Dissociative stress response corresponds with downregulation of the HPA-axis
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The term „dissociation“ (from Latin: dissociare, disuniting, separating) is used in natural sciences to describe processes of falling apart, disintegration, and separation. In the psychology it is defined as lost of information or control over mental processes that, under normal circumstances, are available to conscious awareness, self-attribution, and sensory experience (Cardeña & Carlson, 2011). The relationships between dissociation, stress, trauma exposure and the development of psychopathology, such as Posttraumatic Stress Disorder (PTSD), have been frequently documented (Frewen, Brown, Steuwe, & Lanius, 2015; Soffer-Dudek, 2017; van Dijke, Ford, Frank, & van der Hart, 2015; Vonderlin et al., 2018). However, biological stress processes accompanying dissociative symptoms are still broadly unknown (Brand, Lanius, Vermetten, Loewenstein, & Spiegel, 2012). For this reason, in my dissertation, I focused on mechanisms of psychobiological stress processing in traumatized and non-traumatized healthy controls as well as in PTSD patients. Especially, I was interested in dissociation understood as a stress coping strategy through cognitive distance and emotional downregulation (Ehlers & Clark, 2000; Lanius et al., 2010). The data was gathered in two studies. In the first study, I conducted standardized stress experiments (Trier Social Stress Test, TSST, Kirschbaum, Pirke, & Hellhammer, 1993) in female PTSD patients, traumatized and non-traumatized female healthy controls at the Max Planck Institute of Psychiatry in Munich. At four assessment times, concentrations of blood stress hormones (among others cortisol) as well as parameters of psychological stress reactivity were examined. The second study took part in the Nakivale refugee camp in Uganda, where I conducted interviews on trauma exposure and its clinical consequences, with focus on dissociative symptomatology. Hormonal stress response was examined in saliva samples collected at three different assessment times. Further stress markers were determined in hair samples. In both studies, I aimed at finding relationships between the studied psychological and biological variables. The results from both studies were presented in three papers. In Paper 1, which replicated and extended the findings from my previous work (Zaba et al., 2015), in PTSD patients, two subgroups of hormonal stress response were identified. One PTSD group showed a significant increase of stress hormone, cortisol, that did not differ from that of a control group consisted of non-traumatized, healthy controls. In the second PTSD group, cortisol levels decrease, despite the presence of significant psychological stress response, was observed. The missing biological stress response was accompanied by trauma-related dissociation, psychiatric comorbidity as well as by early life trauma and was best predicted by severity of trauma-related dissociation. Interestingly, traumatized healthy controls showed elevated cortisol levels together with high levels of non-pathological dissociation (absorption) that were comparable with those of PTSD patients. In Paper 2, I focused on the identification and clinical characterization of the Dissociative Subtype of PTSD (DS-PTSD, American Psychiatric Association, 2013) in a highly trauma exposed, non-Western population. The DS-PTSD was identified with an established, statistical stratification method (Latent Profile Analysis) in 14% of all studied individuals and in 26% of all PTSD cases. Sexual trauma, high levels of depressive symptoms, low general functionality as well as elevated suicidality were found as correlates of the DS-PTSD. Interestingly, similar correlates were found in already studied Western populations (e.g., Hansen, Ross, & Armour, 2017). The results of Paper 3 showed that assessments of trauma exposure and its clinical consequences did not evoke a significant biological stress response, within the studied sample. However, a subset of individuals (29% of the whole sample) with high levels of PTSD, especially re-experiencing, and depressive symptoms as well as low levels of emotional and instrumental support as coping strategies, exhibited a significant biological stress response. Similarly to the results from the first study, low reactive cortisol levels were best predicted by sexual trauma, low emotional coping and high dissociative tendencies. Both studies demonstrated that stress- and trauma-related dissociative symptoms correspond with downregulation of the hormonal stress system. This shows that focusing on the emotional stress response can broaden our understanding of the complex relationship between trauma exposure, psychopathology and stress hormone activity. Dissociative symptoms, transdiagnostically and transculturally, have frequently been associated with large illness burden and reduced treatment outcome (Lyssenko et al., 2018; McKinnon et al., 2016, Paper 2). For this reason, prospective studies on the possible causal link between dissociation and downregulation of biological stress system are urgently needed.
