Chronic Stress最新文献

{"title":"A medial prefrontal cortex cell type necessary and sufficient for a rapid antidepressant response.","authors":"Brendan D Hare, Ronald S Duman","doi":"10.1177/2470547019841358","DOIUrl":"https://doi.org/10.1177/2470547019841358","url":null,"abstract":"Commentary on: Hare BD, Shinohara R, Liu RJ, Pothula S, DiLeone RJ and Duman RS. Optogenetic stimulation of medial prefrontal cortex Drd1 neurons produces rapid and long-lasting antidepressant effects. Nature communications. 2019; 10: 223. The discovery of ketamine’s antidepressant effects has generated great excitement due to the rapid and sustained time course (within hours, lasting up to seven days), efficacy in treatment resistant individuals, as well as a pharmacological profile that is distinct from traditional antidepressants. Efforts have been ongoing to identify the molecular, cellular, and circuit mechanisms underlying the actions of ketamine. Regarding circuitry, dysfunction of the medial prefrontal cortex (mPFC) subregions, including the subgenual and anterior cingulate, have been implicated in depression, and preclinical models have been utilized to study the role of mPFC in depressionlike behaviors. Ketamine is an NMDA antagonist yet it produces a burst of glutamate in the mPFC following administration. Preclinical studies have demonstrated that mPFC activity following ketamine administration is necessary for ketamine’s rapid antidepressant effects, and that activation of principal neurons in the mPFC can produce persistent antidepressant responses. These findings indicate that neurons and circuits within the mPFC may represent key targets in depression. Through interaction with downstream targets, the mPFC plays a role in the generation of numerous behaviors as well as the response to stress. This diversity of action is mediated by principal neurons projecting to numerous downstream targets. Notably, mPFC principal neurons are heterogeneous and have been characterized based on their projection targets, dendritic morphology, and response to neuromodulators. Although the burst of glutamate following ketamine administration may excite many types of mPFC pyramidal neurons indiscriminately, we hypothesized that the antidepressant response may be carried by a discriminable population. To probe this hypothesis, we utilized Cre-dependent expression of neuronal effectors in mouse lines carrying the Cre transgene in neurons expressing the D1 dopamine receptor (Drd1-Cre) or the D2 dopamine receptor (Drd2Cre). This approach had previously been demonstrated to allow cell-type-specific access to distinct populations of mPFC pyramidal cells. We observed that utilizing a channelrhodopsin vector to allow optogenetic stimulation of Drd1 containing cells produced a rapid (observable 24 h after stimulation) and sustained (observable seven days after stimulation) antidepressant response (Figure 1). These effects are similar to ketamine and indicate that the circuit function responsible for depressionlike behavior was rapidly and persistently altered by the prior period of stimulation. In contrast, stimulation of the Drd2 cell type did not produce an antidepressant response. Additional experiments produced convergent evidence for the importance of the D","PeriodicalId":52315,"journal":{"name":"Chronic Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/2470547019841358","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36989275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Review of fMRI Affective Processing Paradigms Used in the Neurobiological Study of Posttraumatic Stress Disorder.","authors":"Alyson M Negreira,&nbsp;Chadi G Abdallah","doi":"10.1177/2470547019829035","DOIUrl":"https://doi.org/10.1177/2470547019829035","url":null,"abstract":"<p><p>Posttraumatic stress disorder (PTSD) is a chronic and debilitating psychiatric disorder with a complex clinical presentation. The last two decades have seen a proliferation of literature on the neurobiological mechanisms subserving affective processing in PTSD. The current review will summarize the neuroimaging results of the most common experimental designs used to elucidate the affective signature of PTSD. From this summary, we will provide a heuristic to organize the various paradigms discussed and report neural patterns of activations using this heuristic as a framework. Next, we will compare these results to the traditional functional neurocircuitry model of PTSD and discuss biological and analytic variables which may account for the heterogeneity within this literature. We hope that this approach may elucidate the role of experimental parameters in influencing neuroimaging findings.