Posts Tagged "major depressive disorder"
Prevalence of lifetime DSM-IV affective disorders among older African Americans, Black Caribbeans, Latinos, Asians and Non-Hispanic White people.
Prevalence of lifetime DSM-IV affective disorders among older African Americans, Black Caribbeans, Latinos, Asians and Non-Hispanic White people.
Int J Geriatr Psychiatry. 2011 Oct 10;
Authors: Woodward AT, Taylor RJ, Bullard KM, Aranda MP, Lincoln KD, Chatters LM
Abstract
OBJECTIVES: The purpose of this study is to estimate lifetime prevalence of seven psychiatric affective disorders for older non-Hispanic White people, African Americans, Caribbean Black people, Latinos, and Asian Americans and examine demographic, socioeconomic, and immigration correlates of those disorders. DESIGN: Data are taken from the older sub-sample of the Collaborative Psychiatric Epidemiology Surveys. Selected measures of lifetime DSM-IV psychiatric disorders were examined (i.e., panic disorder, agoraphobia, social phobia, generalized anxiety disorder, post-traumatic stress disorder, major depressive disorder, and dysthymia). SETTING: Community epidemiologic survey. PARTICIPANTS: Nationally representative sample of adults 55 years and older (n = 3046). MEASUREMENTS: Disorders were assessed using the DSM-IV World Mental Health Composite International Diagnostic Interview. RESULTS: Major depressive disorder and social phobia were the two most prevalent disorders among the seven psychiatric conditions. Overall, non-Hispanic White people and Latinos consistently had higher prevalence rates of disorders, African Americans had lower prevalence of major depression and dysthymia, and Asian Americans were typically less likely to report affective disorders than those of their counterparts. There is variation across groups in the association of demographic, socioeconomic, and immigration variables with disorders. CONCLUSIONS: This study furthers our understanding of the racial and ethnic differences in the prevalence of DSM-IV disorders among older adults and the correlates of those disorders. It highlights the importance of examining both between-group and within-group differences in disorders and the complexity of the mechanisms associated with differences across groups. Findings from this study underscore the need for future research that more clearly delineates subgroup differences and similarities. Copyright © 2011 John Wiley & Sons, Ltd.
PMID: 21987438 [PubMed - as supplied by publisher]
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Abnormal ECG Patterns in Chronic Post-War PTSD Patients: A Pilot Study.
Abnormal ECG Patterns in Chronic Post-War PTSD Patients: A Pilot Study.
Int J Behav Med. 2011 Sep 30;
Authors: Khazaie H, Saidi MR, Sepehry AA, Knight DC, Ahmadi M, Najafi F, Parvizi AA, Samadzadeh S, Tahmasian M
Abstract
BACKGROUND: Posttraumatic stress disorder (PTSD) is a psychiatric syndrome associated with high levels of sympathetic activation of the autonomic nervous system. Individuals diagnosed with PTSD have a high propensity for electrocardiogram (ECG) abnormalities, atrioventricular conductive defects, and cerebrovascular incidents. PURPOSE: The aim of this study was to investigate ECG abnormalities in post-war PTSD patients. METHOD: This pilot study compared patients diagnosed with chronic post-war PTSD (n = 30) to patients diagnosed with major depressive disorder (MDD; n = 24) and healthy controls (n = 20). Following the completion of the Structured Clinical Interview for the DSM (SCID), participants were assessed with a standard 12-lead ECG. RESULTS: ECG abnormalities were observed in 66.7% of PTSD patients and 70.8% of MDD patients. In contrast, only 28.6% of the healthy control group showed ECG abnormalities. Multivariate logistic regression was used to adjust for participants’ sex, smoking rate, education level, disease duration, and marital status. The results indicated that PTSD and MDD patients were more likely to have ECG abnormalities than the normal population (odds ratio for PTSD = 12.7, 95% confidence interval 1.9-83.9; and odds ratio for MDD = 14.9, 95% confidence interval 1.3-170.5). CONCLUSION: PTSD and MDD patients showed elevated rates of ECG abnormalities compared to healthy controls. These findings have important implications for the medical treatment of PTSD and MDD given that both of these patient groups appear to be at increased risk of cardiovascular disorder.
