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  1. #1
    Junior Member swifto's Avatar
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    How exactly does total HPTA "shutdown" occur? What causes the Pituitary to stop all hormone output?



    My understanding, though vague, is as follows:



    HPTA "shutdown" occurs when too many androgen/estrogen and progesterone receptors become activated in the Hypothalamus. Different AS act in different ways to cause this.



    For example, "shutdown" via uses Testosterone is caused by too many estrogen/androgen receptors becoming activated, therefore HPTA "shutdown" occursand the pituitary stops hormone output. Not to mention the negative feedback loop...



    Deca and other 19-Nor's will cause HPTA "shutdown" via androgen/progesterone activation as Deca, for example, lacks any estorgenic component.



    Is this correct? I must add, the first person to explain this to me was "Ross". Some of you may be aware of him, others not. Is any of the above correct.



    Thanks.

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    Senior Member RepubCarrier's Avatar
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    that's accurate.... who' Ross?
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  3. #3
    Junior Member swifto's Avatar
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    A AS user with many controversial ideas.



    One of the more intresting ones was how to limit HPTA suppression. As we can see how different AS act...Differently by activating different receptors we can limit/control suppression/shutdown. This would in turn make recovery easier and gains easier to attain post cycle.



    An example cycle would be:



    wk 1-8 Test Prop 75mg/ED

    wk 1-10 Tbol 60mg/ED

    wk 1-12 Primo 600mg/wk.



    From week 1-8 total HPTA shutdown occurs, then after discontinueing Test Prop, the activation of estrogen receptors in the Hypothalamus is removed and only androgen actiavtion will be evident. As Tbol/Primo already lack an progestenic component. Therefore, he states, the Pituitary will begin hormone output and Testosetrone levels will begin to resume production, though somewhat suppressed. This will give a steroid user an advanatge when entering PCT etc...

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    Senior Member rast4man's Avatar
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    To keep it simple, you pretty much have the grasp on the HPTA shutdown. Just think of it on a Testosterone based level; adding synthetic Test, will inevitably signal our HPTA that there is no need to produce our naturally occuring Test, hence the "shutdown". That is why it's imperative to get a proper PCT in order to get the HPTA back and naturally producing the body's own natural Test production.



    I tried the non-PCT route prior to the cycle I'm on now, and I must say it was interesting to say the least. I'm going with a full PCT this time so I can compare results and see where I'm at at the end of the cycle.
    "My life is in the hands of any rascal who chooses to annoy me." -Dr. John Hunter, eighteenth-century physician

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    Site Contributor w_llewellyn's Avatar
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    I think "shutdown" is an improper term, and implies there is some threshold that if you reach, some "total" shutdown occurs, and before it you are much safer. It is all about degrees of suppression, although admittedly you can take enough steroids for long enough to almost nil your andorgen output.



    I have never been in favor of attempting to restore your natural balance of hormones at the sime time as trying to find the right dose of a steroid that will allow muscle retention and prevent any androgen defecit without effecting your testosterone production. It is a situation of trying to have your cake and eat it too. It doesn't work, IMO.
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    Senior Member Benson's Avatar
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    Quote Originally Posted by swifto' post='362311' date='Sep 19 2006, 01:55 PM

    For example, "shutdown" via uses Testosterone is caused by too many estrogen/androgen receptors becoming activated, therefore HPTA "shutdown" occursand the pituitary stops hormone output. Not to mention the negative feedback loop...


    This is essentially correct. Both elevated T and E will signal the hypothalmus to reduce endogenous androgen production in men...I am sure someone here knows the answer but is it correct that non-aromatizing compounds will cause less shutdown because E levels do not rise?
    Remember, believe none of what you hear and half of what you see...





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    Quote Originally Posted by Benson' post='362412' date='Sep 19 2006, 06:03 PM



    I am sure someone here knows the answer but is it correct that non-aromatizing compounds will cause less shutdown because E levels do not rise?


    The concensus seems to be that Tren and Deca shut you down much harder than testosterone for example, so it doesn't seem to be true in all cases.
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    Site Contributor w_llewellyn's Avatar
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    Quote Originally Posted by omnibus' post='362467' date='Sep 19 2006, 09:41 PM

    The concensus seems to be that Tren and Deca shut you down much harder than testosterone for example, so it doesn't seem to be true in all cases.


    Progestational activity also causes inhibition, both at the hypothalamus and likely at the testes directly.
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    So using 100 mg test 2-3 after the other androgens have cleared the system is pointless ? I would think you could get some recovery, albeit not at "full speed" ?



    I guess one could use HCG during these 2-3 weeks instead, would that be a better option ?



    I hate crashing and do not mind prolonging -full-recovery for a few weeks if it means I can have a smoother transition.



    Holding mass is doable on low-normal testosterone IMO. However holding mass when you have castrate levels is damn near impossible, not to mention zero libido and depression to boot.

