Transcortin: corticosteriod-binding gobulin (CBG)
CBG is similar to SHBG in function but it focuses on corticosteroids cortisol, progesterone, aldosterone, & DOC. It’s regulated by estrogen. I found a link between this and something called Pseudo Cushing’s Syndrome.
Excess estrogen can cause a rise in CBG leading to an overall high number and effect, however free cortisol used for metabolism is too low. This is the same issue we have from a high overall testosterone or T3 value but too low free-testosterone or free-T3, the bio-available vs in-use amounts are at incorrect ratios. I believe this can play a factor in a number of our sides from Fin.
Has anyone researched this and is there a way to suppress it like SHBG?