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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
What’s the general consensus on AI’s here?
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<blockquote data-quote="xqfq" data-source="post: 161018" data-attributes="member: 38167"><p>I don't think it's just lipids. I worry about the <em><u>direct</u></em><u> effect that an aromatase inhibitor could have on endothelial function</u>. In some studies on women with aromatase inhibitors, lipids are not necessarily impacted, but in all studies endothelial function is affected. If you google "endothelial anastrozole" you will find many studies.</p><p></p><p>We know that testosterone can be beneficial for endothelial function through aromatase directly in the endothelial cells:</p><p></p><p><a href="https://www.pnas.org/content/pnas/99/6/4055.full.pdf" target="_blank">https://www.pnas.org/content/pnas/99/6/4055.full.pdf</a></p><p></p><p>Here's the study I find most interesting:</p><p></p><p><a href="https://www.ahajournals.org/doi/full/10.1161/01.RES.0000103633.57225.BC" target="_blank">https://www.ahajournals.org/doi/full/10.1161/01.RES.0000103633.57225.BC</a></p><p></p><p>This is in men, who were given a heavy dose (1mg/day) of anastrazole. But keep in mind <em>they were not on TRT</em> - they had a functioning HPTA axis, and thus 1mg/day of anastrazole did *not* crash their E2. Their E2 went from ~23 pg/mL to ~17.5 pg/mL. But if you look at the graph for "Effect of Anastrozole on Flow-Mediated Dilation of the Brachial Artery," you'll see they had a 50% reduction in flow-mediated dilation.</p><p></p><p>How could this be? In my bro-scientist mind, it might have to do with how the drug distributes itself throughout the body. Because it is carried in the blood stream, it would make sense that it could effect the cells in the endothelium more strongly. But that's just my own guess - I really don't know.</p><p></p><p>Does this matter for more sane AI doses? I have no idea! But I do think it gives at least one maybe-datapoint that an AI can have direct effects beyond those equivalent to lowering of E2.</p></blockquote><p></p>
[QUOTE="xqfq, post: 161018, member: 38167"] I don't think it's just lipids. I worry about the [I][U]direct[/U][/I][U] effect that an aromatase inhibitor could have on endothelial function[/U]. In some studies on women with aromatase inhibitors, lipids are not necessarily impacted, but in all studies endothelial function is affected. If you google "endothelial anastrozole" you will find many studies. We know that testosterone can be beneficial for endothelial function through aromatase directly in the endothelial cells: [URL]https://www.pnas.org/content/pnas/99/6/4055.full.pdf[/URL] Here's the study I find most interesting: [URL]https://www.ahajournals.org/doi/full/10.1161/01.RES.0000103633.57225.BC[/URL] This is in men, who were given a heavy dose (1mg/day) of anastrazole. But keep in mind [I]they were not on TRT[/I] - they had a functioning HPTA axis, and thus 1mg/day of anastrazole did *not* crash their E2. Their E2 went from ~23 pg/mL to ~17.5 pg/mL. But if you look at the graph for "Effect of Anastrozole on Flow-Mediated Dilation of the Brachial Artery," you'll see they had a 50% reduction in flow-mediated dilation. How could this be? In my bro-scientist mind, it might have to do with how the drug distributes itself throughout the body. Because it is carried in the blood stream, it would make sense that it could effect the cells in the endothelium more strongly. But that's just my own guess - I really don't know. Does this matter for more sane AI doses? I have no idea! But I do think it gives at least one maybe-datapoint that an AI can have direct effects beyond those equivalent to lowering of E2. [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
What’s the general consensus on AI’s here?
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