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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
First post. Can’t get E2 under control, starting to worry
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<blockquote data-quote="Cataceous" data-source="post: 276876" data-attributes="member: 38109"><p>In this case the burden of proof is on those claiming that exogenous administration is so different that much larger amounts are required. What is the basis for this hypothesis? Clearly at the molecular level, with exogenous testosterone being bioidentical, there is no difference in how it's metabolized. As you suggest, the better argument relates to subtleties associated with the loss of pulsatile delivery regulated by the HPTA. However, this is looking for the cause of a condition that itself has not been shown to exist with any scientific rigor. Otherwise it's easy to dismiss with an argument such as "These individuals started at too high of a dose, suffered from an excess of estrogenic activity, but instead of reducing the dose they increased it, which happened to help with these symptoms by saturating aromatase. But the resulting protocol is unbalanced and non-physiological." I'm not saying this argument is necessary true, but without scientific support the claims about high doses being necessary don't carry much more weight than my willingness to bet on the negative consequences of pushing up thyroid hormones.</p></blockquote><p></p>
[QUOTE="Cataceous, post: 276876, member: 38109"] In this case the burden of proof is on those claiming that exogenous administration is so different that much larger amounts are required. What is the basis for this hypothesis? Clearly at the molecular level, with exogenous testosterone being bioidentical, there is no difference in how it's metabolized. As you suggest, the better argument relates to subtleties associated with the loss of pulsatile delivery regulated by the HPTA. However, this is looking for the cause of a condition that itself has not been shown to exist with any scientific rigor. Otherwise it's easy to dismiss with an argument such as "These individuals started at too high of a dose, suffered from an excess of estrogenic activity, but instead of reducing the dose they increased it, which happened to help with these symptoms by saturating aromatase. But the resulting protocol is unbalanced and non-physiological." I'm not saying this argument is necessary true, but without scientific support the claims about high doses being necessary don't carry much more weight than my willingness to bet on the negative consequences of pushing up thyroid hormones. [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
First post. Can’t get E2 under control, starting to worry
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