Background to question:
There are primarily 2 indications for using medication to increase LH stimulation of the testes during TRT:
1. Preservation of spermatogenesis (Fertility)
2. Preservation of intrinsic testicular production of testosterone (and estradiol) (avoidance of testicular atrophy, promotion of more rapid recovery of endogenous T production if/when TRT stopped).
Indication #1 requires much higher LH levels (in part because the real target is the Sertoli cell rather than the Leydig cell, and LH in this case is standing in for FSH due to complicated less efficient mechanisms). When HCG used for this indication the doses are in the range of 3000-6000 IU per week.
Indication #2 requires much lower LH levels. When HCG is used for this indication the doses are typically 250 or 500 IU 2-3x/week.
Question:
Can enclomiphene, clomiphene, or tamoxifen accomplish something useful as regards indication #2?
It is commonly stated (without data) that the HPA axis is shut down so profoundly with TRT that SERMS are ineffective. However, while I am relatively convinced that this is true regarding Indication #1, and is likely true for testicular atrophy/size, I am not certain it is completely true regarding promotion of endogenous recovery.
It is quite possible, theoretically, that low level LH stimulation of the Leydig cells from SERMS during TRT could allow more rapid recovery upon stopping TRT. Moreover, some men never recover endogenous production depending in part on factors like length of suppression and age. This could potentially be favorably impacted by low level LH stimulation by SERMS as well.
The question comes down to what level of intratesticular testosterone can be achieved with a SERM during TRT and I am not aware of data on this point. One way to look at this would be to measure LH levels during TRT alone and repeat after a suitable period with the addition of a SERM.
Has anyone done this?
Does anyone have additional data or experience?
There are primarily 2 indications for using medication to increase LH stimulation of the testes during TRT:
1. Preservation of spermatogenesis (Fertility)
2. Preservation of intrinsic testicular production of testosterone (and estradiol) (avoidance of testicular atrophy, promotion of more rapid recovery of endogenous T production if/when TRT stopped).
Indication #1 requires much higher LH levels (in part because the real target is the Sertoli cell rather than the Leydig cell, and LH in this case is standing in for FSH due to complicated less efficient mechanisms). When HCG used for this indication the doses are in the range of 3000-6000 IU per week.
Indication #2 requires much lower LH levels. When HCG is used for this indication the doses are typically 250 or 500 IU 2-3x/week.
Question:
Can enclomiphene, clomiphene, or tamoxifen accomplish something useful as regards indication #2?
It is commonly stated (without data) that the HPA axis is shut down so profoundly with TRT that SERMS are ineffective. However, while I am relatively convinced that this is true regarding Indication #1, and is likely true for testicular atrophy/size, I am not certain it is completely true regarding promotion of endogenous recovery.
It is quite possible, theoretically, that low level LH stimulation of the Leydig cells from SERMS during TRT could allow more rapid recovery upon stopping TRT. Moreover, some men never recover endogenous production depending in part on factors like length of suppression and age. This could potentially be favorably impacted by low level LH stimulation by SERMS as well.
The question comes down to what level of intratesticular testosterone can be achieved with a SERM during TRT and I am not aware of data on this point. One way to look at this would be to measure LH levels during TRT alone and repeat after a suitable period with the addition of a SERM.
Has anyone done this?
Does anyone have additional data or experience?
