Originally Posted by
bert003
read the below longhorn1...
Some steroids only REDUCE TESTOSTERONE PRODUCTION(to varying degrees), whereas other steroids will SHUTDOWN the HPTA resulting in a complete cessation of androgen production.
*NOT ALL ANDROGENS CAUSE SHUTDOWN* true, but why would you want to use something that doesnt completely shut down the HPTA. If you are only gonna suppress it (aka anavar only) you are basically spending money to replace your own hormones with no extra anabolic effect.
"Shutdown", is defined by a COMPLETE inhibition of the Pituitary/Testes, resulting in a TOTAL cessation of endogenous androgen production.
SOME androgens will only SUPPRESS endogenous androgen production, resulting in a DECREASED testosterone level, but not a complete shutdown. (Turinabol, Anavar, Halotestin, Wistrol, Equipoise, Dianabol, Masteron, Primobolan)
Very Androgenic/Progestenic/Estrogenic steroids(Trenbolone, Nandrolone, Anadrol, Testosterone) cause a COMPLETE shutdown of endogenous hormone production.
The distinction between SUPRESSION and SHUTDOWN is utterly important, as steroids that cause LESS supression of endogenous hormones will allow for greater retention of gains upon ending the cycle, and a quicker, easier recovery!
no the only difference between suppression and shutdown is the natural occuring levels of LH and FSH, both signs of primary cessation of gonadotropins. Yes you want to try to keep LH and FSH as normal as possible but with exogenous steroids in anabolic doses (supaphysiologic amounts) its going to happen. thats why HCG is such an importance ON cycle because it mimics LH in the male. And HCG has been shown to MAINTAIN spermatogensis in subjects with subpar FSH levels, so that would be essential to recovery. but thats in a different thread i wrote, and I know swifto wrote one also. So using the terms here, using HCG would keep from going to shutdown and keep it in suppression
The Following steroids will NOT SHUTDOWN THE HPTA:
Turinabol, Anavar, Proviron, Halotestin, Wistrol, Equipoise, Dianabol, Masteron, Primobolan, Clostebol, and 4-ADiol.
Pre-PCT: PRE-PCT allows the HPTA to begin LH/FSH output, while still receiving additional anabolic support. This is the peroid of time where we utilize a NON-inhibitory steroid while the endogenous testosterone level begins to recover. This occurs PRIOR TO FULL PCT, so that by the time we begin full PCT the HPTA has already began recovering.
Pre-PCT is dumb. Using HCG on cycle will do everything that this is claimed to do. and with the more suppressive AAS (progestins) it could actually lead to more problems due to not enough test in the body anyways which throws the other hormones out of wack.
Active RECOVERY: The HPTA BEGINS to restore endogenous testosterone production once it detects the body's androgen level beginning to decline(end of cycle).
Therefore, HPTA CAN BEGIN TO RECOVER WHILE STILL IN AN ANABOLIC STATE!
The following drugs can be used during Active Recovery:
Examples...
In a SHORT CYCLE:
Weeks 1-4: Testosterone Propionate, 100mgs ED
Weeks 1-4: Dianabol, 50mgs ED
Weeks 1-4: NPP, 400mgs
Weeks 4-8: **PRE-PCT(ACTIVE RECOVERY)**
Weeks 8-?: **POST CYCLE THERAPY**
so after using NANDROLONE, which was said caused total shutdown, you would wait 4 weeks before beginning PCT? long after all the estered androgens are out of the system, it wouldnt do any good and would put the body in a catabolic state during that time which is counterproductive. Using anavar, or any of those other drugs wouldnt do much either at best somewhat balance the anabolism/catabolism effect that androgens have
A Standard Cycle:
Weeks 1-6: Dianabol, 30mgs ED
Weeks 1-10: Testosterone Enanthate, 500mgs
Weeks 8-12: Winstrol, 100mgs ED
Weeks 12-16: **PRE-PCT(ACTIVE RECOVERY) **
Weeks 16-26: **POST CYCLE THERAPY**
same here, you are saying to wait untill there is virtually NO TESTOSTERONE in the body and then wait a couple of weeks then start PCT? Ineffective and not smart
DO NOT end your cycle ABRUPTLY! Don't just END your cycle cold-turkey! If you are SHUTDOWN, full restoration can take weeks and even MONTHS. Therefore, one should REMAIN ON minimally-inhibitive STEROIDS(HPTA) in an attempt to MAINTAIN the gains they made while ON CYCLE, while STILL BEGINNING TO RECOVER TESTOSTERONE PRODUCTION. On top of that, one still continues to progess from the mild additional anabolic support.Actually, if using HCG on cycle and utilize clomid/nolva combo in PCT then an abrupt end to the cycle would be best. As long as the Testosterone is the last to go, ie run test longer than nandrolone deca to let it clear. That way there would still be some functional testosterone in the body and while using HCG on cycle Intratesticular testosterone volume would be maintained which makes recovery that much easier. testosterone is a key player in Spermatogensis which, in the end, what determines if there is enough functional testosterone in the body
NOT only does it mean that you can run a COMPLETE CYCLE with NO SHUTDOWN whatsoever(as long as the right compounds, dosages, and durations are used), it also means that if you ARE SHUTDOWN from your cycle, you do NOT HAVE TO COME RIGHT OFF CYCLE! Actually, it is BETTER TO STAY ON CYCLE WHILE YOUR ENDOGENOUS TESTOSTERONE LEVEL BEGINS TO INCREASE!
