“…Increased hypothalamic CRF has also been inferred from a number of studies that have found elevated cortisol levels in PTSD (De Bellis et al, 1999;Lemieux and Coe, 1995;Liberzon et al, 1999;Maes et al, 1998;Pitman and Orr, 1990). Despite possible elevated hypothalamic CRF activity, PTSD subjects in a large number of studies have been found to have either normal (Baker et al, 1999) or decreased 24-h urinary cortisol (Mason et al, 1986;Yehuda et al, 1995;Yehuda et al, 1990), normal (Kellner et al, 2002) or decreased plasma cortisol (Jensen et al, 1997;Yehuda et al, 1996b), increased lymphocyte glucocorticoid receptors (Yehuda et al, 1991), normal (Kosten et al, 1990) or increased suppression of cortisol in response to dexamethasone (Goenjian et al, 1996;Grossman et al, 1996;Stein et al, 1997;Yehuda et al, 1993), and a buffered ultradian pattern of cortisol release (Yehuda et al, 1996b). Most of these findings are consistent with the hypothesis that PTSD is associated with enhanced negative feedback of the HPA axis, or reduced adrenal output, or a combination of these two mechanisms (for a review, see Yehuda, 2002).…”