Exposure to War as a Risk Factor for Mental Disorders

The authors discuss a new study on the prevalence of mental disorders in Lebanon

Analysis of Kinase Gene Expression in the Frontal Cortex of Suicide Victims: Implications of Fear and Stress†

Suicide is a serious public health issue that results from an interaction between multiple risk factors including individual vulnerabilities to complex feelings of hopelessness, fear, and stress. Although kinase genes have been implicated in fear and stress, including the consolidation and extinction of fearful memories, expression profiles of those genes in the brain of suicide victims are less clear. Using gene expression microarray data from the Online Stanley Genomics Database1 and a quantitative PCR, we investigated the expression profiles of multiple kinase genes including the calcium calmodulin-dependent kinase (CAMK), the cyclin-dependent kinase, the mitogen-activated protein kinase (MAPK), and the protein kinase C (PKC) in the prefrontal cortex (PFC) of mood disorder patients died with suicide (N = 45) and without suicide (N = 38). We also investigated the expression pattern of the same genes in the PFC of developing humans ranging in age from birth to 49 year (N = 46). The expression levels of CAMK2B, CDK5, MAPK9, and PRKCI were increased in the PFC of suicide victims as compared to non-suicide controls (false discovery rate, FDR-adjusted p < 0.05, fold change >1.1). Those genes also showed changes in expression pattern during the postnatal development (FDR-adjusted p < 0.05). These results suggest that multiple kinase genes undergo age-dependent changes in normal brains as well as pathological changes in suicide brains. These findings may provide an important link to protein kinases known to be important for the development of fear memory, stress associated neural plasticity, and up-regulation in the PFC of suicide victims. More research is needed to better understand the functional role of these kinase genes that may be associated with the pathophysiology of suicide

Posttraumatic Stress Disorder and Community Collective Efficacy following the 2004 Florida Hurricanes

There is a paucity of research investigating the relationship of community-level characteristics such as collective efficacy and posttraumatic stress following disasters. We examine the association of collective efficacy with probable posttraumatic stress disorder and posttraumatic stress disorder symptom severity in Florida public health workers (n = 2249) exposed to the 2004 hurricane season using a multilevel approach. Anonymous questionnaires were distributed electronically to all Florida Department of Health personnel nine months after the 2004 hurricane season. The collected data were used to assess posttraumatic stress disorder and collective efficacy measured at both the individual and zip code levels. The majority of participants were female (80.42%), and ages ranged from 20 to 78 years (median = 49 years); 73.91% were European American, 13.25% were African American, and 8.65% were Hispanic. Using multi-level analysis, our data indicate that higher community-level and individual-level collective efficacy were associated with a lower likelihood of having posttraumatic stress disorder (OR = 0.93, CI = 0.88–0.98; and OR = 0.94, CI = 0.92–0.97, respectively), even after adjusting for individual sociodemographic variables, community socioeconomic characteristic variables, individual injury/damage, and community storm damage. Higher levels of community-level collective efficacy and individual-level collective efficacy were also associated with significantly lower posttraumatic stress disorder symptom severity (b = −0.22, p<0.01; and b = −0.17, p<0.01, respectively), after adjusting for the same covariates. Lower rates of posttraumatic stress disorder are associated with communities with higher collective efficacy. Programs enhancing community collective efficacy may be an important part of prevention practices and possibly lead to a reduction in the rate of posttraumatic stress disorder post-disaster

Chemokines as Potential Biomarkers for PTSD in Military Population

Post-traumatic stress disorder (PTSD) is a serious mental health concern worldwide among civilians and military personnel. Gaps in our understanding of its biological basis create significant obstacles for accurate diagnosis and assessment of therapeutic interventions. In light of this, investigation of biological factors associated with possible molecular cues of inflammation or neuroimmune disorders, could provide new surrogate markers for PTSD or PTSD treatment response. Analyses to date in deployed military personnel have suggested that sets of chemokines may be useful as biomarkers for PTSD acquired in military operations. Specifically, studies to date suggest that CCL2, CCL15, CCL22, CCL25, CXCL2, and CXCL12 are associated with PTSD onset, while CCL13, CCL20, and CXCL6 are correlated to PTSD risk; CX3CL1 are associated with resilience; CCL3; CXCL11, and CXCL16 are associated with stress response. CCL11, CCL13, CCL20, and CCL25 are correlated with the severity of PTSD symptoms. This chapter reviews the current understanding of potential chemokine markers for PTSD, and the potential chemokines associated with PTSD onset, risk, resilience, as well as stress responses in service members. Although the proposed biomarkers require further validation, these findings may lead to additional knowledge for the education and development of diagnostic and therapeutic approaches for PTSD, not only benefiting military personnel, but civilians as well

