I am suffering from non-Cushing hypercorticism. I am considering a Mifepristone treatment. Seems it could be the game changer for me.
I have read some papers, including the links here on this thread. The result from those tests and studies sound very positive and encouraging.
The basic idea is that most receptors in the body tend to react to the presence of a binding antagonist, by "upregulating" or in other words they become more sensitive to their appropriate ligands. So by blocking GR, they should restore their original sensitivity after a certain time. At least that is in theory.
There is one issue however. I have read a post from an endocrinologist on a forum. He says that blocking GR with Mifepristone always lead to some ACTH rebound effect, i.e. the HPA-axis reacts by increasing ACTH secretion. This causes further increase of Cortisol secretion, which is exactly what we are fighting against. So in theory this whole approach is a bad one. But what would explain the generally positive outcomes as in those articles ?
I believe there is one key thing in this matter. As Cortisol increases because of antagonizing GR and the according ACTH rebound, we have increased plasma Cortisol levels. The key here is - PLASMA LEVELS !!! At the same time Mifepristone blocks Cortisol from binding to the GR, thus exhibiting a certain neuroprotective effect on those precious hippocampal neurons. And in the mean time, GR are undergoing expression changes to upregulate in order to cope with the increased amount of Cortisol. It sounds plausible. If true, the only thing to worry about would be possible hypokalemia, which usually comes as a result of elevated Cortisol.
computeTHIS wrote that Mifepristone it helped him with what it appeared to be hypocorticism. But will it really help with hypercorticism ?
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