using those compounds wouldnt increase natural testosterone.
You may also run a cycle that COMPLETELY AVOIDS SHUTDOWN:
Weeks 1-6: Dianabol, 40mgs ED
Weeks 1-10: Anavar, 50mgs ED
Weeks 1-10: Masteron, 100mgs EOD
Or
Weeks 1-6: Dianabol, 40mgs ED
Weeks 1-10: Primobolan, 500mgs
Weeks 6-14: Turinabol, 60mgs ED
talk about harshness on the liver, they are all metabolized by similar enzymes in the liver (same with alot of drugs) and having that much oral androgen would really put a strain on the liver.
And Many many more! There are tons of NON-inhibitory cycles that you can devise using my my list above for your guideline. Your days of HPTA suffering are over!
this sounds like a marketing ploy
By understanding WHICH steroids cause SHUTDOWN and which steroids do NOT, we can formulate a perfect EXTENDED CYCLE.
The Hypothalamus has Androgen, Estrogen, and Progesterone receptors.
Each and EVERY anabolic steroid affects these receptors DIFFERENTLY.
Some steroids affect ALL receptors, while some only affect ONE type of receptor, while others have very little effect on ANY of these receptors.
UNDERSTANDING WHICH steroids affect which receptors, and to WHAT DEGREE, will FULLY enable the steroid user to COMPLETELY and systematically AVOID HPTA SHUTDOWN!
By understanding WHICH steroids cause SHUTDOWN and which steroids do NOT, we can formulate a perfect EXTENDED CYCLE.
Steroids that cause an OVERSATURATION(too many receptors activated) of these various hormone receptors, WILL CAUSE SHUTDOWN.
Steroids that DO NOT CAUSE an OVERSATURATION of ANY of these various hormone receptors, will NOT cause SHUTDOWN!any anabolic dose of androgens will cause suppression, thats how some patients on TRT can maintain spermatogensis, and others lose that ability. One of the biggest reasons AAS failed as a male contraceptive agent
The Following drugs either DIRECTLY or INDIRECTLY activate ESTROGEN receptors, to varying degrees:
Testosterone
Methandrostenolone
Mathandriol
Oxymetholone
Nandrolone
Boldenone
The Following drugs either DIRECTLY or INDIRECTLY activate PROGESTERONE receptors, to varying degrees:
Nandrolone
Trenbolone
Oxymetholone
The Following drugs activate Androgen receptors, to varying degrees:
Testosterone
Methandrostenolone
Mathandriol
Oxymetholone
Nandrolone
Boldenone
Trenbolone
Halotestin
Oxandrolone
Stanzolol
Chlorodehydromethltestosterone
Methyltestosterone
Methenolone...
(ALL AAS*)
As we can see, the steroids that cause HPTA SHUTDOWN either OVERSATURATE ONE SPECIFIC receptor, or they activate too many TOTAL receptors(Androgen/Estrogen/Progesterone)
For instance, Trenbolone causes HPTA SHUTDOWN because it OVERSATURATES BOTH, the ANDROGEN and the PROGESTERONE receptors.
