NiceCupOfTea said...
Anyway, I don't think hormones had anything to do with my Crohn's/colitis, because I have never been pregnant
I became convinced today it does have to do with hormones.
Exit prednisone taper and have a LOT of stubborn blubber. I begin doing everything I can to increase testosterone which in men is the opposite of cortisol. I made a fateful mistake and also got off the RS diet for 10 days and started to slip into a flare ( diet was controlling the problem ).
Now it seems like the leaner I get the more testosterone I have and therefore the more estradiol. My adrenals are not back to full strength and topped out. So THIS is why my diet has to become cleaner and cleaner - I just do not have enough coritisol flying into this headwind.
Turns out that testosterone lowers cortisol and it might be doing so indirectly. Testosterone in men converts to estradiol and dht ( balding hormone ). Estradiol it turns out down regulates cortisol by increasing the enzyme which breaks down cortisol.
So what I felt was happening was confirmed when I went looking for it.
Corticosteroid-binding globulin (CBG), reduces FREE-cortisol, 75% of coritisol is bound to CGB and unusable. CGB is produced by the liver and is regulated by estrogens.
Testosterone in men increases estradiol which increases CBG which decreases available cortisol.
T => E2 => CBF => decrease in free cortisol
If you happen to have been pregnant it connects there as well.
"The portal system carries the CRH to the anterior lobe of the pituitary, where it stimulates corticotropes to secrete adrenocorticotropic hormone (ACTH) and other biologically-active substances (β-endorphin). ACTH stimulates the synthesis of cortisol, glucocorticoids, mineralocorticoids and DHEA."
CRH -> creates ACTH -> Which creates cortisol etc
CRH is also synthesized by the placenta and seems to determine the duration of pregnancy.[8]
Levels rise towards the end of pregnancy just before birth and current theory suggests three roles of CRH in parturition:[9]
Increases levels of dehydroepiandrosterone (DHEA) directly by action on the fetal adrenal gland, and indirectly via the mother's pituitary gland. DHEA has a role in preparing for and stimulating cervical contractions.
Increases prostaglandin availability in uteroplacental tissues. Prostaglandins activate cervical contractions.
Prior to parturition it may have a role inhibiting contractions, through increasing cAMP levels in the myometrium.
In culture, trophoblast CRH is inhibited by progesterone, which remains high throughout pregnancy. Its release is stimultated by glucocorticoids and catecholamines, which increase prior to parturition lifting this progesterone block.