</p>","PeriodicalId":52315,"journal":{"name":"Chronic Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/2470547019829035","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37180657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurosteroid Levels in the Orbital Frontal Cortex of Subjects with PTSD and Controls: A Preliminary Report.","authors":"Dianne A Cruz, Leisa A Glantz, Kara D McGaughey, Gillian Parke, Lawrence J Shampine, Jason D Kilts, Jennifer C Naylor, Christine E Marx, Douglas E Williamson","doi":"10.1177/2470547019838570","DOIUrl":"10.1177/2470547019838570","url":null,"abstract":"<p><strong>Background: </strong>Neurosteroids mediate stress signaling and have been implicated in the pathogenesis of post-traumatic stress disorder (PTSD) in both preclinical and clinical studies. Compared to controls, subjects with PTSD exhibit altered neurosteroid levels in peripheral blood and cerebrospinal fluid as well as hypoactivity in the medial orbital frontal cortex (mOFC). Therefore, the aim of this study was to compare neurosteroid levels in the mOFC of subjects with PTSD (n = 18) and controls (n = 35).</p><p><strong>Methods: </strong>Gray matter was dissected from fresh-frozen mOFC, and levels of the neurosteroids pregnenolone, allopregnanolone, pregnanolone, epiallopregnanolone, epipregnanolone, tetrahydrodeoxycorticosterone, and androsterone were determined by gas chromatography - tandem mass spectrometry (GC/MS/MS).</p><p><strong>Results: </strong>Analyses of unadjusted levels revealed that males with PTSD had significantly decreased levels of allopregnanolone (<i>p</i> = 0.03) compared to control males and females with PTSD had significantly increased levels of pregnenolone (<i>p</i> = 0.03) relative to control females. After controlling for age, postmortem interval, and smoking status, results showed that males with PTSD had significantly decreased levels of androsterone (<i>t</i>₄₆ = 2.37, <i>p</i> = 0.02) compared to control males and females with PTSD had significantly increased levels of pregnanolone (<i>t</i>₄₆ = -2.25, <i>p</i> = 0.03) relative to control females.</p><p><strong>Conclusions: </strong>To our knowledge, this is the first report of neurosteroid levels in postmortem brain tissue of subjects with PTSD. Although replication is required in other brain regions and in a larger cohort of subjects, the results suggest a dysregulation of allopregnanolone and androsterone in males with PTSD and pregnanolone in females with PTSD in the mOFC.</p>","PeriodicalId":52315,"journal":{"name":"Chronic Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/91/6f/10.1177_2470547019838570.PMC6604657.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37133277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dorsal Hippocampus ERK2 Signaling Mediates Anxiolytic-Related Behavior in Male Rats.","authors":"Jorge A Sierra-Fonseca,&nbsp;Lyonna F Parise,&nbsp;Francisco J Flores-Ramirez,&nbsp;Eden H Robles,&nbsp;Israel Garcia-Carachure,&nbsp;Sergio D Iñiguez","doi":"10.1177/2470547019897030","DOIUrl":"https://doi.org/10.1177/2470547019897030","url":null,"abstract":"<p><strong>Background: </strong>Anxiety disorders are the most common neuropathologies worldwide, but the precise neuronal mechanisms that underlie these disorders remain unknown. The hippocampus plays a role in mediating anxiety-related responses, which can be modeled in rodents using behavioral assays, such as the elevated plus maze. Yet, the molecular markers that underlie affect-related behavior on the elevated plus maze are not well understood.</p><p><strong>Methods: </strong>We used herpes simplex virus vector delivery to overexpress extracellular signal-regulated kinase-2, a signaling molecule known to be involved in depression and anxiety, within the dorsal hippocampus of adult Sprague-Dawley male rats. Three days post virus delivery, we assessed anxiety-like responses on the elevated plus maze or general locomotor activity on the open field test.</p><p><strong>Results: </strong>When compared to controls, rats overexpressing extracellular signal-regulated kinase-2 in the dorsal hippocampus displayed an anxiolytic-like phenotype, per increases in time spent in the open arms, and less time in the closed arms, of the elevated plus maze. Furthermore, no changes in locomotor activity as a function of virus infusion were observed on the open field test between the experimental groups.</p><p><strong>Conclusion: </strong>This investigation demonstrates that virus-mediated increases of extracellular signal-regulated kinase-2 signaling, within the hippocampus, plays a critical role in decreasing anxiogenic responses on the rat elevated plus maze. As such, our data provide construct validity, at least in part, to the molecular mechanisms that mediate anxiolytic-like behavior in rodent models for the study of anxiety.