Accelerated ageing and effects of psychotherapy on DNA strand break accumulation in individuals suffering from posttraumatic stress disorders
2015, Moreno-Villanueva, Maria, Morath, Julia, Vanhooren, Valerie, Elbert, Thomas, Libert, Claude, Bürkle, Alexander, Kolassa, Iris-Tatjana
The prevalence of age-related diseases is increased in individuals with Posttraumatic Stress Disorder (PTSD). At the molecular level, N-Glycosylation is an age-dependent process, identified as a biomarker for physiological aging (GlycoAge Test). Individuals with PTSD and trauma-exposed individuals presented an upward shift in the GlycoAge Test, equivalent to an advancement of the aging process by 15 additional years.
On the other hand traumatic stress may increase carcinogenesis via increased DNA damage and impaired DNA repair mechanisms. We found higher levels of basal DNA breakage in individuals with PTSD and trauma-exposed subjects than in controls. However, single-strand break repair was unimpaired in individuals with PTSD.
In conclusion, our results suggest that cumulative exposure to traumatic stressors accelerates the process of physiological aging and show – for the first time in vivo – an association between traumatic stress and DNA breakage. Moreover, we demonstrate changes at the molecular level, i.e. the integrity of DNA, after psychotherapeutic interventions.
Effects of Psychotherapy on DNA Strand Break Accumulation Originating from Traumatic Stress
2014, Morath, Julia, Moreno-Villanueva, Maria, Hamuni, Gilava, Kolassa, Stephan, Ruf-Leuschner, Martina, Schauer, Maggie, Elbert, Thomas, Bürkle, Alexander, Kolassa, Iris-Tatjana
Background: Previous research reveals an association between traumatic stress and an increased risk for numerous diseases, including cancer. At the molecular level, stress may increase carcinogenesis via increased DNA damage and impaired DNA repair mechanisms. We assessed DNA breakage in peripheral blood mononuclear cells from individuals with post-traumatic stress disorder (PTSD) and measured the cellular capacity to repair single-strand breaks after exposure to ionizing X-radiation. We also investigated the effect of psychotherapy on both DNA breakage and DNA repair. Methods: In a first study we investigated DNA breakage and repair in 34 individuals with PTSD and 31 controls. Controls were subdivided into 11 trauma-exposed subjects and 20 individuals without trauma exposure. In a second study, we analysed the effect of psychotherapy (Narrative Exposure Therapy) on DNA breakage and repair. Thirty-eight individuals with PTSD were randomly assigned to either a treatment or a waitlist control condition. Follow-up was performed 4 months and 1 year after therapy. Results: In study 1 we found higher levels of basal DNA breakage in individuals with PTSD and trauma-exposed subjects than in controls, indicating that traumatic stress is associated with DNA breakage. However, single-strand break repair was unimpaired in individuals with PTSD. In study 2, we found that psychotherapy reversed not only PTSD symptoms, but also DNA strand break accumulation. Conclusion: Our results show - for the first time in vivo - an association between traumatic stress and DNA breakage; they also demonstrate changes at the molecular level, i.e., the integrity of DNA, after psychotherapeutic interventions.
Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells
2013, Gola, Hannah, Engler, Harald, Sommershof, Annette, Adenauer, Hannah, Kolassa, Stephan, Schedlowski, Manfred, Gröttrup, Marcus, Elbert, Thomas, Kolassa, Iris-Tatjana
Posttraumatic stress disorder (PTSD) is associated with an enhanced risk for cardiovascular and other inflammatory diseases. Chronic low-level inflammation has been suggested as a potential mechanism linking these conditions. METHODS: We investigated plasma cytokine levels as well as spontaneous and lipopolysaccharide (LPS)-stimulated cytokine production by peripheral blood mononuclear cells (PBMCs) in a group of 35 severely traumatized PTSD patients compared to 25 healthy controls. RESULTS: Spontaneous production of interleukin (IL)-1beta, IL-6 and tumor necrosis factor (TNF)-alpha by isolated PBMCs was significantly higher in the PTSD compared to the control group and even correlated with PTSD symptom severity within the PTSD group. In contrast, circulating plasma levels of pro- and anti-inflammatory cytokines such as IL-6, IL-8, IL-10, TNF-alpha, or monocyte chemotactic protein (MCP)-1 were not significantly altered in PTSD patients compared to healthy controls.
Our findings indicate that PBMCs of PTSD patients are already pre-activated in vivo, providing further evidence for low-grade inflammation in PTSD. This might possibly represent one psychobiological pathway from PTSD to poor physical health.