Comorbidity of PTSD and depression in Korean War veterans: Prevalence, predictors, and impairment
ABSTRACT Rates of PTSD and depression are high in Korean War veterans. The prevalence and impact of the two disorders occurring comorbidly, however, has not been investigated. This paper aims to investigate the extent to which PTSD and depression co-occur in Australian veterans of the Korean War, the symptom severity characteristics of comorbidity, the impact on life satisfaction and quality, and the association with war-related predictors.
Veterans (N=5352) completed self-report questionnaires including the Posttraumatic Stress Disorder Checklist, the Hospital Anxiety and Depression Scale, the Life Satisfaction Scale, the brief World Health Organisation Quality of Life questionnaire and the Combat Exposure Scale.
Seventeen percent of veterans met criteria for comorbid PTSD and depression, 15% had PTSD without depression, and a further 6% had depression without PTSD. Compared with either disorder alone, comorbidity was associated with impaired life satisfaction, reduced quality of life, and greater symptom severity. Several war-related factors were associated with comorbidity and with PTSD alone, but not with depression alone.
The reliance on self-reported measures and the necessity for retrospective assessment of some deployment-related factors renders some study data vulnerable to recall bias.
Comorbid PTSD and depression, and PTSD alone, are prevalent among Korean War veterans, are both associated with war-related factors 50 years after the Korean War, and may represent a single traumatic stress construct. The results have important implications for understanding complex psychopathology following trauma.
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ABSTRACT: BACKGROUND: Posttraumatic stress disorder (PTSD) and depressive disorder are over represented in combat veterans. Veterans with both disorders have an increased risk of suicide. The nitric oxide synthase 1 adaptor protein (NOS1AP) gene, which modulates stress-evoked N-methyl-d-aspartate (NMDA) activity, was investigated in combat veterans. METHODS: A comprehensive genetic analysis of NOS1AP and its association with PTSD was investigated in Vietnam combat veterans with PTSD (n=121) and a group of healthy control individuals (n=237). PTSD patients were assessed for symptom severity and level of depression using the Mississippi Scale for Combat-Related PTSD and the Beck Depression Inventory-II (BDI). RESULTS: The G allele of NOS1AP SNP rs386231 was significantly associated with PTSD (p=0.002). Analysis of variance revealed significant differences in BDI-II and Mississippi scores between genotypes for rs386231 with the GG genotype associated with increased severity of depression (p=0.002 F=6.839) and higher Mississippi Scale for Combat-Related PTSD scores (p=0.033). Haplotype analysis revealed that the C/G haplotype (rs451275/rs386231) was significantly associated with PTSD (p=0.001). LIMITATIONS: The sample sizes in our study were not sufficient to detect SNP associations with very small effects. In addition the study was limited by its cross sectional design. CONCLUSIONS: This is the first study reporting that a variant of the NOS1AP gene is associated with PTSD. Our data also suggest that a genetic variant in NOS1AP may increase the susceptibility to severe depression in patients with PTSD and increased risk for suicide.Journal of Affective Disorders 01/2014; 147:87-93. DOI:10.1016/j.jad.2012.10.013
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ABSTRACT: Posttraumatic stress disorder (PTSD), major depressive disorder (MDD), and severe fatigue may develop in response to severe stress and trauma. These conditions have all been shown to be associated with altered sensitivity of leukocytes for regulation by glucocorticoids (GCs). However, it remains unknown whether sensitivity of leukocytes for GCs is a pre-existing vulnerability factor, or whether GC-sensitivity of leukocytes alters as a consequence of stress and stress-related conditions. Our aim was to investigate whether sensitivity of T-cells and monocytes for regulation by GCs (i.e. dexamethasone: DEX) assessed before military deployment predicts high levels of PTSD, depressive, and/or fatigue symptoms 6 months after return from deployment. We included 526 male military personnel before deployment to Afghanistan. Logistic regression analysis was performed to predict fatigue, depressive, and PTSD symptoms 6 months after deployment based on sensitivity of LPS-induced TNF-α production and PHA-induced T-cell proliferation to DEX-inhibition before deployment. Severe fatigue 6 months after deployment was independently associated with low DEX-sensitivity of monocyte TNF-α production before deployment. A high level of depressive symptoms