Attention Deficit Hyperactivity Disorder and Risk of Posttraumatic Stress and Related Disorders: A Prospective Longitudinal Evaluation in U.S. Army Soldiers

Crossâ sectional associations between attention deficit hyperactivity disorder (ADHD) and posttraumatic stress disorder (PTSD) have been observed, but longitudinal studies assessing this association are lacking. This prospective study evaluated the association between predeployment ADHD and postdeployment PTSD among U.S. Army soldiers. Soldiers who deployed to Afghanistan were surveyed before deployment (T0) and approximately 1 month (T1), 3 months (T2), and 9 months (T3) after their return. Logistic regression was performed to estimate the association between predeployment ADHD and postdeployment (T2 or T3) PTSD among 4,612 soldiers with data at all waves and no record of stimulant medication treatment during the study. To evaluate specificity of the ADHDâ PTSD association, we examined associations among predeployment ADHD, postdeployment major depressive episode (MDE), generalized anxiety disorder (GAD), and suicidal ideation. Weighted prevalence of ADHD predeployment was 6.1% (SE = 0.4%). Adjusting for other risk factors, predeployment ADHD was associated with risk of postdeployment PTSD, adjusted odds ratio (AOR) = 2.13, 95% CI [1.51, 3.00], p < .001, including incidence among soldiers with no predeployment history of PTSD, AOR = 2.50, 95% CI [1.69, 3.69], p < .001. ADHD was associated with postdeployment MDE, AOR = 2.80, 95% CI [2.01, 3.91], p < .001, and GAD, AOR = 3.04, 95% CI [2.10, 4.42], p < .001, but not suicidal ideation. Recognition of associations between predeployment ADHD and postdeployment PTSD, MDE, and GAD may inform targeted prevention efforts. Future research should examine whether treatment of ADHD is protective against PTSD and related disorders in traumaâ exposed individuals.ResumenSpanish Abstracts by Asociación Chilena de Estrés Traumático (ACET)El trastorno de déficit atencional con hiperactividad y el riesgo del trastorno de estrés postraumático y trastornos relacionados: Una evaluación longitudinal prospectiva en soldados del ejército estadounidenseTDAH Y RIESGO DE TEPT EN SOLDADOS DEL EJà RCITO DE EE.UU.Se han observado asociaciones transversales entre el trastorno por déficit de atención con hiperactividad (TDAH) y el trastorno por estrés postraumático (TEPT), pero faltan estudios longitudinales que evalúen esta asociación. Este estudio prospectivo evaluó la asociación entre el TDAH previo al despliegue y el TEPT posterior al despliegue entre los soldados del Ejército de Estados Unidos. Los soldados desplegados en Afganistán fueron encuestados antes del despliegue (T0) y aproximadamente 1 mes (T1), 3 meses (T2), y 9 meses (T3) después de su regreso del despliegue. Se realizó una regresión logística para estimar la asociación entre el TDAH previo al despliegue y el TEPT posterior al despliegue (T2 o T3) en 4.612 soldados con datos en todas las etapas y sin registro de tratamiento con medicamentos estimulantes durante el estudio. Para evaluar la especificidad de la asociación TDAHâ TEPT, examinamos las asociaciones entre el TDAH previo al despliegue, el episodio depresivo mayor posterior al despliegue (EDM), el trastorno de ansiedad generalizada (TAG), y la ideación suicida. La prevalencia ponderada del TDAH previo al despliegue fue de 6.1% (SE = 0.4%). Al controlar los otros factores de riesgo, el TDAH previo al despliegue se asoció con el riesgo de TEPT posterior al despliegue, odds ratio ajustado (AOR en su sigla en inglés) = 2.13, IC del 95% [1.51, 3.00], p <.001, incluida la incidencia entre soldados sin historial previo al despliegue de TEPT, AOR = 2.50, IC del 95% [1.69, 3.69], p <.001. El TDAH se asoció con el EDM posterior al despliegue, AOR = 2.80, IC del 95% [2.01, 3.91], p <.001, y TAG, AOR = 3.04, IC del 95% [2.10, 4.42], p <.001, pero no con ideación suicida. El reconocimiento de las asociaciones entre el TDAH previo al despliegue y el TEPT, el EDM, y el TAG posterior al despliegue puede informar los esfuerzos de prevención específicos. Las investigaciones futuras deberían examinar si el tratamiento del TDAH protege contra el TEPT y los trastornos relacionados en personas expuestas a trauma.