NR3C1 and post-traumatic stress disorder: Speculatively, increased output after trauma may evolve as a compensatory anti-glucocorticoid mechanism, to inhibit negative effects of a long-term increase in negative glucocorticoid feedback and sensitivity of glucocorticoid receptors that has been observed in trauma-exposed participants irrespective of PTSD status (Nawata et al., 1985; Zenko et al., 2018).