There is heated debate on what is a viable option as an ancillary while on cycle, both for adverse side effect prevention and for easier recovery. Regarding recovery, most substances are used for their ability to salvage some function of an axis part, with the most prominenent and widely used being hCG. This hormone is used to preserve testicular function and form in the absence of LH, and FSH or its analog hMG have been proposed to support its spermatogenetic function.
But what about the other 2 parts of the axis? Granted, hypothalamus is a brain region with milllions and diverse inputs, both hormonal and neuronal. Lastly, is there anything we can do to preserve the third part of the HPTA, the pituitary?
The pituitary receives input from the hypothalamus via pulses of GnRH and from the testes via T and a few other hormones (namely activin and inhibin). It produces LH, which tells the testis to produce T, and FSH, which tells the testis to produce spermatozoa.
Regular pulses of GnRH promote the production of LH and FSH in the anterior pituitary, while prolonged and intense GnRH input blocks it. Most importantly, gonadal hormones like T and E reduce GnRH activity. Testosterone and estrogen on the other hand inhibit LH and FSH production. It is our body's way of telling that we have enough gonadal hormones and the testes do not need to produce more.
These tissues (the pituitary and the testes) undergo a process call sensitization.Put simply, if left for a long period without any excitation, even a small stimulus will produce great effect. The reverse is also true, if for a long period they are over-stimulated, a great stimulus will produce miniscule effect.
While on cycle, we provide the body with a supra-physiological amount of androgens. This leads eventually to a reduction in hypothalamic, pituitary and testicular activity. If there were a way to prevent GnRH and T/E sensitization of the pituitary, the recovery and the preserved function of it would be benefited.
Older studies (PMID: 3931502, 323393, 6781360, 3516082, sorry cant post links yet) suggest that is the case with a low dose of SERMs.
Specifically, there is a dose-dependent bell shaped curve where a low dose of tamoxifen will actually raise LH (and subsequently T) levels, and at the same time, sensitize the pituitary's input to GnRH. The dose studied was 20 mg / day. At higher doses of clomiphene or tamoxifen the reverse was true, as the pituitary was desensitized. There are specific limitations: these were mostly done in cell cultures, where GnRH input is absent by default; mainly female subjects were used; there was no supplementation.
In another study (PMID: 22946848) tamoxifen increased a marker of testicular function while on replacement therapy, indicating an increase in FSH activity. The replacement dose in this study was 120 mg / day of testorone undecanoate per os.
Other unecdotal evidence point to numerous steroid (ab)users to supplement their on cycle protocol with a low dose of SERM for the same reason.
On another substance, we have hMG. This is a hormone, analog in its action to both LH and FSH. It's sole role in the male is found in the testis, where it both increases T production and spermatogenesis. Its use has been documented reverse steroid-induce hypogonadism (PMID: 12801577). It is also supported by many that use of the substance up to the start of PCT helps recovery and preserves testicular function, as with hCG preserving another part of testicular function, T production.
Therefor, it would be interesting to assert whether there is the need for a low dose of tamoxifen and hMG during cycle, whether it would ease recovery and help preserve both pituitary and testicular function.
But what about the other 2 parts of the axis? Granted, hypothalamus is a brain region with milllions and diverse inputs, both hormonal and neuronal. Lastly, is there anything we can do to preserve the third part of the HPTA, the pituitary?
The pituitary receives input from the hypothalamus via pulses of GnRH and from the testes via T and a few other hormones (namely activin and inhibin). It produces LH, which tells the testis to produce T, and FSH, which tells the testis to produce spermatozoa.
Regular pulses of GnRH promote the production of LH and FSH in the anterior pituitary, while prolonged and intense GnRH input blocks it. Most importantly, gonadal hormones like T and E reduce GnRH activity. Testosterone and estrogen on the other hand inhibit LH and FSH production. It is our body's way of telling that we have enough gonadal hormones and the testes do not need to produce more.
These tissues (the pituitary and the testes) undergo a process call sensitization.Put simply, if left for a long period without any excitation, even a small stimulus will produce great effect. The reverse is also true, if for a long period they are over-stimulated, a great stimulus will produce miniscule effect.
While on cycle, we provide the body with a supra-physiological amount of androgens. This leads eventually to a reduction in hypothalamic, pituitary and testicular activity. If there were a way to prevent GnRH and T/E sensitization of the pituitary, the recovery and the preserved function of it would be benefited.
Older studies (PMID: 3931502, 323393, 6781360, 3516082, sorry cant post links yet) suggest that is the case with a low dose of SERMs.
Specifically, there is a dose-dependent bell shaped curve where a low dose of tamoxifen will actually raise LH (and subsequently T) levels, and at the same time, sensitize the pituitary's input to GnRH. The dose studied was 20 mg / day. At higher doses of clomiphene or tamoxifen the reverse was true, as the pituitary was desensitized. There are specific limitations: these were mostly done in cell cultures, where GnRH input is absent by default; mainly female subjects were used; there was no supplementation.
In another study (PMID: 22946848) tamoxifen increased a marker of testicular function while on replacement therapy, indicating an increase in FSH activity. The replacement dose in this study was 120 mg / day of testorone undecanoate per os.
Other unecdotal evidence point to numerous steroid (ab)users to supplement their on cycle protocol with a low dose of SERM for the same reason.
On another substance, we have hMG. This is a hormone, analog in its action to both LH and FSH. It's sole role in the male is found in the testis, where it both increases T production and spermatogenesis. Its use has been documented reverse steroid-induce hypogonadism (PMID: 12801577). It is also supported by many that use of the substance up to the start of PCT helps recovery and preserves testicular function, as with hCG preserving another part of testicular function, T production.
Therefor, it would be interesting to assert whether there is the need for a low dose of tamoxifen and hMG during cycle, whether it would ease recovery and help preserve both pituitary and testicular function.
Preserving HPT axis functions on cycle
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