</p>","PeriodicalId":52315,"journal":{"name":"Chronic Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/2470547019897030","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37675059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Salience Network Disruption in U.S. Army Soldiers With Posttraumatic Stress Disorder.","authors":"Chadi G Abdallah,&nbsp;Christopher L Averill,&nbsp;Amy E Ramage,&nbsp;Lynnette A Averill,&nbsp;Selin Goktas,&nbsp;Samaneh Nemati,&nbsp;John H Krystal,&nbsp;John D Roache,&nbsp;Patricia A Resick,&nbsp;Stacey Young-McCaughan,&nbsp;Alan L Peterson,&nbsp;Peter Fox","doi":"10.1177/2470547019850467","DOIUrl":"https://doi.org/10.1177/2470547019850467","url":null,"abstract":"Background Better understanding of the neurobiology of posttraumatic stress disorder (PTSD) may be critical to developing novel, effective therapeutics. Here, we conducted a data-driven investigation using a well-established, graph-based topological measure of nodal strength to determine the extent of functional dysconnectivity in a cohort of active duty U.S. Army soldiers with PTSD compared to controls. Methods A total of 102 participants with (n = 50) or without PTSD (n = 52) completed functional magnetic resonance imaging at rest and during symptom provocation using subject-specific script imagery. Vertex/voxel global brain connectivity with global signal regression (GBCr), a measure of nodal strength, was calculated as the average of its functional connectivity with all other vertices/voxels in the brain gray matter. Results In contrast to resting state, where there were no group differences, we found a significantly higher GBCr during symptom provocation, in PTSD participants compared to controls, in areas within the right hemisphere, including anterior insula, caudal-ventrolateral prefrontal, and rostral-ventrolateral parietal cortices. Overall, these clusters overlapped with the ventral and dorsal salience networks. Post hoc analysis showed increased GBCr in these salience clusters during symptom provocation compared to resting state. In addition, resting-state GBCr in the salience clusters predicted GBCr during symptom provocation in PTSD participants but not in controls. Conclusion In PTSD, increased connectivity within the salience network has been previously hypothesized, based primarily on seed-based connectivity findings. The current results strongly support this hypothesis using whole-brain network measure in a fully data-driven approach. It remains to be seen in future studies whether these identified salience disturbances would normalize following treatment.","PeriodicalId":52315,"journal":{"name":"Chronic Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/2470547019850467","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37279523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"\"Does the opioid system block or enhance the antidepressant effects of ketamine?\"","authors":"Sanjay J Mathew,&nbsp;Ana Maria Rivas-Grajales","doi":"10.1177/2470547019852073","DOIUrl":"https://doi.org/10.1177/2470547019852073","url":null,"abstract":"Commentary on: Williams NR, Heifets BD, Blasey C, et al. Attenuation of antagonism effects of ketamine by opioid receptor antagonism. Am J Psychiatry. 2018;175(12):1205–1215; Yoon G, Petrakis IL, Krystal JH. Association of combined naltrexone and ketamine with depressive symptoms in a case series of patients with depression and alcohol use disorder. JAMA Psychiatry. 2019;76(3):337–338. Despite tremendous growth in the off-label use of racemic ketamine for psychiatric indications and the recent U.S. Food and Drug Administration approval of esketamine nasal spray for treatment-resistant depression (TRD), neural mechanisms underlying the induction and maintenance of ketamine’s rapid but transient antidepressant effects remain obscure. Ketamine’s initial pharmacological target is not disputed: it acts as a nonselective, noncompetitive N-methyl-D-aspartate receptor (NMDAR) antagonist. Converging preclinical evidence indicates that this NMDAR blockade inhibits (1) Gamma-aminobutyric acid (GABA) interneurons (resulting in enhanced presynaptic release of glutamate and stimulation of postsynaptic a-Amino-3-hydroxy-5methyl-4-isoxazole-propionic acid (AMPA) receptors), (2) extrasynaptic GluN2B-containing NMDARs (resulting in de-suppression of mTORC1 function), and (3) spontaneous neurotransmission (resulting in inhibition of eukaryotic elongation factor 2 kinase activity). A final common pathway for these effects involves activation of neurotrophic factor signaling pathways, increased synaptic protein synthesis, and dendritic spine formation and restoration of lost spines (‘‘spinogenesis’’). There is considerably less consensus in defining the role of non-NMDAR receptor activity in mediating the rapid (within several hours) and sustained (24 h to 7 days) antidepressant effects observed in numerous clinical trials. Indeed, the sustained antidepressant responses seen in some individuals are particularly puzzling, given the short elimination of half-life of ketamine and its primary metabolite norketamine. Recent preclinical experiments have shown that a different metabolite— hydroxynorketamine [(2R,6R)-HNK]—promotes AMPA-mediated synaptic