Pre-Disaster Salivary Cortisol Prospectively Predicts Post-Disaster Posttraumatic Stress Disorder Symptoms in Children

• In Event: 2-073 - Early Adversity, Biology, and Behavior: Examining Biological Consequences and Contingencies of Early Life Stress

Integrative Statement

BACKGROUND. A growing body of research suggests links between altered levels of cortisol (a major stress hormone of the hypothalamic-pituitary-adrenal [HPA] axis) and posttraumatic stress disorder (PTSD; Zoladz & Diamond, 2013). However, most evidence linking cortisol dysfunctions to PTSD is based on studies examining the concurrent associations between cortisol and PTSD. Thus, it remains an unresolved question as to whether cortisol alterations develop in response to PTSD or represent a pre-existing vulnerability. Further, few studies have investigated the association between cortisol and PTSD in children. To our knowledge, the current study is the first to examine whether salivary cortisol and cortisol reactivity to stressful laboratory stimuli prospectively predict the development of PTSD symptomatology in young children who later experienced a natural disaster (i.e., Hurricane Katrina).

METHODS. Participants were 35 children (65.7% male) between the ages of three and six at Time 1. Participants included children who had experienced at least one trauma between 36 and 83 months of age (n = 17) and children without trauma who were recruited as healthy controls. Children were evaluated on baseline cortisol, cortisol reactivity, and PTSD symptoms both prior to (Time 1) and following (Time 2) a natural disaster. Structured diagnostic interviews were used to assess PTSD symptoms. At each lab visit, cortisol samples were collected prior to (baseline) and immediately following exposure to a series of trauma-related stimuli (i.e., emotional videos and recall of trauma memory). Cortisol reactivity was calculated by subtracting the baseline cortisol value from the post-stimuli cortisol value.

RESULTS. To determine the contributions of baseline cortisol level and cortisol reactivity in predicting subsequent PTSD symptoms, two hierarchical regression analyses were conducted. The first model tested whether Time 1 baseline cortisol predicted Time 2 PTSD symptoms. As shown in Table 1, after controlling for gender (β = −.29, p = 0.07), the significant effects of prior trauma exposure (β = .45, p < 0.01) and Time 1 PTSD symptoms (β = .73, p < 0.01), Time 1 baseline cortisol significantly predicted Time 2 PTSD symptoms (β = −.40, p < 0.01). Specifically, lower baseline cortisol predicted higher levels of PTSD symptomatology. Baseline cortisol accounted for 16% of the unexplained variance in Time 2 PTSD symptoms, and the total variance explained by Model 1 was 74.1%. Model 2 was identical to the first except that Time 1 cortisol reactivity was entered as the dependent variable. Results revealed that cortisol reactivity at Time 1 did not significantly predict Time 2 PTSD symptoms (β = .15, p = 0.27).

DISCUSSION. Overall, in this first study examining cortisol prior to trauma exposure in children, the findings provide evidence that baseline salivary cortisol level may be a risk marker for subsequent development of PTSD symptomatology following trauma exposure. This contrasts with the body of mostly cross-sectional studies that have characterized cortisol dysregulation as a consequence of trauma exposure in those who develop PTSD. Future studies may benefit from examining whether HPA-axis alterations would be a practical target for prevention efforts aimed at decreasing risk for the development of psychopathology.

Authors

• Rebecca Lynch, Tulane University
  Presenting Author

• Amy J. Mikolajewski, Tulane University
  Non-Presenting Author

• Michael S. Scheeringa, Tulane University
  Non-Presenting Author