  10. #10
    Junior Member swifto's Avatar
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    Quote Originally Posted by w_llewellyn' post='362359' date='Sep 19 2006, 10:42 PM

    I think "shutdown" is an improper term, and implies there is some threshold that if you reach, some "total" shutdown occurs, and before it you are much safer. It is all about degrees of suppression, although admittedly you can take enough steroids for long enough to almost nil your andorgen output.



    I have never been in favor of attempting to restore your natural balance of hormones at the sime time as trying to find the right dose of a steroid that will allow muscle retention and prevent any androgen defecit without effecting your testosterone production. It is a situation of trying to have your cake and eat it too. It doesn't work, IMO.


    So you dont think its possible to restore ANY hormone output after discontinueing suppressive androgens, such as Testosterone, Tren, Deca, whilst still using less suppressive androgens, like Var, Primo.



    Is it also true the Pituitary, if not shutdown, can not be permanently suppressed from suppression only..If you follow. There will be no long term health effects if the Pituitary is mearly suppressed, not shutdown?

  11. #11
    Junior Member swifto's Avatar
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    Quote Originally Posted by Benson' post='362412' date='Sep 20 2006, 03:03 AM

    This is essentially correct. Both elevated T and E will signal the hypothalmus to reduce endogenous androgen production in men...I am sure someone here knows the answer but is it correct that non-aromatizing compounds will cause less shutdown because E levels do not rise?


    This is what I have been led to believe.



    Less suppressive androgens only act on certain receptors. Var lasks any estrogenic, progestenic component, therefore can only activate a number of androgenic receptors. Enough to casue "shutdown"...Well...Who knows? I guess thats another question.

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    Who knows ? I do . Blood worked showed essentially no test on 80 mg/day of Var.



    15 mg ED has been show to supress T 30% according to a study.



    Just another myth.



    If it (androgen) binds to the AR - negative feedback and HPTA sup.



    The question is : if you are already shutdown -end of cycle. Can you use a moderate dose and still recover T albeit more slowly ?

  13. #13
    Site Contributor w_llewellyn's Avatar
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    Quote Originally Posted by swifto' post='362545' date='Sep 20 2006, 10:45 AM

    So you dont think its possible to restore ANY hormone output after discontinueing suppressive androgens, such as Testosterone, Tren, Deca, whilst still using less suppressive androgens, like Var, Primo.


    No, it would seem logically possible, although Anavar and Primobolan are both more suppressive than people think. The problem is, the PCT window is when you are trying to restore your natural balance, and throwing things like AI's, reductase inhibitors, low doses of this or that, etc. IMO complicate things. If some people can do it and it works, defintiely good to hear..



    Is it also true the Pituitary, if not shutdown, can not be permanently suppressed from suppression only..If you follow. There will be no long term health effects if the Pituitary is mearly suppressed, not shutdown?


    No, I don't think it is this simple. Your pituitary glad is the "master endocrine gland" in the body. It controls many other things than testosterone, and isn't going to atrophy like your testes do because LH levels are low. It is more an issue of your body, after long periods of acquired hypogonadism, having a problem recognizing its old hormonal balance. Often even after long periods away from steroids, abusers will have testosterone levels on the low end of the spectrum, even though considered normal clinically. This isn't because the pituitary is atrophied or "smaller", but because it thinks this state is normal. This isn't always the case, of course, but illustrates how complicated the issue of recovery can be. I think we should stop focusing on this "shutdown" thing so much; it is just symmantics. Just focus on NOT putting yourself in a place where you have interfered with your natural hormonal balance for too long a period of time.
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    Site Contributor w_llewellyn's Avatar
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    Quote Originally Posted by avantgarde' post='362530' date='Sep 20 2006, 09:40 AM

    So using 100 mg test 2-3 after the other androgens have cleared the system is pointless ? I would think you could get some recovery, albeit not at "full speed" ?



    I guess one could use HCG during these 2-3 weeks instead, would that be a better option ?



    I hate crashing and do not mind prolonging -full-recovery for a few weeks if it means I can have a smoother transition.



    Holding mass is doable on low-normal testosterone IMO. However holding mass when you have castrate levels is damn near impossible, not to mention zero libido and depression to boot.


    I see what you are saying. I think the focus should be a moderate cycle and a strong PCT course (HCG/CLOM/NOLV), or perhaps trying to maintain testicular volume with very low doses of HCG during. This way you are not faced with castrate levels for a long PCT window.



    If going this other route, I would prob recommend doing low dose transdermal. The injectables have too sharp a peak at 24-48 hours. You aren't going to get that balanced low level you are looking for. Each 100mg shot will result in a short window of gonadotropin suppression.
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    Senior Member Benson's Avatar
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    Quote Originally Posted by avantgarde' post='362553' date='Sep 20 2006, 04:49 PM

    The question is : if you are already shutdown -end of cycle. Can you use a moderate dose and still recover T albeit more slowly ?


