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The ability to identify persons at elevated risk for post-traumatic stress disorder (PTSD) soon after exposure to trauma, could aid clinical decision-making and treatment. In this study, we explored whether cytosine methylation of the 1 F promoter of the  NR3C1  (glucocorticoid receptor [GR]) gene obtained immediately following a trauma could predict PTSD. Our sample comprised 52 trauma survivors (28 women, 24 men), presenting to the Emergency Department (ED) within six hours of a traumatic event and followed for 13 months. Blood samples were taken at intake ( n  = 42) and again at the end of the study (13 months later,  n  = 27) to determine  NR3C1-1F  promoter methylation as well as plasma levels of cortisol, adrenocorticotropic-hormone (ACTH), and neuropeptide-Y (NPY). At the 13-month follow-up, participants who met the PTSD criteria ( n  = 4) showed significantly lower  NR3C1-1F  promoter sum percent methylation compared to the non-PTSD group ( n  = 38). Further,  NR3C1-1F  methylation at ED intake was inversely correlated with PTSD severity 13 months later, indicating that lower  NR3C1-1F  promoter methylation in the immediate aftermath of trauma was associated with the development of PTSD. To the extent that reduced promoter methylation is associated with greater GR expression and responsivity, this finding is consistent with the hypothalamic-pituitary-adrenal dysregulation previously described for PTSD.

Promoter methylation of the glucocorticoid receptor following trauma may be associated with subsequent development of PTSD