Can a hormone disclose the psychological impact of an accidental injury?

Dehydroepiandrosterone (DHEA) and its metabolite dehydroepiandrosterone sulfate (DHEAS), which are adrenal gland products like cortisol, show neuroprotective action in animal studies and generally act as noncompetitive antagonists at the GABA A receptor. A relationship between DHEA(S) concentration, depression, and anxiety disorders including posttraumatic stress disorder (PTSD) has been previously reported. The current findings on DHEA(S) concentration in PTSD are however contradictory.
While the majority of studies have identified a higher DHEA(S) concentration in PTSD subjects than in control subjects, as well as increases in the DHEA(S)-to-cortisol ratio, others have reported no group differences or even lower DHEA(S) concentrations in PTSD.

The aim of this study was to test chronic/long-term DHEA(S) changes in participants who had developed PTSD after severe accidental injury. In order to disentangle the influence of manifest PTSD symptoms on the plasma DHEA(S) concentrations, the investigators tested only participants with remitted PTSD. In addition, they included a comparison group of survivors of severe accidental injury who had not developed PTSD (trauma controls), and a group of age- and gender-matched nontraumatized healthy subjects (no-trauma controls). Twenty-nine subjects who experienced severe accidental injury 10 years ago were recruited from our past studies. Thirteen participants were diagnosed with PTSD or sub-threshold PTSD according to the DSM-IV in the year following the accident. Fourteen had not developed PTSD during the year after the accident and had no lifetime diagnosis of PTSD.

Blood samples were taken by venipuncture between 8 and 10 a.m. Cortisol and DHEAS were assessed with competitive electrochemiluminescence immunoassay. DHEA was measured with radioimmunoassay. A significant group effect was found for plasma DHEA concentration (p = 0.03). No significant group effects were obtained in DHEAS concentration (p = 0.4) and DHEA-cortisol ratio (p = 0.1). Post hoc tests only evidenced a significantly lower DHEA concentration in trauma controls compared to the no-trauma group (p = 0.03, Bonferroni corrected for multiple comparisons). Adding age as a covariate showed a significant main effect of age, but no significant age-bygroup interactions on DHEA, DHEAS, and the DHEA-cortisol ratio, respectively. After controlling for the effect of age, there was a medium effect size of the group factor on DHEA concentration (p=0.09). Gender as an additional between-subject factor in the model did not show any significant main effect.

The unexpected lack of significant differences between the remitted PTSD group and the no-trauma control group could be associated with the remission of the PTSD symptoms, suggesting that there is no difference in DHEA concentrations between PTSD subjects and control subjects after remission. It
has been suggested that the increase in DHEA in PTSD is salutary rather than pathophysiologic, and there is some indication that effective psychotherapy for PTSD elevates DHEA levels. Thus, the process of remission might have influenced DHEA concentrations in the remitted PTSD group. This cross-sectional study design could not explain any causality and intrapersonal chronological hormonal changes, e.g. the decline with aging on DHEA concentration. Blood sampling was done at a single time point; therefore, the investigators could not assess diurnal variation. The sample size is small and the results remain exploratory. Future prospective larger studies are needed to confirm the longitudinal endocrinological influences on accident survivors.