potentiation via an entirely NMDAR independent pathway. Furthermore, ketamine has significant central antinociceptive effects, with activity at mu-, kappa-, and delta-opioid receptors. Inasmuch as the U.S. continues to face an alarming increase in the number of opioid-related overdose fatalities, some have urged more caution in the use of ketamine (and esketamine) for depression, particularly in the face of recent experimental evidence by Williams et al. that ketamine’s antidepressant effects may be mediated by mu-opioid receptor activity. In this Commentary, we evaluate the evidence presented in Williams’ et al. intriguing article as well as counterevidence. The study, a randomized, double-blind, placebo-controlled cross-over study in 12 participants with TRD, showed that pretreatment with the nonselective opioid antagonist ","PeriodicalId":52315,"journal":{"name":"Chronic Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/2470547019852073","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37398044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"\"Association of Severity of Posttraumatic Stress Disorder With Inflammation: Using Total White Blood Cell Count as a Marker\".","authors":"Farrukh M Koraishy,&nbsp;Joanne Salas,&nbsp;Thomas C Neylan,&nbsp;Beth E Cohen,&nbsp;Paula P Schnurr,&nbsp;Sean Clouston,&nbsp;Jeffrey F Scherrer","doi":"10.1177/2470547019877651","DOIUrl":"https://doi.org/10.1177/2470547019877651","url":null,"abstract":"<p><strong>Background: </strong>Inflammation is known to be associated with posttraumatic stress disorder (PTSD). It is not known if total white blood cell (WBC) count, a routinely checked inflammatory marker, is associated with PTSD symptom trajectories using medical record data.</p><p><strong>Methods: </strong>We used latent class growth analysis to identify three-year PTSD symptom trajectories using PTSD Checklist (PCL) scores. The outcome for each patient was maximum WBC count from index PTSD diagnosis to last PCL. Using linear regression analysis, we then calculated and compared the average WBC count for each trajectory before and after controlling for age, gender, race, obesity, smoking, diabetes, hypertension, cardiovascular disease, depression and other co-morbid inflammatory conditions.</p><p><strong>Results: </strong>Patients were 40.2 (SD±13.5) years of age, 83.7% male and 67.9% white. We identified three PCL trajectory groups based on symptom severity over time: 'moderate-large decrease', 'moderate severe-slight decrease', and 'severe-persistent'. In adjusted analyses, 'severe-persistent' vs. 'moderate-large decrease' had significantly higher WBC count (B=0.64; 95%CI=0.18, 1.09; p=.006). Although non-significant, 'moderate severe-slight decrease' vs. 'moderate-large decrease' also had a higher WBC count (B=0.42; 95% CI: -0.02, 0.86; p=.061).</p><p><strong>Conclusion: </strong>Persistently severe PTSD is associated with a higher WBC count than improving PTSD. WBC appears to have utility for measuring the association between psychiatric disorders and inflammation in retrospective cohort studies involving large administrative medical record data bases.</p>","PeriodicalId":52315,"journal":{"name":"Chronic Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/2470547019877651","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37723439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"What Is the Confusion With Cortisol?","authors":"B. McEwen","doi":"10.1177/2470547019833647","DOIUrl":"https://doi.org/10.1177/2470547019833647","url":null,"abstract":"Cortisol has many roles not only in mediating the response to stress but also in the circadian rhythm, and it does so by both genomic and nongenomic cellular and molecular mechanisms. Yet, it is common to associate cortisol only with stress and, in particular, with the negative aspects of stress even though we would not survive without it. This commentary provides a brief overview not only of the diverse roles of cortisol but also of how to measure it to get meaningful information in the context of other mediators of stress and adaptation and the concepts of allostasis and allostatic load and overload. In particular, the adaptive plasticity of the brain mediated by glucocorticoids and excitatory amino acids is discussed in relation to misconceptions about what constitutes brain damage. Thus the confusion with cortisol is that it does too many important things both positive and negative!","PeriodicalId":52315,"journal":{"name":"Chronic Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/2470547019833647","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42070336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reduced Salience and Enhanced Central Executive Connectivity Following PTSD Treatment.","authors":"Chadi G Abdallah,&nbsp;Christopher L Averill,&nbsp;Amy E Ramage,&nbsp;Lynnette A Averill,&nbsp;Evelyn Alkin,&nbsp;Samaneh Nemati,&nbsp;John H Krystal,&nbsp;John D Roache,&nbsp;Patricia Resick,&nbsp;Stacey Young-McCaughan,&nbsp;Alan L Peterson,&nbsp;Peter Fox","doi":"10.1177/2470547019838971","DOIUrl":"https://doi.org/10.1177/2470547019838971","url":null,"abstract":"<p><strong>Background: </strong>In soldiers with posttraumatic stress disorder (PTSD), symptom provocation was found to induce increased connectivity within the salience network, as measured by functional magnetic resonance imaging (<i>f</i>MRI) and global brain connectivity with global signal regression (GBCr). However, it is unknown whether these GBCr disturbances would normalize following effective PTSD treatment.