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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
How fast can hematocrit rise?
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<blockquote data-quote="johndoesmith" data-source="post: 46124" data-attributes="member: 13404"><p>I read the study, and it doesn't give you the levels of testosterone or estradiol during treatment. It does give a rather confusing graph correlating changes in T and E2 to changes in HCT, HGB, and ferritin.</p><p></p><p>Although directly regarding E2 and HCT I copied this from the study:</p><p></p><p>"Interestingly, we also observed that TE administration elevated circulating E2 and BioE2 and that the magnitude of change in E2 was correlated to the increases in RBC count and HGB. These findings raise the possibility that estrogens may mediate several of the effects we observed. In this regard, estrogen has been shown to suppress hepcidin, and an estrogen response element is present in the promoter region of the hepcidin gene (<a href="http://ajpendo.physiology.org/content/307/5/E456#ref-20" target="_blank">20</a>, <a href="http://ajpendo.physiology.org/content/307/5/E456#ref-21" target="_blank">21</a>). However, we find it highly unlikely that E2 mediated the erythropoietic effects of T given that T administration results in elevated RBC count and HGB in aromatase-deficient men (<a href="http://ajpendo.physiology.org/content/307/5/E456#ref-30" target="_blank">30</a>) and that RBC count and HGB are elevated following T plus letrozole (a potent aromatase inhibitor) treatment in boys with constitutional delay of puberty (<a href="http://ajpendo.physiology.org/content/307/5/E456#ref-19" target="_blank">19</a>). Similarly, preclinical evidence from our laboratory indicates that trenbolone (a nonaromatizable and non-5&#945;-reducible T analog) and TE elevate HGB in an identical manner in orchiectomized rats (<a href="http://ajpendo.physiology.org/content/307/5/E456#ref-26" target="_blank">26</a>, <a href="http://ajpendo.physiology.org/content/307/5/E456#ref-36" target="_blank">36</a>). Together, these results demonstrate that aromatase activity is not necessary for androgen-stimulated erythropoiesis, although the possibility remains that the suppression of hepcidin was at least partially influenced by the elevated E2 following TE administration."</p><p></p><p>So it seems that E2 doesn't, according to this study, although I am not certain I am understanding this study completely.</p></blockquote><p></p>
[QUOTE="johndoesmith, post: 46124, member: 13404"] I read the study, and it doesn't give you the levels of testosterone or estradiol during treatment. It does give a rather confusing graph correlating changes in T and E2 to changes in HCT, HGB, and ferritin. Although directly regarding E2 and HCT I copied this from the study: "Interestingly, we also observed that TE administration elevated circulating E2 and BioE2 and that the magnitude of change in E2 was correlated to the increases in RBC count and HGB. These findings raise the possibility that estrogens may mediate several of the effects we observed. In this regard, estrogen has been shown to suppress hepcidin, and an estrogen response element is present in the promoter region of the hepcidin gene ([URL="http://ajpendo.physiology.org/content/307/5/E456#ref-20"]20[/URL], [URL="http://ajpendo.physiology.org/content/307/5/E456#ref-21"]21[/URL]). However, we find it highly unlikely that E2 mediated the erythropoietic effects of T given that T administration results in elevated RBC count and HGB in aromatase-deficient men ([URL="http://ajpendo.physiology.org/content/307/5/E456#ref-30"]30[/URL]) and that RBC count and HGB are elevated following T plus letrozole (a potent aromatase inhibitor) treatment in boys with constitutional delay of puberty ([URL="http://ajpendo.physiology.org/content/307/5/E456#ref-19"]19[/URL]). Similarly, preclinical evidence from our laboratory indicates that trenbolone (a nonaromatizable and non-5α-reducible T analog) and TE elevate HGB in an identical manner in orchiectomized rats ([URL="http://ajpendo.physiology.org/content/307/5/E456#ref-26"]26[/URL], [URL="http://ajpendo.physiology.org/content/307/5/E456#ref-36"]36[/URL]). Together, these results demonstrate that aromatase activity is not necessary for androgen-stimulated erythropoiesis, although the possibility remains that the suppression of hepcidin was at least partially influenced by the elevated E2 following TE administration." So it seems that E2 doesn't, according to this study, although I am not certain I am understanding this study completely. [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
How fast can hematocrit rise?
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