectable GnRH for bodybuilders.

Upon further review it appears this may work to some degree. Since GnRH is pulsatile(peaks occur every 90-120 minutes) and if it were administered in such a fashion it would and has shone to increase LH and FSH. The pulsatile pattern of GnRH release appears to be essential for stimulatory effects on LH and FSH release.

[Property of Steroid.com]

Can HCG be used to keep the leydig cells responsive when shutdown from androgens? Or when LH/FSH arnt being naturally produced ie, shutdown?

If, yes. Then wouldnt PCT be easier as the leydig cells are still responsive?

Isnt it a wise idea to use low amounts of HCG during a cycle then?

Maybe. I'm not so sure it matters, honestly. I'll also shoot you straight, and say 2 things:

1. I've been doing a lot of reading on HCG and I think it's effects on hypogonadic males is very different than normal males, and is again different in steroid using males, and it's ability to raise estrogen again, may be different in all those cases, and it's even different in athletes...etc...I need to centralize all my thoughts to be as lucid as possible.

2. At the level of athlete I work with, they fall into one of 2 categories:

a. Professional athlete in a drug tested sport...meaning they need undetectable stuff, and very mild cycles, and barely any pct

b. Bodybuilder/Powerlifter...meaning they don't ever come off.


So PCT has kind of gone on the back burner for me. I've been talking a lot to Eric Potratz (author/supp designer) about AIs (his new supplement which isn't out yet), and HCG...and that's the only reason I'm even researching it. But I think there's likely alot we don't know about it yet.

2.

[vitor]

I was on a 3 year straight cycle, and my total testosterone levels were roughly 250ish (300 is the low end of normal) 3 weeks upon cessation. When I was 19, before ever using steroids, my test levels were 650ish. I doubt I would ever get back there, but I would bet that within a few more weeks, my test levels would be in the low/medium/normal range.

Although I should mention that the last 6 months of my 3 year cycle, I was on HRT doses (100mgs of prop/EOD) which got my test levels to 950ish, which is still High/Normal.

From your example it would indicate that the amount of time youre ON, doesnt make a big diffrence as far as pct/recovery in concerned...

Do you think that your last 3 months with HRT dose was the key factor in your recovery there?
(b/c 3 years is a freaky long time)

[Swifto]

Upon further review it appears this may work to some degree. Since GnRH is pulsatile(peaks occur every 90-120 minutes) and if it were administered in such a fashion it would and has shone to increase LH and FSH. The pulsatile pattern of GnRH release appears to be essential for stimulatory effects on LH and FSH release.

Which means it would be very difficult for a bodybuilder to dose accordingly. Injections would be very frequent indeed.

[Swifto]

Maybe. I'm not so sure it matters, honestly. I'll also shoot you straight, and say 2 things:

1. I've been doing a lot of reading on HCG and I think it's effects on hypogonadic males is very different than normal males, and is again different in steroid using males, and it's ability to raise estrogen again, may be different in all those cases, and it's even different in athletes...etc...I need to centralize all my thoughts to be as lucid as possible.

2. At the level of athlete I work with, they fall into one of 2 categories:

a. Professional athlete in a drug tested sport...meaning they need undetectable stuff, and very mild cycles, and barely any pct

b. Bodybuilder/Powerlifter...meaning they don't ever come off.


So PCT has kind of gone on the back burner for me. I've been talking a lot to Eric Potratz (author/supp designer) about AIs (his new supplement which isn't out yet), and HCG...and that's the only reason I'm even researching it. But I think there's likely alot we don't know about it yet.

2.

Thanks. I appreciate your response.

[Swifto]

From your example it would indicate that the amount of time youre ON, doesnt make a big diffrence as far as pct/recovery in concerned...

Do you think that your last 3 months with HRT dose was the key factor in your recovery there?
(b/c 3 years is a freaky long time)

I was under the impression, that if your leydig cells were shot, PCT is going to be very counterproductive with SERM/AI's. This is often why PCT protocols are nothing but useless and a waste of money.

There often too short. 3-4 weeks, isnt sufficient time IMHO. 4-8 weeks is. It also ***ends greatly on what compounds you've used, AI's, HCG or not, length of shutdown, inhibition. Ones PCT protocol duration should change accordingly.

[Swifto]

Just had a thought...

Prolactin is also very inhibitory to ones HPTA. So would the use Cabergoline be crucial when cycling 19-Nors, or be a must when conducting a PCT protocol when one's used 19-Nor's previously?

[vitor]

Just had a thought...

Prolactin is also very inhibitory to ones HPTA. So would the use Cabergoline be crucial when cycling 19-Nors, or be a must when conducting a PCT protocol when one's used 19-Nor's previously?

I find all AAS raises prolactin (from pre cycle BW), but tren and deca even more so.

User Caber when cycling would always be a good thing imo. High prolactin levels will drive libido in the ground too.

[perfectbeast2001]

I was under the impression, that if your leydig cells were shot, PCT is going to be very counterproductive with SERM/AI's. This is often why PCT protocols are nothing but useless and a waste of money.

There often too short. 3-4 weeks, isnt sufficient time IMHO. 4-8 weeks is. It also ***ends greatly on what compounds you've used, AI's, HCG or not, length of shutdown, inhibition. Ones PCT protocol duration should change accordingly.

Very true, the "industry standard" 4 week PCT of a SERM and an AI (or worse two SERMS) is a pointless waste of money IMO. PCT length should be dicatated by how long it takes to actually work!! In my experience 60 days would be a more appropriate length.