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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
Arimidex - Pain Caused by Crashing E2 or Another Reason?
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<blockquote data-quote="PhantomFear" data-source="post: 179831" data-attributes="member: 38928"><p>Most people don't understand that AI's aren't selective to solely aromatase.</p><p></p><p>The enzymes in the steroid hormone cascade all belong to the same family. As a result, any substance that inhibits one will have an effect on another, albeit to a lesser degree. You can see this in the hormones themselves. Estradiol can bind to the estrogen, androgen, progestin and glucocorticoid receptor. Testosterone can do the same, as can progesterone, as can DHEA, as can most steroid metabolites. This doesn't mean they all bind with the same affinity or elicit the same response, however. This same idea applies to aromatase inhibitors and their interaction with armomatase and the other steroid producing enzymes.</p><p></p><p>When you take an ai, you're also reducing the production of pregnenolone, progesterone, dhea and all of their associated metabolites. Most people on T are already low in these hormones due to hpta suppression, and I believe this is why very small doses can cause a large, undesired response despite little changes to serum estradiol (not that serum estradiol is a good indicator of estrogenic activity in the tissue anyway)</p><p></p><p>I personally don't subscribe to the idea that a poor response to a low dose (emphais on low; 1mg of adex a day is a different matter entirely) of ai is because of reduced estradiol when estradiol isn't significantly lowered. I find it more likely that it's due to the reduction in already low progesterone, evidenced by the complaint that even small doses can cause joint issues. Progesterone is just as important for joints as estrogen, which is why there is the current craze of everyone wanting to add nandrolone, a progestin, to their trt for the joint health benefits.</p></blockquote><p></p>
[QUOTE="PhantomFear, post: 179831, member: 38928"] Most people don't understand that AI's aren't selective to solely aromatase. The enzymes in the steroid hormone cascade all belong to the same family. As a result, any substance that inhibits one will have an effect on another, albeit to a lesser degree. You can see this in the hormones themselves. Estradiol can bind to the estrogen, androgen, progestin and glucocorticoid receptor. Testosterone can do the same, as can progesterone, as can DHEA, as can most steroid metabolites. This doesn't mean they all bind with the same affinity or elicit the same response, however. This same idea applies to aromatase inhibitors and their interaction with armomatase and the other steroid producing enzymes. When you take an ai, you're also reducing the production of pregnenolone, progesterone, dhea and all of their associated metabolites. Most people on T are already low in these hormones due to hpta suppression, and I believe this is why very small doses can cause a large, undesired response despite little changes to serum estradiol (not that serum estradiol is a good indicator of estrogenic activity in the tissue anyway) I personally don't subscribe to the idea that a poor response to a low dose (emphais on low; 1mg of adex a day is a different matter entirely) of ai is because of reduced estradiol when estradiol isn't significantly lowered. I find it more likely that it's due to the reduction in already low progesterone, evidenced by the complaint that even small doses can cause joint issues. Progesterone is just as important for joints as estrogen, which is why there is the current craze of everyone wanting to add nandrolone, a progestin, to their trt for the joint health benefits. [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
Arimidex - Pain Caused by Crashing E2 or Another Reason?
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