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Keep it beefy
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though it may not be highly effective, it may still have some effect, and this is my reasoning.
there are several feedback mechanisms that control testosterone production in the human body. two of the most important are the estrogenic and testosterone routes.
the first being the estrogenic one. most people know about this. this is why people take clomid postcycle. clomid is a selective estrogen receptor modulator, and binds in the hypothalamus to prevent the brain from thinking there is any estrogen in the blood. the hypo. reacts by releasing GNRH, which tells the pituitary to release LH and FSH.
the testosterone negative feedback route occurs through inhibin. which is released from the testes and acts on the hypothalamus to regulate testosterone the same way the above feedback route did. considering both of these, you can see that doing clomid on-cycle isn't entirely pointless. when you take clomid in the presence of supraphysiological levels of testosterone (or it's derivatives, some haveing more pronouced effects on inhibin than others, and affecting other feedback routes, though that's a different thread), the hypothalamus thinks it's not getting estrogen, which would normally cause for an increase in LH production. but because inhibin levels are high (because the testes see that there is tons of test. floating around), the feedback via the estrogenic route is less effective, BUT STILL EFFECTIVE TO AN EXTENT. studies have shown that in healthy men, clomid alone will raise testosterone levels up to 57% (i don't have the abstract on me, someone else may). the endocrine system is extremely multifaceted, and is not an on or off thing. when both negative feedback systems are in full effect, as is the case on cycle most of the time, you shut yourself down from two separate pathways. if you knock out one of those pathways (i.e. with clomid oncycle), LH levels will increase.
there are several feedback mechanisms that control testosterone production in the human body. two of the most important are the estrogenic and testosterone routes.
the first being the estrogenic one. most people know about this. this is why people take clomid postcycle. clomid is a selective estrogen receptor modulator, and binds in the hypothalamus to prevent the brain from thinking there is any estrogen in the blood. the hypo. reacts by releasing GNRH, which tells the pituitary to release LH and FSH.
the testosterone negative feedback route occurs through inhibin. which is released from the testes and acts on the hypothalamus to regulate testosterone the same way the above feedback route did. considering both of these, you can see that doing clomid on-cycle isn't entirely pointless. when you take clomid in the presence of supraphysiological levels of testosterone (or it's derivatives, some haveing more pronouced effects on inhibin than others, and affecting other feedback routes, though that's a different thread), the hypothalamus thinks it's not getting estrogen, which would normally cause for an increase in LH production. but because inhibin levels are high (because the testes see that there is tons of test. floating around), the feedback via the estrogenic route is less effective, BUT STILL EFFECTIVE TO AN EXTENT. studies have shown that in healthy men, clomid alone will raise testosterone levels up to 57% (i don't have the abstract on me, someone else may). the endocrine system is extremely multifaceted, and is not an on or off thing. when both negative feedback systems are in full effect, as is the case on cycle most of the time, you shut yourself down from two separate pathways. if you knock out one of those pathways (i.e. with clomid oncycle), LH levels will increase.
