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Resilience as a mediator in the relationship between posttraumatic stress and posttraumatic growth among adult accident or crime victims: the moderated mediating effect of childhood trauma.

ABSTRACT: Background: Results on the association between posttraumatic stress symptoms (PTSS) and posttraumatic growth (PTG) are inconsistent, and there may be unknown factors mediating or moderating this relationship. Identifying these factors could help in developing an intervention strategy for promoting PTG. However, few studies have examined relationships among PTSS, resilience, and PTG concurrently, and no study has investigated the effect of childhood trauma on these relationships in adulthood. Objective: The aim of this study was to examine the moderated mediating effect of childhood trauma on resilience and its associations with PTSS and PTG in adult victims of traumatic accidents or crimes. We hypothesized that resilience would mediate relationships between PTSS and PTG and that its mediating effects would differ depending on childhood trauma. Methods: We included adult victims of accidents or crimes referred to a university hospital or specialized support centre (n = 143). PTSS, resilience, childhood trauma, and PTG were measured with the following questionnaires: PTSD Checklist for DSM-5, Connor-Davidson Resilience Scale, Adverse Childhood Experiences Questionnaire, and the Short Form of the Posttraumatic Growth Inventory, respectively. Results: The effect of PTSS on PTG was found to be fully mediated by resilience, and this mediating effect was moderated according to childhood trauma: the more childhood traumatic experiences, the greater the mediating effect of resilience was between PTSS and PTG. The effect of resilience on PTG was highest in the high childhood trauma group. Conclusion: Therapists treating individuals with psychological trauma should attempt to identify a history of childhood trauma and to evaluate resilience. Therapeutic approaches tailored according thereto may improve PTG among individuals with PTSS symptoms, especially those with high levels of childhood trauma.

SUBMITTER: Lee D

PROVIDER: S-EPMC6968590 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:While the paradigm that genetic predisposition and environmental exposures interact to shape development and function of the human brain and ultimately the risk of psychiatric disorders has drawn wide interest, the corresponding molecular mechanisms have not been elucidated yet. Here we show that a functional polymorphism altering chromatin interaction between the transcription start site and long range enhancers in the FK506 binding protein 5 (FKBP5) gene, an important regulator of the stress hormone system, increases the risk of developing stress-related psychiatric disorders in adulthood by allele-specific, childhood trauma-dependent DNA demethylation in functional glucocorticoid response elements (GREs) of FKBP5. This demethylation is linked to increased stress-dependent gene transcription followed by a long-term dysregulation of the stress hormone system and a global impact on the function of immune cells and brain areas associated with stress regulation. This first identification of molecular mechanisms of genotype-directed long-term environmental reactivity will also critically contribute to designing more effective treatment strategies for stress-related disorders. Effects of FKBP5 rs1360780 genotype x environment interaction on peripheral blood mRNA expression of GR responsive genes, as measured by gene expression arrays, were explored in 129 individuals (child abuse/risk allele carrier N = 40, child abuse/protective allele carrier N = 15; and no child abuse/risk allele carrier N = 60, no child abuse/protective allele carrier N = 14). In all 129 individuals, 1627 transcripts showed a significant correlation with plasma cortisol concentrations, suggesting their GR responsiveness. The correlation of 76 of these transcripts with cortisol plasma levels showed significant differences when stratifying by FKBP5 genotype in individuals with child abuse (Fisher z score ≥ 1.96) For these 76 transcripts, the mean absolute correlation coefficient with plasma cortisol was R = 0.23 in the risk allele carriers with child abuse, that is those exhibiting a demethylation of FKBP5 intron 7 as compared to R = 0.74 in the carriers of the protective genotype with child abuse where intron 7 methylation remains largely stable. This indicates a relative GR-resistance in the trauma exposed FKBP5 risk allele vs. protective genotype carriers. These 76 transcripts did not show a genotype-dependent difference in correlation coefficients in non-trauma exposed individuals suggesting that exposure to early trauma enhances FKBP5 genotype-dependent effect of GR sensitivity, most likely by epigenetic mechanisms. These findings suggest that the combination of FKBP5 risk allele carrier status and early trauma exposure alters the stress hormone-dependent regulation of several genes in peripheral blood cells, and might thereby enhance the reported association of early trauma with immune and inflammatory dysregulation, further promoting system-wide symptoms of stress-related disorders.

Project description:Background: Supporting wellbeing beyond symptom reduction is necessary in trauma care. Research suggests increased posttraumatic growth (PTG) may promote wellbeing more effectively than posttraumatic stress disorder (PTSD) symptom reduction alone. Understanding neurobiological mechanisms of PTG would support PTG intervention development. However, most PTG research to-date has been cross-sectional data self-reported through surveys or interviews.Objective: Neural evidence of PTG and its coexistence with resilience and PTSD is limited. To advance neural PTG literature and contribute translational neuroscientific knowledge necessary to develop future objectively measurable neural-based PTG interventions.Method: Alpha frequency EEG and validated psychological inventories measuring PTG, resilience, and PTSD symptoms were collected from 30 trauma-exposed healthy adults amidst the COVID-19 pandemic. EEG data were collected using custom MNE-Python software, and a wireless OpenBCI 16-channel dry electrode EEG headset. Psychological inventory scores were analysed in SPSS Statistics and used to categorise the EEG data. Power spectral density analyses, t-tests and ANOVAs were conducted within EEGLab to identify brain activity differentiating high and low PTG, resilience, and PTSD symptoms.Results: Higher PTG was significantly differentiated from low PTG by higher alpha power in the left centro-temporal brain area around EEG electrode C3. A trend differentiating high PTG from PTSD was also indicated in this same location. Whole-scalp spectral topographies revealed alpha power EEG correlates of PTG, resilience and PTSD symptoms shared limited, but potentially meaningful similarities.Conclusion: This research provides the first comparative neural topographies of PTG, resilience and PTSD symptoms in the known literature. Results provide objective neural evidence supporting existing theory depicting PTG, resilience and PTSD as independent, yet co-occurring constructs. PTG neuromarker alpha C3 significantly delineated high from low PTG and warrants further investigation for potential clinical application. Findings provide foundation for future neural-based interventions and research for enhancing PTG in trauma-exposed individuals.

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Resilience as a mediator in the relationship between posttraumatic stress and posttraumatic growth among adult accident or crime victims: the moderated mediating effect of childhood trauma.

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