After prolonged use of AAS , the pituitary is downregulated to LHRH . We know this because even with extensive use of HCG , sometimes LH and FSH levels remain absent.
Another proof of this is that people with Kallmann syndrome (that never produced LHRH naturally) do not show initial response with an LHRH test even without any defect in his pituitary gland.
Because of this ( and because of a success story presented in a paper) , some people advocate the use of 100 mcg of trip at the beginning of PCT for pituitary priming.
However, this method IMHO is terrible.
The physiological dose of LHRH is 2-20 mcg in pulses every 60 ~ 90 minutes. Repeated use of supraphysiological doses in the beginning increases pituitary response (this is the priming) but then the pituitary begins to be downregulated. Furthermore, the use of constante levels of LHRH (rather than pulsatile fashion) also desensitizate the pituitary.
Trip is an LHRH agonist, which is not only more powerful than LHRH, 130 to 150 times more, also remain acting as longer (as opposed to LHRH which is short acting), some says that it`s effects lasts up to one month.
That would be counterproductive in a PCT for two reasons: first the risk of downregulation of the pituitary and second because while trip is acting, the hypothalamus is not working.
More seriously, the result could trick the person. The result of the blood test appeared the HPTA axis funcioando properly after using trip but a month later the person would be in a stronger shutdown than the original.
So LHRH is useless for PCT? I do not believe that. But the use of trip certainly should be rejected.
What could be useful in IMHO , it`s a correct protocol for priming the pituitary.
There is a vast literature on the use of LHRH for priming the pituitary, especially for the diagnosis of some diseases, like Kallmann syndrome.
Some protocols that I saw :
- A long time pulses in physiological doses of LHRH (there was no success in all the cases, this is what usually happens to a person in a regular PCT);
- In the paper " Application of gonadotropin releasing hormone in hypogonadotropic hypogonadism - diagnostic and Therapeutic Aspects " it uses pulses of LHRH 20 mcg every 90 minutes ( this would be impossible for a PCT);
- In the book "LHRH and it`s analogs" (LHRH and Its Analogs) , the author presents some commonly used protocols. The most successful one being used was 5 100 mcg shots IM LHRH (LHRH not an LHRH agonist).
This protocol also was used in the paper "Clinical and inheritance profiles of Kallmann syndrome in Jordan"
- In another interesting case, reported in the paper "GnRH (LHRH) restores HPTA in AAS induced hypogonadism", a bodybuilder who was in ASIH for more than a year had its pituitary primed with 3 doses of 200 mcg LHRH (IM, 1 x per day)
- Yet another case, priming was achieved with 20 pulses of 20 mcg of LHRH (5 pulses of 20 mcg every hour for 5 hours done on 4 consecutive days).
Thus, in the case of a person that is sure in shutdown after prolonged use of AAS or have been diagnosed with ASIH, IMHO the dose of 100 mcg of LHRH IM for five days in a row seems useful.
There would be the risk of suppression of the pituitary?
I think unlikely. I saw no case dna medical literature suppression pulse of LHRH (all cases I saw were of LHRH agonists, such as trip, or antagonists or LHRH administered in a continuously way rather than pulsatile)
The most recommended way , if you have the financial means and the medical follow-up , it`s get a proper exam, the GnRH stimulation test (basically evaluates the response of your pituitary after a dose of 100 mcg of LHRH ), at the end of your cycle to see if your pituitary is downregulated . If so, perform with your doctor the priming of the pituitary . This would probably greatly reduce the risk of ASIH and also shorten your recovery time.
Then I could use in theory LHRH pulses during a cycle instead of HCG ?
Probably not. LHRH pulses at very long intervals LH would probably not produce enough LH to keep the operation of the tests .
Anyway , the use of LHRH ( Gonadorelin Acetate ) as shown may prove useful . But the use of trip should be avoided on PCT.
Another proof of this is that people with Kallmann syndrome (that never produced LHRH naturally) do not show initial response with an LHRH test even without any defect in his pituitary gland.
Because of this ( and because of a success story presented in a paper) , some people advocate the use of 100 mcg of trip at the beginning of PCT for pituitary priming.
However, this method IMHO is terrible.
The physiological dose of LHRH is 2-20 mcg in pulses every 60 ~ 90 minutes. Repeated use of supraphysiological doses in the beginning increases pituitary response (this is the priming) but then the pituitary begins to be downregulated. Furthermore, the use of constante levels of LHRH (rather than pulsatile fashion) also desensitizate the pituitary.
Trip is an LHRH agonist, which is not only more powerful than LHRH, 130 to 150 times more, also remain acting as longer (as opposed to LHRH which is short acting), some says that it`s effects lasts up to one month.
That would be counterproductive in a PCT for two reasons: first the risk of downregulation of the pituitary and second because while trip is acting, the hypothalamus is not working.
More seriously, the result could trick the person. The result of the blood test appeared the HPTA axis funcioando properly after using trip but a month later the person would be in a stronger shutdown than the original.
So LHRH is useless for PCT? I do not believe that. But the use of trip certainly should be rejected.
What could be useful in IMHO , it`s a correct protocol for priming the pituitary.
There is a vast literature on the use of LHRH for priming the pituitary, especially for the diagnosis of some diseases, like Kallmann syndrome.
Some protocols that I saw :
- A long time pulses in physiological doses of LHRH (there was no success in all the cases, this is what usually happens to a person in a regular PCT);
- In the paper " Application of gonadotropin releasing hormone in hypogonadotropic hypogonadism - diagnostic and Therapeutic Aspects " it uses pulses of LHRH 20 mcg every 90 minutes ( this would be impossible for a PCT);
- In the book "LHRH and it`s analogs" (LHRH and Its Analogs) , the author presents some commonly used protocols. The most successful one being used was 5 100 mcg shots IM LHRH (LHRH not an LHRH agonist).
This protocol also was used in the paper "Clinical and inheritance profiles of Kallmann syndrome in Jordan"
- In another interesting case, reported in the paper "GnRH (LHRH) restores HPTA in AAS induced hypogonadism", a bodybuilder who was in ASIH for more than a year had its pituitary primed with 3 doses of 200 mcg LHRH (IM, 1 x per day)
- Yet another case, priming was achieved with 20 pulses of 20 mcg of LHRH (5 pulses of 20 mcg every hour for 5 hours done on 4 consecutive days).
Thus, in the case of a person that is sure in shutdown after prolonged use of AAS or have been diagnosed with ASIH, IMHO the dose of 100 mcg of LHRH IM for five days in a row seems useful.
There would be the risk of suppression of the pituitary?
I think unlikely. I saw no case dna medical literature suppression pulse of LHRH (all cases I saw were of LHRH agonists, such as trip, or antagonists or LHRH administered in a continuously way rather than pulsatile)
The most recommended way , if you have the financial means and the medical follow-up , it`s get a proper exam, the GnRH stimulation test (basically evaluates the response of your pituitary after a dose of 100 mcg of LHRH ), at the end of your cycle to see if your pituitary is downregulated . If so, perform with your doctor the priming of the pituitary . This would probably greatly reduce the risk of ASIH and also shorten your recovery time.
Then I could use in theory LHRH pulses during a cycle instead of HCG ?
Probably not. LHRH pulses at very long intervals LH would probably not produce enough LH to keep the operation of the tests .
Anyway , the use of LHRH ( Gonadorelin Acetate ) as shown may prove useful . But the use of trip should be avoided on PCT.