PMID: 21960258 [PubMed - as supplied by publisher]
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Investigating anxiety and depressive-like phenotypes in genetic mouse models of serotonin depletion.
Investigating anxiety and depressive-like phenotypes in genetic mouse models of serotonin depletion.
Neuropharmacology. 2011 Sep 21;
Authors: Fernandez SP, Gaspar P
Abstract
Emotional disorders such as depression, panic attacks, generalized anxiety, phobias and post-traumatic stress have been associated to decreased serotonin (5-HT) function, based on the positive effects of treatments that enhance 5-HT neurotransmission. However, it has been difficult to establish a primary role for 5-HT deficiency in these diseases, making preclinical models particularly useful. Over the last ten years a variety of genetic mouse models of 5-HT depletion have been produced, complementing previous pharmacologically-based models. Initial models hindered the differentiation of the raphe 5-HT neurons, while more recently produced models suppressed 5-HT production or incapacitated 5-HT vesicular packaging and release in normally developed raphe neurons. Here, we provide an overview of 11 genetic strains with lowered serotonin transmission and summarize the available behavioural investigations concerning their anxiety and depression phenotypes. Although these studies are still ongoing, some common anxiety-related traits and behavioural phenotypes have emerged. Most studies have associated lowered 5-HT levels with decreased innate anxiety to novelty and heightened fear responses to conditioned aversive cues. This complex phenotype is in general agreement with the proposed dual function of 5-HT in modulating different defensive behaviours. Surprisingly, the depressive-like behaviours have been less studied and, so far, did not yield a consistent phenotype in standard tests, and future studies should be conducted using more ethological relevant models to conclude on the causal role of 5-HT depletion in depression. This review also describes the differences in level and regional distribution of 5-HT depletion among the available mouse models, which could contribute to the diverse phenotypes observed. This article is part of a Special Issue entitled ‘Anxiety and Depression‘.
PMID: 21945798 [PubMed - as supplied by publisher]
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The neurogenesis hypothesis of affective and anxiety disorders: Are we mistaking the scaffolding for the building?
The neurogenesis hypothesis of affective and anxiety disorders: Are we mistaking the scaffolding for the building?
Neuropharmacology. 2011 Sep 19;
Authors: Petrik D, Lagace DC, Eisch AJ
Abstract
Hypotheses are scaffoldings erected in front of a building and then dismantled when the building is finished. They are indispensable for the workman; but you mustn’t mistake the scaffolding for the building. Johann Wolfgang von Goethe. The neurogenesis hypothesis of affective disorders – in its simplest form – postulates that the generation of neurons in the postnatal hippocampal dentate gyrus is involved in the etiology and treatment efficacy of major depressive disorder (MDD). The hypothesis was established in the 1990s but was built on a broad foundation of earlier research on the hippocampus, serotonin and MDD. It has gone through several growth phases fueled by discoveries both correlative and causative in nature. Recently, the hypothesis has also been broadened to also include potential relevance for anxiety disorders, like post-traumatic stress disorder (PTSD). As any hypothesis should be, it has been tested and challenged, sometimes vigorously. Here we review the current standing of the neurogenesis hypothesis of affective and anxiety disorders, noting in particular how a central postulate – that decreased neurogenesis results in depression or anxiety – has, in general, been rejected. We also review the controversies on whether treatments for these disorders, like antidepressants, rely on intact neurogenesis for their efficacy, and the existence of neurogenesis-dependent and -independent effects of antidepressants. In addition, we review the implications that the hypothesis has for the response to stress, PTSD, and the neurobiology of resilience, and highlight our own work showing that adult-generated neurons are functionally important for the behavioral response to social stress. We conclude by emphasizing how advancements in transgenic mouse technology, rodent behavioral analyses, and our understanding of the neurogenesis process will allow us to refine our conclusions and perform ever more specific experiments. Such scrutiny is critical, since if we “mistake the scaffolding for the building” we could overlook opportunities for translational impact in the clinic. This article is part of a special Issue entitled ‘Anxiety and Depression‘.
PMID: 21945290 [PubMed - as supplied by publisher]
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