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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
Can estrogen crash cause desensitization/knock out of the estrogen receptor - lets discuss!
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<blockquote data-quote="Wuinz" data-source="post: 245607" data-attributes="member: 45016"><p>Hey all, I’m coming from a Reddit thread/discord. A guy (Sweaty_Literature_69) posted a theory about how AI induced low E2 symptoms, PFS and PSSD are pretty much the same. It all comes down to estrogen receptors being desensitized. And it’s not oversensitized receptors leading to high E2 symptoms. A clear indicator of this is aching/painful joints. High E2 does not typically show this symptom. Emotional numbness is another one. Blood work is all normal, but your estrogen receptors are so downregulated that you feel low E2. </p><p></p><p>How did this happen? In the AI cases people deprived their receptors of E2 leading to estrogen receptor upregulation. And then when you come off the AI it leads to a sudden burst of estrogen, downregulating your receptors. Your estrogen stays up/normal but your receptors’ sensitivity don’t change because of a lack of rapid hormonal change. And then it gets stuck. Maybe it’s a genetic thing or maybe it’s due to how quickly the estrogen came back. Regardless, the victims here suffer from estrogen receptor persistent down regulation.</p><p></p><p>How do we fix this? We have had proof from this very thread. You need to take estrogen directly. You need to abruptly raise your estrogen (also taking T and HCG to protect androgen function) for a few months. This will kickstart your receptors, allowing them to self regulate and regulate other receptors. [USER=16355]@nurselyfe[/USER] please try this.</p></blockquote><p></p>
[QUOTE="Wuinz, post: 245607, member: 45016"] Hey all, I’m coming from a Reddit thread/discord. A guy (Sweaty_Literature_69) posted a theory about how AI induced low E2 symptoms, PFS and PSSD are pretty much the same. It all comes down to estrogen receptors being desensitized. And it’s not oversensitized receptors leading to high E2 symptoms. A clear indicator of this is aching/painful joints. High E2 does not typically show this symptom. Emotional numbness is another one. Blood work is all normal, but your estrogen receptors are so downregulated that you feel low E2. How did this happen? In the AI cases people deprived their receptors of E2 leading to estrogen receptor upregulation. And then when you come off the AI it leads to a sudden burst of estrogen, downregulating your receptors. Your estrogen stays up/normal but your receptors’ sensitivity don’t change because of a lack of rapid hormonal change. And then it gets stuck. Maybe it’s a genetic thing or maybe it’s due to how quickly the estrogen came back. Regardless, the victims here suffer from estrogen receptor persistent down regulation. How do we fix this? We have had proof from this very thread. You need to take estrogen directly. You need to abruptly raise your estrogen (also taking T and HCG to protect androgen function) for a few months. This will kickstart your receptors, allowing them to self regulate and regulate other receptors. [USER=16355]@nurselyfe[/USER] please try this. [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
Can estrogen crash cause desensitization/knock out of the estrogen receptor - lets discuss!
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