    In theory, you should be able to taper your exogenous androgen intake, encourage endogenous production with a SERM or, better yet, HCG and avoid the crash altogether...in theory...
    Remember, believe none of what you hear and half of what you see...





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    Bill : so how bout something like this



    7-10 days - 5 grams Androgel ED

    7-10 days - 2,5 grams Androgel ED

    7-10 days - 1,25 gram Androgel ED



    I take it HCG should be used prior to this as both at the same time would mean high T levels and no recovery ?



    I´m thinking



    8 weeks of testosterone @ 500 mg (2 inj/week, frontload with double dose to quickly get to steady state levels).



    2 weeks - the test from previous weeks clears, 10 days of HCG (should be clear after the 4 remaining days of week 2).



    3-4 weeks - Androgel as above + SERM (nolva).



    3-4 weeks - SERM



    I read your comment on AI´s and lipids but I would think a moderate dose of Aromasin - 6,25 mg ED, would be ok to control estrogen on cycle ?



    EDIT : Androgel raise DHT and Estrogen more compared to injections - this may be problematic.



    I guess one could have small injections of test instead and avoid the pesky pharmacokinetics of having one 100 mg shot.

    I´m thinking 25 mg EOD should do the trick (1/10 ml standard 250 mg/ml AMP) with a slin pin for accuracy - may an option ?

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    Quote Originally Posted by w_llewellyn' post='362558' date='Sep 20 2006, 01:31 PM

    . Just focus on NOT putting yourself in a place where you have interfered with your natural hormonal balance for too long a period of time.




    ....And how long would that be? I've heard that the anterior pituitary become more "sensitized" to GHRH in the first two weeks of a cycle since less of it is generated by the hypothalamus. Would this set the system for aggressive recovery was the cycle abruptly ended at that point?
    Morality is herd instinct in the individual.
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    ...not GHRH.....GnRH.
    Morality is herd instinct in the individual.
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    Senior Member BIGGUNS101's Avatar
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    Quote Originally Posted by w_llewellyn' post='362561' date='Sep 20 2006, 05:39 PM

    I see what you are saying. I think the focus should be a moderate cycle and a strong PCT course (HCG/CLOM/NOLV), or perhaps trying to maintain testicular volume with very low doses of HCG during. This way you are not faced with castrate levels for a long PCT window.



    If going this other route, I would prob recommend doing low dose transdermal. The injectables have too sharp a peak at 24-48 hours. You aren't going to get that balanced low level you are looking for. Each 100mg shot will result in a short window of gonadotropin suppression.
    What do you consider a very low dose of HCG, also will this dosage work for someone on HRT.

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    Quote Originally Posted by BIGGUNS101' post='362715' date='Sep 21 2006, 12:41 PM

    What do you consider a very low dose of HCG, also will this dosage work for someone on HRT.


    In case you haven't seen this:



    Coviello AD, Matsumoto AM, Bremner WJ, et al. Low-dose human chorionic gonadotropin maintains intratesticular testosterone in normal men with testosterone-induced gonadotropin suppression. J Clin Endocrinol Metab. 2005;90(5):2595-602.



    ABSTRACT



    In previous studies of testicular biopsy tissue from healthy men, intratesticular testosterone (ITT) has been shown to be much higher than serum testosterone (T), suggesting that high ITT is needed relative to serum T for normal spermatogenesis in men. However, the quantitative relationship between ITT and spermatogenesis is not known. To begin to address this issue experimentally, we determined the dose-response relationship between human chorionic gonadotropin (hCG) and ITT to ascertain the minimum dose needed to maintain ITT in the normal range. Twenty-nine men with normal reproductive physiology were randomized to receive 200 mg T enanthate weekly in combination with either saline placebo or 125, 250, or 500 IU hCG every other day for 3 wk. ITT was assessed in testicular fluid obtained by percutaneous fine needle aspiration at baseline and at the end of treatment. Baseline serum T (14.1 nmol/liter) was 1.2% of ITT (1174 nmol/liter). LH and FSH were profoundly suppressed to 5% and 3% of baseline, respectively, and ITT was suppressed by 94% (1234 to 72 nmol/liter) in the T enanthate/placebo group. ITT increased linearly with increasing hCG dose (P < 0.001). Posttreatment ITT was 25% less than baseline in the 125 IU hCG group, 7% less than baseline in the 250 IU hCG group, and 26% greater than baseline in the 500 IU hCG group. These results demonstrate that relatively low dose hCG maintains ITT within the normal range in healthy men with gonadotropin suppression. Extensions of this study will allow determination of the ITT concentration threshold required to maintain spermatogenesis in man.
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