Interesting discussion . . . let me explain what we REALLY know about Clomid . . . granted what we really know refers to women.
Clomid is a very good drug for women having moderate problems with conception (ie nothing is wrong with the family jewels or plumbing but for some reason twice-weekly joy sessions with the lover isn't getting the job done). Clomid, which structurally looks like estrogen, acts on hypothalamus causing it to release gonadotropin releasing hormone (GnRH). From this point on, it's business as usual. GnRH stimulates the pituitary to release follicle-stimulating hormone (FSH) and lutenizing hormone (LH). FSH primarily primes the ovaries to jiggle some oocytes from their 2-4 decade slumber while LH is responsible for increasing estrogen production and ultimately for ovulation. A woman on Clomid typically pumps out 2-3X more estrogen than before treatment.
Clearly (well as clear as human medical science gets), Clomid acts by blocking estrogenic feedback to hypothalamus. It is unlikely that Clomid would desensitize the ovaries (or testes) to LH b/c if that happened what's the point of boosting LH? It's unlikely that Clomid desensitizes the pituitary to LH . . . since it's acting through intracellular steroid receptors while LH/FSH are peptide hormones with cell surface receptors. If Clomid does desensitize the pituitary to LH . . . that might be GOOD. If you block LH feedback to the pituitary, it might keep on pumping out LH. Obviously, feedback from FSH and steroid hormones would likely supercede the blockade of LH signalling.
St'd dose for women is 50mg x 5d (before mid-cycle). If that fails to bump LH/estrogen then during the NEXT cycle you try 100mg x 5d. If that fails then 150mg x 5d (during the next month) +/- another fertility drug like Pergonal(LH and FSH purified from urine). Some go all the way to 250mg . . . but that's a damn unhappy woman.
So what happens in guys? Damn if anybody really knows b/c why would you ever use Clomid in a guy?! The basic biology is the same. Clomid primes the hypothalamus by inhibiting steroid hormone feedback on the hypothalamus (early post cycle this would be T and E, while after enough half-lives it would be primarily aromatized E). If you put enough Clomid in your system, you can overcome steroid-mediated shutdown of the HPT axis.
In fact, the addition of an aromatase inhibitor increases your odds of being successful . . . if you were using aromatizing gear . . . b/c the enemy to re-starting the HP part of the axis is serum steroid levels.
Clomid is a very good drug for women having moderate problems with conception (ie nothing is wrong with the family jewels or plumbing but for some reason twice-weekly joy sessions with the lover isn't getting the job done). Clomid, which structurally looks like estrogen, acts on hypothalamus causing it to release gonadotropin releasing hormone (GnRH). From this point on, it's business as usual. GnRH stimulates the pituitary to release follicle-stimulating hormone (FSH) and lutenizing hormone (LH). FSH primarily primes the ovaries to jiggle some oocytes from their 2-4 decade slumber while LH is responsible for increasing estrogen production and ultimately for ovulation. A woman on Clomid typically pumps out 2-3X more estrogen than before treatment.
Clearly (well as clear as human medical science gets), Clomid acts by blocking estrogenic feedback to hypothalamus. It is unlikely that Clomid would desensitize the ovaries (or testes) to LH b/c if that happened what's the point of boosting LH? It's unlikely that Clomid desensitizes the pituitary to LH . . . since it's acting through intracellular steroid receptors while LH/FSH are peptide hormones with cell surface receptors. If Clomid does desensitize the pituitary to LH . . . that might be GOOD. If you block LH feedback to the pituitary, it might keep on pumping out LH. Obviously, feedback from FSH and steroid hormones would likely supercede the blockade of LH signalling.
St'd dose for women is 50mg x 5d (before mid-cycle). If that fails to bump LH/estrogen then during the NEXT cycle you try 100mg x 5d. If that fails then 150mg x 5d (during the next month) +/- another fertility drug like Pergonal(LH and FSH purified from urine). Some go all the way to 250mg . . . but that's a damn unhappy woman.
So what happens in guys? Damn if anybody really knows b/c why would you ever use Clomid in a guy?! The basic biology is the same. Clomid primes the hypothalamus by inhibiting steroid hormone feedback on the hypothalamus (early post cycle this would be T and E, while after enough half-lives it would be primarily aromatized E). If you put enough Clomid in your system, you can overcome steroid-mediated shutdown of the HPT axis.
In fact, the addition of an aromatase inhibitor increases your odds of being successful . . . if you were using aromatizing gear . . . b/c the enemy to re-starting the HP part of the axis is serum steroid levels.
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