I am reposting the following post for you (below). From the other posts, it is clear there is no good understanding for PCT. A few comments:
The use of cabergoline without a clinical indication of hyperprolactinemia is worthless and probably harmful.
There is published literature (mine) on successfully restoring the HPTA after AAS cessation.
It is fully expected the LH and FSH will decrease after hCG administration. The measuring of these hormones during hCG treatment is a waste of time, money, and resources. They provide nothing! The TT is the important level. See bold-faced in repost.
Tapering is a myth. It is also worthless. All drugs have half-lives, which act as an inherent taper. Further, there is absolutely no evidence to support tapering to restore the HPTA.
Repost:
https://thinksteroids.com/community/posts/662426
I am a proponent of hCG use during TRT or cycling. The question is the dose. I have written often that 250 IU is inadequate. I prefer 500 IU SC Q3D throughout the AAS administration. I do think that it aids it bringing the testes back online. However, this does not mean to stop hCG after stopping AAS. One must have a sense of the testes response to hCG. Also, from the posts I have read, the HPTA is not in an environment for functioning after AAS administration. The half-lives of the AAS must be taken into consideration.
The first phase of the HPTA protocol examines the functionality of the testicles by the direct action of hCG.
hCG raises sex hormone levels directly through the stimulation of testis and secondarily decreases the production and level of the gonadotropin LH. The increase in serum testosterone with the hCG stimulation is useful in determining whether any primary testicular dysfunction is present.
This initial value is a measure of the ability of the testicles to respond to stimulation from the hCG. Demonstration of HPTA functionality is by an adequate response of the testicles to raise the serum level of T well into the normal range. If this is observed the hCG is discontinued. The failure of the testes to respond to an hCG challenge is indicative of primary testicular failure.
In the simplest terms, the first half of the protocol is determine testicular production and reserve by direct stimulation with hCG. If one is unable to obtain adequate (normal) levels successfully to the first half there is little cause or reason to proceed to the second half.
The second phase of the HPTA protocol, clomiphene and tamoxifen, examines the ability of the hypothalamo-pituitary to respond to stimulation by producing LH levels within the normal reference range.
Clomiphene is a mixed agonist/antagonist. This is due o the fact that clomiphene is composed of two isomers: enclomiphene (trans-clomiphene) and zuclomiphene (cis-clomiphene). Enclomiphene is an estradiol receptor antagonist. Zuclomiphene is an estradiol receptor agonist. In all likelihood, the net antagonist effect might be due to the composition being 70% trans (enclomiphene) and 30% cis (zuclomiphene). Tamoxifen is more of a strict antiestrogen, decreases the effect of estrogen in the body, and potentiates the action of clomiphene. This combination came about after 100s of clinical experience.
Tamoxifen and clomiphene citrate compete with estrogen for estrogen receptor binding sites, thus eliminating excess estrogen circulation at the level of the hypothalamus and pituitary allowing gonadotropin production to resume. Administration produces an elevation of LH and secondarily gonadal sex hormones. The administration leads to an appropriate rise in the levels of LH, suggesting that the negative feedback control on the hypothalamus is intact and that the storage and release of gonadotropins by the pituitary is normal. If there was a successful stimulation of testicular T levels by hCG but an inadequate or no response in LH production than the patient has hypogonadotropic, secondary, hypogonadism.
In the simplest terms, the second half of the protocol is to determine hypothalamo-pituitary production and reserve with clomiphene and tamoxifen. The physiological type of hypogonadismhypogonadotropic or secondaryis characterized by abnormal low or low normal gonadotropin (LH) production in response to clomiphene citrate and tamoxifen. In the functional type of hypogonadism, the ability to stimulate is present.
Further, in my experience, an inadequate gonadotropin response is not reason for giving up on HPTA restoration. As I have said, discontinuing on a 12-18 month basis is still advocated. I have had success by this regimen.