æ ½è±¡Traditional and Simplified Chinese Abstracts by the Asian Society for Traumatic Stress Studies (AsianSTSS)ç°¡é« å ç¹ é« ä¸­æ æ ®è¦ ç ±äº æ´²å µå ·å¿ ç ç  ç©¶å­¸æ 翻譯Attention Deficit Hyperactivity Disorder and Risk of Posttraumatic Stress and Related Disorders: A Prospective Longitudinal Evaluation in US Army SoldiersTraditional Chineseæ¨ é¡ : å° æ³¨å ä¸ è¶³æ é åº¦æ´»èº ç è æ £å µå ·å¾ å£ å ç å ç ¸é ç ¾ç ç é¢¨é ª:å° ç¾ å è» äººé ²è¡ ç å ç »ç¸±è²«ç  ç©¶æ ®è¦ : é å¾ ä¸ ç ´æ ç  ç©¶æª¢è¦ å° æ³¨å ä¸ è¶³æ é åº¦æ´»èº ç (ADHD)è å µå ·å¾ å£ å ç (PTSD)ä¹ é ç æ©«æ ·æ §é é £, å ¯æ ¯, æ å ä» æ¬ ç¼ºæª¢è¦ å ©è é é £ç ç¸±è²«ç  ç©¶ã æ ¬å ç »ç  ç©¶æ ¨å ¨é é ç¾ è» æ¨£æ ¬, è© ä¼°æ å½¹å ADHDè· æ å½¹å¾ PTSDç é é £ã æ¨£æ ¬ç ºå å¾ é ¿å¯ æ± æ å½¹ç è» äºº, å ¨æ å½¹å (T0)å å® æ æ å½¹å¾ ç´ 1å æ (T1)ã 3å æ (T2)å 9å æ (T3)æ ¥å èª¿æ ¥ã æ å 以é 輯迴歸å æ å æ æ 波段ç æ ¸æ , ä¼°è¨ 4,612å è» äººæ å½¹å ADHDè· æ å½¹å¾ (T2 æ T3)PTSDç é é £ã ç  ç©¶ä¸­, æ¨£æ ¬ä¸¦ç ¡æ ç ¨è å¥®è ¥ç ©ã ç ºäº è§£ADHDâ PTSDç ç ¹æ® é é £, æ å æª¢è¦ ä»¥ä¸ é  ç ®ä¹ é ç é é £:æ å½¹å ADHDã å® æ æ å½¹å¾ ç å ´é æ é¬±ç¯ æ®µ(MDE)ã å»£æ³ æ §ç ¦æ ®ç (GAD)ã è ªæ®ºæ 念ã æ å½¹å ADHDæ ®é åº¦ç º6.1% (SE = 0.4%)ã å° å ¶ä» é¢¨é ªå  ç´ ä½ èª¿ç¯ å¾ , æ å½¹å ADHDè· æ å½¹å¾ æ £PTSDç é¢¨é ªæ æ é é £(å·²èª¿ç¯ å ç® æ¯ (AOR) = 2.13, 95% CI [1.51, 3.00], p < .001), ç ¶ä¸­å æ ¬æ å½¹å ä¸¦ç ¡PTSDç è» äºº(AOR = 2.50, 95% CI [1.69, 3.69], p < .001)ã ADHDè· å® æ æ å½¹å¾ æ £MDEç (AOR = 2.80, 95% CI [2.01, 3.91], p < .001)å GAD(AOR = 3.04, 95% CI [2.10, 4.42] p < .001)é ½æ é , ä½ è· è ªæ®ºæ å¿µç ¡é ã äº è§£æ å½¹å ADHDè· æ å½¹å¾ PTSDã MDEå GADç é é £, å ¯è ½æ å ©ç ¼å± é å° æ §ç é  é ²å·¥ä½ ã æ ªä¾ ç  ç©¶æ æª¢è¦ å° å å µäººå£«æ ä¾ ADHDæ²»ç , æ ¯å ¦å° å ¶PTSDå ç ¸é ç ¾ç æ ä¿ è­·æ æ ã Simplified Chineseæ  é¢ : ä¸ æ³¨å ä¸ è¶³æ è¿ åº¦æ´»è· ç ä¸ æ £å 伤å å å ç å ç ¸å ³ç ¾ç ç é£ é ©:å¯¹ç¾ å ½å äººè¿ è¡ ç å ç »çºµè´¯ç  ç©¶æ ®è¦ : è¿ å¾ ä¸ ç ´æ ç  ç©¶æ£ è§ ä¸ æ³¨å ä¸ è¶³æ è¿ åº¦æ´»è· ç (ADHD)ä¸ å 伤å å å ç (PTSD)ä¹ é ´ç æ¨ªæ ­æ §å ³è¿ , å ¯æ ¯, æ ä»¬ä» æ¬ ç¼ºæ£ è§ ä¸¤è å ³è¿ ç çºµè´¯ç  ç©¶ã æ ¬å ç »ç  ç©¶æ ¨å ¨é è¿ ç¾ å æ ·æ ¬, è¯ ä¼°æ å½¹å ADHDè· æ å½¹å PTSDç å ³è¿ ã æ ·æ ¬ä¸ºå å¾ é ¿å¯ æ± æ å½¹ç å 人, å ¨æ å½¹å (T0)å å® æ æ å½¹å 约1个æ (T1)ã 3个æ (T2)å 9个æ (T3)æ ¥å è° æ ¥ã æ ä»¬ä»¥é »è¾ å å½ å æ å æ æ 波段ç æ °æ ®, 估计4,612å å 人æ å½¹å ADHDè· æ å½¹å (T2 æ T3)PTSDç å ³è¿ ã ç  ç©¶ä¸­, æ ·æ ¬å¹¶æ  æ ç ¨å ´å¥ è ¯ç ©ã ä¸ºäº è§£ADHDâ PTSDç ç ¹æ® å ³è¿ , æ ä»¬æ£ è§ ä»¥ä¸ é¡¹ç ®ä¹ é ´ç å ³è¿ :æ å½¹å ADHDã å® æ æ å½¹å ç 严é æ é è 段(MDE)ã å¹¿æ³ æ §ç ¦è ç (GAD)ã è ªæ æ 念ã æ å½¹å ADHDæ ®é 度为6.1% (SE = 0.4%)ã å¯¹å ¶ä» é£ é ©å  ç´ ä½ è° è å , æ å½¹å ADHDè· æ å½¹å æ £PTSDç é£ é ©æ æ å ³è¿ (å·²è° è è ç® æ¯ (AOR) = 2.13, 95% CI [1.51, 3.00], p < .001), å½ ä¸­å æ ¬æ å½¹å å¹¶æ  PTSDç å 人(AOR = 2.50, 95% CI [1.69, 3.69], p < .001)ã ADHDè· å® æ æ å½¹å æ £MDEç (AOR = 2.80, 95% CI [2.01, 3.91], p < .001)å GAD(AOR = 3.04, 95% CI [2.10, 4.42] p < .001)é ½æ å ³, ä½ è· è ªæ æ å¿µæ  å ³ã äº è§£æ å½¹å ADHDè· æ å½¹å PTSDã MDEå GADç å ³è¿ , å ¯è ½æ å ©å å± é å¯¹æ §ç é¢ é ²å·¥ä½ ã æ ªæ ¥ç  ç©¶åº æ£ è§ å¯¹å å 人士æ ä¾ ADHDæ²»ç , æ ¯å ¦å¯¹å ¶PTSDå ç ¸å ³ç ¾ç æ ä¿ æ ¤æ åº ãPeer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/146971/1/jts22347_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146971/2/jts22347.pd