Testosterone causes SHUTDOWN because it converts to ESTROGEN and DHT, therefore, it oversaturates the Androgen/Estrogen receptors.
As we can ALSO SEE, the steroids that DO NOT cause SHUTDOWN of the HPTA, do NOT oversaturate ANY of the different hormone receptors, and thus, do NOT cause SHUTDOWN.
Methenolone(Primobolan) does not possess ANY Estrogenic or Progestational ACTIVITY WHATSOEVER. It does, by virtue of being an anabolic steroid, posses a SMALL Androgenic component. Because it lacks ANY ESTROGENIC/PROGESTATIONAL component, and it lacks a strong Androgenic component, it WILL NOT CAUSE SHUTDOWN!
Oxandrolone(Anavar) posseses NO Estrogenic/Progestational component either. AND, it also lacks a strong androgenic component. Thus, Anavar will NOT cause shutdown.
By understanding WHICH steroids cause SHUTDOWN and which steroids do NOT, we can formulate a perfect EXTENDED CYCLE.
*It must also be noted, that ANY steroid in LARGE enough DOSAGES for long enough DURATIONS, can cause SHUTDOWN of the HPTA.
NOT ALL ANDROGENS CAUSE SHUTDOWN*
"Shutdown", is defined by a COMPLETE inhibition of the Pituitary/Testes, resulting in a TOTAL cessation of endogenous androgen production.
SOME androgens will only SUPPRESS endogenous androgen production, resulting in a DECREASED testosterone level, but not a complete shutdown. (Tbol, Var, Wistrol, EQ, Dianabol, masteron, proviron, halo, primo)
Very Androgenic/Progestenic/Estrogenic steroids(Tren, Deca, Drol, Test) cause a COMPLETE shutdown of endogenous hormone production.
The distinction between SUPRESSION and SHUTDOWN is utterly important, as steroids that cause LESS supression of endogenous hormones will allow for greater retention of gains upon ending the cycle, and a quicker, easier PCT.
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Horm Metab Res. 1984 Sep;16(9):492-7.Related Articles, Links
Effect of non aromatizable androgens on LHRH and TRH responses in primary testicular failure.
Spitz IM, Margalioth EJ, Yeger Y, Livshin Y, Zylber-Haran E, Shilo S.
We have assessed the gonadotropin, TSH and PRL responses to the non aromatizable androgens, mesterolone and fluoxymestrone, in 27 patients with primary testicular failure. All patients were given a bolus of LHRH (100 micrograms) and TRH (200 micrograms) at zero time. Nine subjects received a further bolus of TRH at 30 mins. The latter were then given mesterolone 150 mg daily for 6 weeks. The remaining subjects received fluoxymesterone 5 mg daily for 4 weeks and 10 mg daily for 2 weeks. On the last day of the androgen administration, the subjects were re-challenged with LHRH and TRH according to the identical protocol. When compared to controls, the patients had normal circulating levels of testosterone, estradiol, PRL and thyroid hormones. However, basal LH, FSH and TSH levels, as well as gonadotropin responses to LHRH and TSH and PRL responses to TRH, were increased the gonadotropin response to LHRH normally a lower gonad response to LH. . Mesterolone administration produced no changes in steroids, thyroid hormones, gonadotropins nor PRL. There was, however, a reduction in the integrated and incremental TSH secretion after TRH. Fluoxymesterone administration was accompanied by a reduction in thyroid binding globulin (with associated decreases in T3 and increases in T3 resin uptake). The free T4 index was unaltered, which implies that thyroid function was unchanged. In addition, during fluoxymesterone administration, there was a reduction in testosterone, gonadotropins and LH response to LHRH. Basal TSH did not vary, but there was a reduction in the peak and integrated TSH response to TRH. PRL levels were unaltered during fluoxymesterone treatment.
This study isnt applicable to this situation. Who actually has access to LHRH and TRH. thats essentially 'cheating' the body in its feedback loops, both long and short. And by repeating the bolus of releasing hormones essentially reduces the "power" of LH to stimulate testosterone. The TRH feedback loop is long enough it was avoided (in testosterone's case) but had a negative impact on T3, which plays a key part in metabolism. why do people take T3 to lose weight?
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Excellent...
its really not that big of a deal. 