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SCHRECKENBACH, Monika, 2019. Dissociative stress response corresponds with downregulation of the HPA-axis [Dissertation]. Konstanz: University of KonstanzBibTex
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<dcterms:abstract xml:lang="eng">The term „dissociation“ (from Latin: dissociare, disuniting, separating) is used in natural sciences to describe processes of falling apart, disintegration, and separation. In the psychology it is defined as lost of information or control over mental processes that, under normal circumstances, are available to conscious awareness, self-attribution, and sensory experience (Cardeña & Carlson, 2011). The relationships between dissociation, stress, trauma exposure and the development of psychopathology, such as Posttraumatic Stress Disorder (PTSD), have been frequently documented (Frewen, Brown, Steuwe, & Lanius, 2015; Soffer-Dudek, 2017; van Dijke, Ford, Frank, & van der Hart, 2015; Vonderlin et al., 2018). However, biological stress processes accompanying dissociative symptoms are still broadly unknown (Brand, Lanius, Vermetten, Loewenstein, & Spiegel, 2012). For this reason, in my dissertation, I focused on mechanisms of psychobiological stress processing in traumatized and non-traumatized healthy controls as well as in PTSD patients. Especially, I was interested in dissociation understood as a stress coping strategy through cognitive distance and emotional downregulation (Ehlers & Clark, 2000; Lanius et al., 2010). The data was gathered in two studies. In the first study, I conducted standardized stress experiments (Trier Social Stress Test, TSST, Kirschbaum, Pirke, & Hellhammer, 1993) in female PTSD patients, traumatized and non-traumatized female healthy controls at the Max Planck Institute of Psychiatry in Munich. At four assessment times, concentrations of blood stress hormones (among others cortisol) as well as parameters of psychological stress reactivity were examined. The second study took part in the Nakivale refugee camp in Uganda, where I conducted interviews on trauma exposure and its clinical consequences, with focus on dissociative symptomatology. Hormonal stress response was examined in saliva samples collected at three different assessment times. Further stress markers were determined in hair samples. In both studies, I aimed at finding relationships between the studied psychological and biological variables. The results from both studies were presented in three papers. In Paper 1, which replicated and extended the findings from my previous work (Zaba et al., 2015), in PTSD patients, two subgroups of hormonal stress response were identified. One PTSD group showed a significant increase of stress hormone, cortisol, that did not differ from that of a control group consisted of non-traumatized, healthy controls. In the second PTSD group, cortisol levels decrease, despite the presence of significant psychological stress response, was observed. The missing biological stress response was accompanied by trauma-related dissociation, psychiatric comorbidity as well as by early life trauma and was best predicted by severity of trauma-related dissociation. Interestingly, traumatized healthy controls showed elevated cortisol levels together with high levels of non-pathological dissociation (absorption) that were comparable with those of PTSD patients. In Paper 2, I focused on the identification and clinical characterization of the Dissociative Subtype of PTSD (DS-PTSD, American Psychiatric Association, 2013) in a highly trauma exposed, non-Western population. The DS-PTSD was identified with an established, statistical stratification method (Latent Profile Analysis) in 14% of all studied individuals and in 26% of all PTSD cases. Sexual trauma, high levels of depressive symptoms, low general functionality as well as elevated suicidality were found as correlates of the DS-PTSD. Interestingly, similar correlates were found in already studied Western populations (e.g., Hansen, Ross, & Armour, 2017). The results of Paper 3 showed that assessments of trauma exposure and its clinical consequences did not evoke a significant biological stress response, within the studied sample. However, a subset of individuals (29% of the whole sample) with high levels of PTSD, especially re-experiencing, and depressive symptoms as well as low levels of emotional and instrumental support as coping strategies, exhibited a significant biological stress response. Similarly to the results from the first study, low reactive cortisol levels were best predicted by sexual trauma, low emotional coping and high dissociative tendencies. Both studies demonstrated that stress- and trauma-related dissociative symptoms correspond with downregulation of the hormonal stress system. This shows that focusing on the emotional stress response can broaden our understanding of the complex relationship between trauma exposure, psychopathology and stress hormone activity. Dissociative symptoms, transdiagnostically and transculturally, have frequently been associated with large illness burden and reduced treatment outcome (Lyssenko et al., 2018; McKinnon et al., 2016, Paper 2). For this reason, prospective studies on the possible causal link between dissociation and downregulation of biological stress system are urgently needed.</dcterms:abstract>
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