alex3619
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One of the problems in discussing the impact of things like corticosteroids is we are relying on highly reductionistic research. They are taking a snapshot in time and only looking at a few things. Cortisol primarily (but I think it has other functions, probably) acts by suppressing the release of arachidonic acid, if I recall correctly. Its a one pathway wonder. Arachidonic acid is processed by cyclo-oxygenase to make inflammatory hormones. The balance of those hormones determine the symptoms - and that balance depends on things like oxidative stress, cytokines and so on. The entire balance determines the outcome, not just one chemical, and this balance is constantly changing. I have heard it discussed as trying to shoot a flying bumblebee at a hundred yards, or trying to play a symphony with the metabolism and immune system without a conductor or musical score. Its complicated. Its not completely reliable.
In any case the only way to find out for most patients is to very very cautiously test something to see if it works, then to monitor to see its still working and not causing problems over time. This isn't easy either as most patients are doing many things at once - so which one is responsible for what?
There is another reason to use DHEA though - it can simulate mitochondrial replication. Since we have mitochondrial issues that could be a good thing.
Bye, Alex
In any case the only way to find out for most patients is to very very cautiously test something to see if it works, then to monitor to see its still working and not causing problems over time. This isn't easy either as most patients are doing many things at once - so which one is responsible for what?
There is another reason to use DHEA though - it can simulate mitochondrial replication. Since we have mitochondrial issues that could be a good thing.
Bye, Alex