Post-traumatic Stress Disorder Symptoms Mediate the Relationship Between Trauma Exposure and Smoking Status in College Students

2014 ◽  
Vol 31 (1) ◽  
pp. 78-82 ◽  
Author(s):  
Crystal A. Gabert-Quillen ◽  
Arielle Selya ◽  
Douglas L. Delahanty
Keyword(s):  
College Students ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Smoking Status ◽  
Trauma Exposure ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
The Relationship

scholarly journals Mediating role of avoidance of trauma disclosure and social disapproval in ICD-11 post-traumatic stress disorder and complex post-traumatic stress disorder: cross-sectional study in a Lithuanian clinical sample

BJPsych Open ◽  
2021 ◽  
Vol 7 (6) ◽  
Author(s):  
Monika Kvedaraite ◽  
Odeta Gelezelyte ◽  
Thanos Karatzias ◽  
Neil P. Roberts ◽  
Evaldas Kazlauskas
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Clinical Sample ◽  
Trauma Exposure ◽  
Traumatic Experiences ◽  
Post Traumatic Stress ◽  
Mediating Role ◽  
Post Traumatic ◽  
The Relationship

Background ICD-11 includes a new diagnosis of complex post-traumatic stress disorder (CPTSD), resulting predominantly from reoccurring or prolonged trauma. Previous studies showed that lack of social support is among the strongest predictors of PTSD, but social factors have been sparsely studied in the context of the ICD-11 definition of PTSD and CPTSD. Aims To analyse the factor structure of the International Trauma Questionnaire (ITQ) in a Lithuanian clinical sample and to evaluate the mediating role of social and interpersonal factors in the relationship between trauma exposure and ICD-11 PTSD and CPTSD. Method The sample comprised 280 adults from out-patient mental health centres (age, years: mean 39.48 (s.d. = 13.35); 77.5% female). Trauma-related stress symptoms were measured with the ITQ. Social disapproval was measured with the Social Acknowledgment Questionnaire (SAQ) and trauma disclosure using the Disclosure of Trauma Questionnaire (DTQ). Results ICD-11 PTSD and CPTSD prevalence among the participants in this study was 13.9% and 10.0% respectively. Results indicated that avoidance of trauma disclosure mediated the relationship between trauma exposure and PTSD as well as CPTSD, whereas social disapproval mediated only the relationship between trauma exposure and CPTSD. Conclusions The findings suggest that disclosure of traumatic experiences and support from closest friends and family members might mitigate the effects of traumatic experiences, potentially reducing the risk of developing CPTSD.

scholarly journals An epistasis between dopaminergic and oxytocinergic systems confers risk of post-traumatic stress disorder in a traumatized Chinese cohort

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Kunlin Zhang ◽  
Gen Li ◽  
Li Wang ◽  
Chengqi Cao ◽  
Ruojiao Fang ◽  
...  
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Trauma Exposure ◽  
Environment Interaction ◽  
Post Traumatic Stress ◽  
Ptsd Diagnosis ◽  
Psychiatric Syndrome ◽  
Chinese Cohort ◽  
Post Traumatic

AbstractPost-traumatic stress disorder (PTSD) is a psychiatric syndrome that occurs after trauma exposure. Neurotransmitters such as dopamine and oxytocin have been reported to be involved in neuropathology of PTSD. Previous studies indicated that the dopamine–oxytocin interaction may contribute to behavioral disorders. Thus, exploring the epistasis (gene–gene interaction) between oxytocinergic and dopaminergic systems might be useful to reveal the genetic basis of PTSD. In this study, we analyzed two functional single nucleotide polymorphisms (SNPs), rs2268498 for oxytocinergic gene OXTR and rs1801028 for dopaminergic gene DRD2 based on putative oxytocin receptor–dopamine receptor D2 (OTR–DR2) heterocomplex in a Chinese cohort exposed to the 2008 Wenchuan earthquake (156 PTSD cases and 978 controls). Statistical analyses did not find any single variant or gene–environment interaction (SNP × earthquake-related trauma exposure) associated with provisional PTSD diagnosis or symptoms. An OXTR–DRD2 interaction (rs2268498 × rs1801028) was identified to confer risk of provisional PTSD diagnosis (OR = 9.18, 95% CI = 3.07–27.46 and P = 7.37e-05) and further subset analysis indicated that rs2268498 genotypes controlled the association directions of rs1801028 and rs1801028 genotypes also controlled the association directions of rs2268498. Rs2268498 × rs1801028 is also associated with PTSD symptoms (P = 0.043). Our study uncovered a genetic and putative function-based contribution of dopaminergic–oxytocinergic system interaction to PTSD.