</p><p><strong>Methods: </strong>69 US Army soldiers with (n = 42) and without PTSD (n = 27) completed <i>f</i>MRI at rest and during symptom provocation using subject-specific script imagery. Then, participants with PTSD received 6 weeks (12 sessions) of group cognitive processing therapy (CPT) or present-centered therapy (PCT). At week 8, all participants repeated the <i>f</i>MRI scans. The primary analysis used a region-of-interest approach to determine the effect of treatment on salience GBCr. A secondary analysis was conducted to explore the pattern of GBCr alterations posttreatment in PTSD participants compared to controls.</p><p><strong>Results: </strong>Over the treatment period, PCT significantly reduced salience GBCr (<i>p</i> = .02). Compared to controls, salience GBCr was high pretreatment (PCT, <i>p</i> = .01; CPT, <i>p</i> = .03) and normalized post-PCT (<i>p</i> = .53), but not post-CPT (<i>p</i> = .006). Whole-brain secondary analysis found high GBCr within the central executive network in PTSD participants compared to controls. <i>Post hoc</i> exploratory analyses showed significant increases in executive GBCr following CPT treatment (<i>p</i> = .01).</p><p><strong>Conclusion: </strong>The results support previous models relating CPT to central executive network and enhanced cognitive control while unraveling a previously unknown neurobiological mechanism of PCT treatment, demonstrating treatment-specific reduction in salience connectivity during trauma recollection.</p>","PeriodicalId":52315,"journal":{"name":"Chronic Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/2470547019838971","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37348472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Purpose in Life and Conscientiousness Protect Against the Development of Suicidal Ideation in U.S. Military Veterans With PTSD and MDD: Results From the National Health and Resilience in Veterans Study.","authors":"Elizabeth Straus, Sonya B Norman, Jessica C Tripp, Michelle Pitts, Robert H Pietrzak","doi":"10.1177/2470547019872172","DOIUrl":"10.1177/2470547019872172","url":null,"abstract":"<p><strong>Background: </strong>Although several studies have examined risk factors for suicidal ideation among veterans, little is known about risk and protective factors for suicidal ideation in high-risk veteran samples. Thus, this study examined a broad range of risk and protective factors associated with the development of suicidal ideation in a high-risk sample of U.S. veterans who screened positive for current posttraumatic stress disorder (PTSD) and/or major depressive disorder (MDD).</p><p><strong>Methods: </strong>Data were analyzed from the National Health and Resilience in Veterans Study, a nationally representative, prospective cohort study of U.S. veterans. Veterans completed self-report measures to screen for PTSD and MDD and to assess for risk and protective factors. The sample included 222 veterans with PTSD and/or MDD who did not endorse suicidal ideation at baseline and completed at least one assessment over a seven-year follow-up period. A multivariable binary logistic regression analysis was conducted to examine baseline factors associated with incident suicidal ideation.</p><p><strong>Results: </strong>Nearly one in three (27.1%) of veterans with PTSD and/or MDD developed suicidal ideation over the seven-year follow-up period. Non-Caucasian race and lower scores on measures of purpose in life, conscientiousness, and frequency of religious service attendance were independently associated with incident suicidal ideation. Lower purpose in life (52.3%) and conscientiousness (33.2%) explained the vast majority of variance in incident suicidal ideation.</p><p><strong>Conclusion: </strong>Nearly 30% of veterans with PTSD and/or MDD who did not endorse suicidal ideation at baseline developed suicidal ideation over a seven-year period. Prevention and treatment efforts designed to bolster purpose in life and conscientiousness may help mitigate risk for suicidal ideation in this high-risk population.</p>","PeriodicalId":52315,"journal":{"name":"Chronic Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6880965/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47112772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}