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Testosterone Replacement, Low T, HCG, & Beyond
Clomid for PCT, fertility or low T
Why Clomid Fails: The Zuclomiphene Threshold
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<blockquote data-quote="socks" data-source="post: 37935" data-attributes="member: 13240"><p><u><strong>Part One: Clomid Introduction</strong></u></p><p>- Selective estrogen receptor modulator, which occupies e2 receptors acting as a weak estrogen</p><p> </p><p>- Two parts/isomers, 30-50% zuclomiphene(estrogenic) and 50-70% enclomiphene (non-estrogenic) <a href="https://pubchem.ncbi.nlm.nih.gov/compound/clomiphene#section=Formulations-Preparations" target="_blank">(1)</a></p><p> </p><p>- Inhibits negative feedback of e2 primarily at the hypothalamus/pituitary, thus stimulating the following: GnRH-->LH/FSH-->Leydig Cells-->Testosterone</p><p> </p><p>- Antagonist at Hypothalamus and pituitary</p><p> </p><p>- Agonist (increased estradiol) in the liver, hippocampus, brain stem, neocortex, fat, blood plasma <a href="https://books.google.com/books?id=ZaNhPcwrJkAC&lpg=PA29&dq=thalamus%20clomiphene&pg=PA29#v=onepage&q=clomiphene&f=false" target="_blank">(2)</a></p><p></p><p><u><strong>Part 2: The Zuclomiphene Threshold</strong></u></p><p>It seems that most Clomid patients experience some positive results before Zuclomiphene, the estrogenic isomer, accumulates and begins agonizing (pun intended) brain centers associated with mood/libido <a href="https://books.google.com/books?id=ZaNhPcwrJkAC&lpg=PA29&dq=thalamus%20clomiphene&pg=PA29#v=onepage&q=clomiphene&f=false" target="_blank">(2)</a>. Thus, it follows that these patients, the majority, are hitting a threshold accumulation of Zuclomiphene and it's primarily this, not e2 levels, which leads to therapy failure. e2 is a <em>red herring</em>, Zuclomiphene appears the culprit. </p><p></p><p>Doc Saya on Zuclomiphene:</p><p></p><p></p><p><u>Why is dosage a MORE powerful tool than any estrogen management ancillary in Clomid treatment?</u> The LONG half-life of the zuclomiphene isomer, it's corresponding threshold (different for each individual), and the novel effects it has upon brain regions. This, you will find is the mechanism to Clomid therapy failure in the treatment of Low T symptoms.</p><p></p><p></p><p>For the "great 1st week, bad 2nd week" responders @25mg ED, the threshold appears around 50-75mg (<a href="https://books.google.com/books?id=UxecCgAAQBAJ&lpg=PA49&dq=zuclomiphene%20half%20life&pg=PA49#v=onepage&q=zuclomiphene%20half%20life&f=false" target="_blank">assuming 11day HL</a> pg.49). Although as seen in the introduction, the wildly non-standard quantities of each isomer makes calculations difficult.</p><p></p><p>Let's hear some patient experiences who had a great first week on Clomid before the Zuclomiphene threshold began negating the benefits of the Enclomiphene isomer.</p><p></p><p><u><strong>Part Three: to follow</strong></u></p></blockquote><p></p>
[QUOTE="socks, post: 37935, member: 13240"] [U][B]Part One: Clomid Introduction[/B][/U] - Selective estrogen receptor modulator, which occupies e2 receptors acting as a weak estrogen - Two parts/isomers, 30-50% zuclomiphene(estrogenic) and 50-70% enclomiphene (non-estrogenic) [URL="https://pubchem.ncbi.nlm.nih.gov/compound/clomiphene#section=Formulations-Preparations"](1)[/URL] - Inhibits negative feedback of e2 primarily at the hypothalamus/pituitary, thus stimulating the following: GnRH-->LH/FSH-->Leydig Cells-->Testosterone - Antagonist at Hypothalamus and pituitary - Agonist (increased estradiol) in the liver, hippocampus, brain stem, neocortex, fat, blood plasma [URL="https://books.google.com/books?id=ZaNhPcwrJkAC&lpg=PA29&dq=thalamus%20clomiphene&pg=PA29#v=onepage&q=clomiphene&f=false"](2)[/URL] [U][B]Part 2: The Zuclomiphene Threshold[/B][/U] It seems that most Clomid patients experience some positive results before Zuclomiphene, the estrogenic isomer, accumulates and begins agonizing (pun intended) brain centers associated with mood/libido [URL="https://books.google.com/books?id=ZaNhPcwrJkAC&lpg=PA29&dq=thalamus%20clomiphene&pg=PA29#v=onepage&q=clomiphene&f=false"](2)[/URL]. Thus, it follows that these patients, the majority, are hitting a threshold accumulation of Zuclomiphene and it's primarily this, not e2 levels, which leads to therapy failure. e2 is a [I]red herring[/I], Zuclomiphene appears the culprit. Doc Saya on Zuclomiphene: [U]Why is dosage a MORE powerful tool than any estrogen management ancillary in Clomid treatment?[/U] The LONG half-life of the zuclomiphene isomer, it's corresponding threshold (different for each individual), and the novel effects it has upon brain regions. This, you will find is the mechanism to Clomid therapy failure in the treatment of Low T symptoms. For the "great 1st week, bad 2nd week" responders @25mg ED, the threshold appears around 50-75mg ([URL="https://books.google.com/books?id=UxecCgAAQBAJ&lpg=PA49&dq=zuclomiphene%20half%20life&pg=PA49#v=onepage&q=zuclomiphene%20half%20life&f=false"]assuming 11day HL[/URL] pg.49). Although as seen in the introduction, the wildly non-standard quantities of each isomer makes calculations difficult. Let's hear some patient experiences who had a great first week on Clomid before the Zuclomiphene threshold began negating the benefits of the Enclomiphene isomer. [U][B]Part Three: to follow[/B][/U] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Clomid for PCT, fertility or low T
Why Clomid Fails: The Zuclomiphene Threshold
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