Support for the mutual maintenance of pain and post-traumatic stress disorder symptoms

2009 ◽  
Vol 40 (7) ◽  
pp. 1215-1223 ◽  
Author(s):  
A. Liedl ◽  
M. O'Donnell ◽  
M. Creamer ◽  
D. Silove ◽  
A. McFarlane ◽  
...  
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Structural Equation ◽  
Stress Disorder ◽  
Traumatic Event ◽  
Saturated Model ◽  
Post Traumatic Stress ◽  
Post Injury ◽  
Post Traumatic ◽  
The Relationship

BackgroundPain and post-traumatic stress disorder (PTSD) are frequently co-morbid in the aftermath of a traumatic event. Although several models attempt to explain the relationship between these two disorders, the mechanisms underlying the relationship remain unclear. The aim of this study was to investigate the relationship between each PTSD symptom cluster and pain over the course of post-traumatic adjustment.MethodIn a longitudinal study, injury patients (n=824) were assessed within 1 week post-injury, and then at 3 and 12 months. Pain was measured using a 100-mm Visual Analogue Scale (VAS). PTSD symptoms were assessed using the Clinician-Administered PTSD Scale (CAPS). Structural equation modelling (SEM) was used to identify causal relationships between pain and PTSD.ResultsIn a saturated model we found that the relationship between acute pain and 12-month pain was mediated by arousal symptoms at 3 months. We also found that the relationship between baseline arousal and re-experiencing symptoms, and later 12-month arousal and re-experiencing symptoms, was mediated by 3-month pain levels. The final model showed a good fit [χ2=16.97, df=12, p>0.05, Comparative Fit Index (CFI)=0.999, root mean square error of approximation (RMSEA)=0.022].ConclusionsThese findings provide evidence of mutual maintenance between pain and PTSD.

scholarly journals Gene Expression Differences Between Young Adults Based on Trauma History and Post-traumatic Stress Disorder

2021 ◽  
Vol 12 ◽  
Author(s):  
Kaitlin E. Bountress ◽  
Vladimir Vladimirov ◽  
Gowon McMichael ◽  
Z. Nathan Taylor ◽  
Gary Hardiman ◽  
...  
Keyword(s):  
Gene Expression ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Gene Network ◽  
Stress Disorder ◽  
Trauma Exposure ◽  
Differentially Expressed ◽  
Post Traumatic Stress ◽  
Network Analyses ◽  
Post Traumatic

Background: The purpose of this study was to identify gene expression differences associated with post-traumatic stress disorder (PTSD) and trauma exposure (TE) in a three-group study design comprised of those with and without trauma exposure and PTSD.Methods: We conducted gene expression and gene network analyses in a sample (n = 45) composed of female subjects of European Ancestry (EA) with PTSD, TE without PTSD, and controls.Results: We identified 283 genes differentially expressed between PTSD-TE groups. In an independent sample of Veterans (n = 78) a small minority of these genes were also differentially expressed. We identified 7 gene network modules significantly associated with PTSD and TE (Bonferroni corrected p ≤ 0.05), which at a false discovery rate (FDR) of q ≤ 0.2, were significantly enriched for biological pathways involved in focal adhesion, neuroactive ligand receptor interaction, and immune related processes among others.Conclusions: This study uses gene network analyses to identify significant gene modules associated with PTSD, TE, and controls. On an individual gene level, we identified a large number of differentially expressed genes between PTSD-TE groups, a minority of which were also differentially expressed in the independent sample. We also demonstrate a lack of network module preservation between PTSD and TE, suggesting that the molecular signature of PTSD and trauma are likely independent of each other. Our results provide a basis for the identification of likely disease pathways and biomarkers involved in the etiology of PTSD.

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