Diverse therapeutic developments for post-traumatic stress disorder (PTSD) indicate common mechanisms of memory modulation

Post-traumatic stress disorder (PTSD), characterized by abnormally persistent and distressing memories, is a chronic debilitating condition in need of new treatment options. Current treatment guidelines recommend psychotherapy as first line management with only two drugs, sertraline and paroxetine, approved by U.S. Food and Drug Administration (FDA) for treatment of PTSD. These drugs have limited efficacy as they only reduce symptoms related to depression and anxietywithout producing permanent remission. PTSD remains a significant public health problem with high morbidity and mortality requiring major advances in therapeutics. Early evidence has emerged for the beneficial effects of psychedelics particularly in combination with psychotherapy for management of PTSD, including psilocybin,MDMA, LSD, cannabinoids, ayahuasca and ketamine. MDMA and psilocybin reduce barrier to therapy by increasing trust between therapist and patient, thus allowing for modification of trauma related memories. Furthermore, research into the memory reconsolidation mechanisms has allowed for identification of various pharmacological targets to disrupt abnormally persistent memories. A number of preclinical and clinical studies have investigated novel and re-purposed pharmacological agents to disrupt fear memory in PTSD. Novel therapeutic approaches like neuropeptide Y, oxytocin, cannabinoids and neuroactive steroids have also shown potential for PTSD treatment. Here,we focus on the role of fear memory in the pathophysiology of PTSD and propose that many of these newtherapeutic strategies produce benefits through the effect on fear memory. Evaluation of recent research findings suggests that while a number of drugs have shown promising results in preclinical studies and pilot clinical trials, the evidence from large scale clinical trials would be needed for these drugs to be incorporated in clinical practice

Approximating A Dsm‐5 Diagnosis Of Ptsd Using Dsm‐Iv Criteria

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/111929/1/da22364.pd

Trends in mental illness and suicidality after Hurricane Katrina

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/58324/1/kessler_trends in mental illness_2008.pd