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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
Here's a scary thought: Long term LH suppression on TRT- What are the effects?
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<blockquote data-quote="AbsoluteZ3R0" data-source="post: 101196" data-attributes="member: 15174"><p>Bodybuilders use exceptionally large quantities of HCG because their goal is to hard-restart the gonadotropin system after prolonged periods of complete shutdown. They also use exceptionally large doses of SERMs following HCG use as well. HCG is an analog to LH, which means that it is exactly the same. As I explained earlier, conventional doses of HCG barely replicate the effects of below range LH, and there is absolutely no reason to think that HCG has a stronger binding affinity for LH receptors than regular LH. The evidence of that is guys on HCG monotherapy who fail to produce large quantities of total testosterone (even at the beginning of therapy) despite high doses of HCG. The amount of HCG necessary to replicate the effects of LH in the 4-6miu/mL range would be extraordinary, so the "hammering LH sites" hypothesis doesn't really hold any water. </p><p></p><p>Also, when bodybuilders refer to HCG as suppressive, they are referring to its down-regulating effect on LH production, not receptor density. That is why they will only use HCG for a relatively short amount of time (usually two weeks) to resensitize the Leydig cells, and then come off to allow the SERMs to kick-start LH production. Even an incredibly low dose of clomid, such as 12.5mg twice a week will hammer LH receptor sites a dozen times harder than a conventional HCG protocol. The difference is that clomid facilitates the production of LH, while HCG attenuates it. As far as receptor activation goes, the effects of HCG are relatively paltry.</p></blockquote><p></p>
[QUOTE="AbsoluteZ3R0, post: 101196, member: 15174"] Bodybuilders use exceptionally large quantities of HCG because their goal is to hard-restart the gonadotropin system after prolonged periods of complete shutdown. They also use exceptionally large doses of SERMs following HCG use as well. HCG is an analog to LH, which means that it is exactly the same. As I explained earlier, conventional doses of HCG barely replicate the effects of below range LH, and there is absolutely no reason to think that HCG has a stronger binding affinity for LH receptors than regular LH. The evidence of that is guys on HCG monotherapy who fail to produce large quantities of total testosterone (even at the beginning of therapy) despite high doses of HCG. The amount of HCG necessary to replicate the effects of LH in the 4-6miu/mL range would be extraordinary, so the "hammering LH sites" hypothesis doesn't really hold any water. Also, when bodybuilders refer to HCG as suppressive, they are referring to its down-regulating effect on LH production, not receptor density. That is why they will only use HCG for a relatively short amount of time (usually two weeks) to resensitize the Leydig cells, and then come off to allow the SERMs to kick-start LH production. Even an incredibly low dose of clomid, such as 12.5mg twice a week will hammer LH receptor sites a dozen times harder than a conventional HCG protocol. The difference is that clomid facilitates the production of LH, while HCG attenuates it. As far as receptor activation goes, the effects of HCG are relatively paltry. [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
Here's a scary thought: Long term LH suppression on TRT- What are the effects?
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