2010, Kolassa, Iris-Tatjana, Ertl, Verena, Eckart, Cindy, Kolassa, Stephan, Onyut, Lamaro Patience, Elbert, Thomas

As exposure to different types of traumatic stressors increases, the prevalence of PTSD increases. However, little is known about the effects of cumulative exposure to traumatic stress on the maintenance and remission from PTSD. In 2006/2007, we investigated 444 refugees from the 1994 Rwandan genocide, assessing exposure to traumatic events, current and lifetime PTSD, and PTSD symptom severity. Higher trauma exposure was associated with higher prevalence of current and lifetime PTSD, with lower probability of spontaneous remission from PTSD, and with higher current and lifetime PTSD symptom severity in clear dose-response effects. The results suggest traumatic load as a root cause of both PTSD chronicity and symptom severity and support the hypothesis of a neural fear network in the etiology of PTSD.

2009, Eckart, Cindy, Engler, Harald, Riether, Carsten, Kolassa, Stephan, Elbert, Thomas, Kolassa, Iris-Tatjana

Posttraumatic stress disorder (PTSD) has been associated with reduced cortisol levels. Opposing results have been interpreted as resulting from methodological differences between studies.We investigated the diurnal profile of salivary cortisol in a population of highly traumatized adult males from Rwanda with and without PTSD, who spent the whole day of examination together under amaximally standardized schedule. Besides the detection of PTSDrelated alterations in cortisol release we aimed at determining physiologically relevant effects of cumulative trauma exposure on HPA functioning in interaction with or independent of diagnosis. There were no differences in the diurnal pattern of cortisol release between subjects with and without PTSD. We observed an increasing prevalence of PTSD with increasing number of different traumatic event types experienced, replicating earlier results on a building-block effect of multiple traumatization. However, size of cumulative exposure was not related to any of the cortisol measures. The results suggest that besides methodological constraints also confounding factors not previously controlled for, e.g., sex differences or current life stress, might contribute to the diverging results of lowered, unchanged or enhanced cortisol secretion in PTSD. Future research should therefore closely monitor these possible confounds to optimize models for cortisol in research on stress-dependent illnesses.