after deployment was independently associated with a low DEX-sensitivity of T-cell proliferation. In contrast, a high level of PTSD symptoms after deployment was independently associated with a high DEX-sensitivity of T-cell proliferation before deployment, but only in individuals who reported PTSD symptoms without depressive symptoms. The predictive value of DEX-sensitivity was independent of childhood trauma and GR number, GR subtype and GR target gene mRNA expression in leukocytes. We present here for the first time that the sensitivity of leukocytes for GCs prior to deployment is a predictive factor for the development of PTSD, depressive and fatigue symptomatology in response to deployment. Notably, PTSD, depressive and fatigue symptoms were differentially associated with GC-sensitivity of monocytes and T-cells and therefore may have different biological underpinnings.Psychoneuroendocrinology 04/2012; 37(11):1822-36. DOI:10.1016/j.psyneuen.2012.03.018
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ABSTRACT: Three decades of posttraumatic stress disorder (PTSD) research have placed it well on the map. PTSD is a young disorder that started being properly understood only from 1980 with incorporation in DSM-III, in which it was acknowledged that exposure to traumatic events can lead to long-term psychopathology. This chapter reviews the history and nosology of the disorder, epidemiology, and etiology, as well as the clinical features. It lists the diagnostic assessments and provides an overview of the biological framework of the disorder by addressing brain, neurohormonal, and transmitter alterations. Exposure to traumatic events is commonplace. The majority of exposed subjects are resilient, as this is still the rule rather than the exception. The reported prevalence of PTSD is twice as common in females compared to males. The A criterion in PTSD expressed the traumatic event, after which the symptom clusters are based on intrusions, avoidance, and irritability. Gene-environmental studies are needed, with a focus on specific, distinct endophenotypes and influences from environmental factors (e.g., traumatic early-life experiences, with abuse or neglect, as well as exposure to disasters or combat). PTSD is often accompanied by comorbid disorders, such as depression and other anxiety disorders, as well as drug and alcohol abuse and dependence. The disorder is heterogeneous, sometimes with complex features that focus on emotional dysregulation, attachment, and dissociation. Several validated trauma assessments are available that allow quantification of trauma symptomatology. The biological framework is based on the concepts of stress sensitization and fear conditioning as well as failure of inhibition. After the decade of the hippocampus we have seen a shift to the decade of the amygdala in the new millennium. Given the specific role of the prefrontal cortex in (neuro)psychological functions in patients with PTSD (i.e., attention and cognitive interference), interest in the role of the prefrontal cortex will increase significantly. Increased multidisciplinary involvement, with inclusion of genetics, endocrinology, immunology, (neuro)psychology, and psychopathology, is essential to find consistency between biological, emotional, and cognitive dysfunction in PTSD. A variety of effective psychological and pharmacological interventions can be used to treat PTSD. The mechanisms of exposure therapy and cognitive therapy in influencing neurobiological markers need to be further investigated. The same goes for emerging therapies such as eye movement desensitization and reprocessing, virtual reality exposure, internet therapy, and neurofeedback. There are no specific drugs for PTSD, except for the treatment of irritability and depressive features with selective serotonin reuptake inhibitors. Other options, such as specific serotonergic agents, e.g., 5-HT(1A) antagonists, norepinephrine blockers, corticotropin-releasing factor antagonists, glucocorticoid receptor antagonists, prazosin and α(1)-adrenergic blocker with nightmares, and use of beta-blockers early after trauma exposure, are investigated. New treatment options such as d-cycloserine and cortisol seem to offer opportunities to influence memory consolidation of traumatic experiences in timed relation to exposure. For health economy it is important to be aware that there is an economic burden associated with PTSD, and treatments require the use of scarce resources. They will ultimately provide tools to ascertain the relative efficiency of different treatment options and plan the availability of these for the affected population. This can be seen as the biggest challenge for the future evolution of the disorder.Handbook of Clinical Neurology 01/2012; 106:291-342. DOI:10.1016/B978-0-444-52002-9.00018-8