CRH and Sepsis: We hypothesized that sepsis-induced critical illness, further referred to as ‘sepsis,’ indeed immediately and continuously activates the hypothalamus to generate, via CRH and AVP, ACTH-induced hypercortisolism, but as soon as free cortisol is elevated, feedback inhibition at the pituitary level interferes with normal processing of POMC into ACTH, explaining the typical ACTH–cortisol dissociation.