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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
Kisspeptin-10 Potential Cardiovascular risk?
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<blockquote data-quote="Cataceous" data-source="post: 253701" data-attributes="member: 38109"><p>First, the assumption of clomiphene tolerance is asking a lot. Clomiphene combines an anti-estrogen with a <em>de facto</em> estrogen. Responses appear to vary widely and unpredictably. The consequences of long-term use are uncertain. Kisspeptin-10 is closer to being endogenous—as a shortened form of the native KP-54. But this alone isn't enough to recommend it over clomiphene if the latter is tolerated.</p><p></p><p>The contrast is greater for those on TRT. Most of them will not see HPTA activation with clomiphene. Some may feel better—or worse or just different—due to the changes in estrogen signaling. On the other hand, kisspeptin possibly confers direct benefits through receptor activation outside of the HPTA. Kisspeptin also spurs production of GnRH, another hormone with independent activity. However, the HPTA stimulation ends at the pituitary, because there the negative feedback from estradiol blocks production of LH and FSH. This is why the combination of a SERM and kisspeptin has potential appeal. The SERM reduces the negative feedback from estradiol at the pituitary, allowing stimulation of the rest of the HPTA. This is the route I've gone, though I hedge my bets by including exogenous GnRH (gonadorelin). Enclomiphene is my preferred SERM, but in some cases—low native aromatization?—clomiphene could be the better choice.</p></blockquote><p></p>
[QUOTE="Cataceous, post: 253701, member: 38109"] First, the assumption of clomiphene tolerance is asking a lot. Clomiphene combines an anti-estrogen with a [I]de facto[/I] estrogen. Responses appear to vary widely and unpredictably. The consequences of long-term use are uncertain. Kisspeptin-10 is closer to being endogenous—as a shortened form of the native KP-54. But this alone isn't enough to recommend it over clomiphene if the latter is tolerated. The contrast is greater for those on TRT. Most of them will not see HPTA activation with clomiphene. Some may feel better—or worse or just different—due to the changes in estrogen signaling. On the other hand, kisspeptin possibly confers direct benefits through receptor activation outside of the HPTA. Kisspeptin also spurs production of GnRH, another hormone with independent activity. However, the HPTA stimulation ends at the pituitary, because there the negative feedback from estradiol blocks production of LH and FSH. This is why the combination of a SERM and kisspeptin has potential appeal. The SERM reduces the negative feedback from estradiol at the pituitary, allowing stimulation of the rest of the HPTA. This is the route I've gone, though I hedge my bets by including exogenous GnRH (gonadorelin). Enclomiphene is my preferred SERM, but in some cases—low native aromatization?—clomiphene could be the better choice. [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
Kisspeptin-10 Potential Cardiovascular risk?
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