Resting mononuclear cell NR3C1 and SKA2 expression levels predict blunted cortisol reactivity to combat training stress among elite army cadets exposed to childhood adversity.

Childhood adversity (CA) may alter reactivity to stress throughout life, increasing risk for psychiatric and medical morbidity, yet long-term correlates of milder CA levels among high functioning healthy adolescents are less studied. The current study examined the prevalence and impact of CA exposure among a cohort of healthy motivated elite parachute unit volunteers, prospectively assessed at rest and at the height of an intensive combat-simulation exposure. We found significantly reduced gene expression levels in resting mononuclear cell nuclear receptor, subfamily 3, member 1 (NR3C1), and its transactivator spindle and kinetochore-associated protein 2 (SKA2), that predict blunted cortisol reactivity to combat-simulation stress among CA exposed adolescents. Long-term alterations in endocrine immune indices, subjective distress, and executive functions persist among healthy high functioning adolescents following milder CA exposure, and may promote resilience or vulnerability to later real-life combat exposure.

The imprint of childhood adversity on emotional processing in high functioning young adults.

Adverse childhood experiences (ACEs) have been acknowledged as risk factors for increased mental health complications in adulthood, specifically increasing susceptibility to developing psychopathology upon exposure to trauma. Yet, little is known regarding the impact of mild ACEs on highly functioning population. In this study forty participants were selected from a group of 366 highly selected military parachute trainees using the self-report "childhood trauma questionnaire," and classified into two groups of 20 each, with and without ACEs. Behavioral measurements were obtained before and at the peak of an intensive combat training period, including anxiety, depression and executive function assessment. Functional MRI including a negative emotional face perception task was conducted at the first time point. Psychometric and cognitive measurements revealed higher levels of anxiety and depressive symptoms, and more difficulties in executive functioning in the ACE group at baseline. Slower reaction time to emotional faces presentation was found in the ACE group. Lower activation in response to negative emotional faces stimuli was found in this group in bilateral secondary visual areas, left anterior insula, left parietal cortex and left primary motor and sensory regions. In contrast, higher activation in the ACE group was found in the right ventral lateral prefrontal cortex (Vlpfc). No significant differences between groups were detected in the amygdala. To conclude, mild adverse childhood experiences produce long-term sequela on psychological wellbeing and neurocircuitry even in high functioning population. Brain regions modulated by childhood trauma may instigate avoidance mechanisms dampening the emotional and cognitive effects of intensive stress.