DSM–III Major Depressive Disorder in the Community

1989 ◽  
Vol 155 (1) ◽  
pp. 48-54 ◽  
Author(s):  
William W. Eaton ◽  
Amy Dryman ◽  
Ann Sorenson ◽  
Allan McCutcheon

The fit of the structure of DSM–III major depressive disorder to data from two large epidemiological surveys is assessed by latent class analysis. The surveys were conducted at the Baltimore and Raleigh–Durham sites of the National Institute of Mental Health (NIMH) Epidemiologic Catchment Area Program. Three classes are required to fit the data, and the third class bears a strong resemblance to major depressive disorder, although it requires slightly more symptoms to be present than DSM–III. The derived structure replicates successfully for Baltimore and Raleigh-Durham, with a prevalence of the major depression category of 0.9% for both sites.

1999 ◽  
Vol 174 (2) ◽  
pp. 112-120 ◽  
Author(s):  
Hartwin S. Sadowski ◽  
Blanca Ugarte ◽  
Israel Kolvin ◽  
Carole E. Kaplan ◽  
Jacqueline Barnes

BackgroundThere is evidence that exposure to social and family disadvantages in childhood are a risk factor for adult depression.AimsTo explore the effects of multiple adversity in early childhood on adult depression, and the relative effects of the different adversities.MethodThis study utilises data from the Newcastle Thousand Family Study. Information on childhood disadvantages was collected when the participants were 5 years old, and information on mental health was gathered when they were 33 years old. Mental health data were scrutinised blind to the evidence of early disadvantage, and best-estimate diagnoses of major depressive disorder were made according to DSM–III–R criteria.ResultsMultiple family disadvantages in childhood substantially increase the risk of suffering a major depressive disorder in adulthood. Such disadvantages include family or marital relationship instability, a combination of poor mothering and poor physical care, and a combination of dependence on social welfare and overcrowding. For females major depression was linked in particular to the quality of parenting in early life.ConclusionsSocial and family (especially multiple family) disadvantages during childhood predispose individuals to an increased risk of major depression in adulthood.


2021 ◽  
Vol 11 (1) ◽  
pp. 8
Author(s):  
Carol S. North ◽  
David Baron

Agreement has not been achieved across symptom factor studies of major depressive disorder, and no studies have identified characteristic postdisaster depressive symptom structures. This study examined the symptom structure of major depression across two databases of 1181 survivors of 11 disasters studied using consistent research methods and full diagnostic assessment, addressing limitations of prior self-report symptom-scale studies. The sample included 808 directly-exposed survivors of 10 disasters assessed 1–6 months post disaster and 373 employees of 8 organizations affected by the September 11, 2001 terrorist attacks assessed nearly 3 years after the attacks. Consistent symptom patterns identifying postdisaster major depression were not found across the 2 databases, and database factor analyses suggested a cohesive grouping of depression symptoms. In conclusion, this study did not find symptom clusters identifying postdisaster major depression to guide the construction and validation of screeners for this disorder. A full diagnostic assessment for identification of postdisaster major depressive disorder remains necessary.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jakub Tomasik ◽  
Sung Yeon Sarah Han ◽  
Giles Barton-Owen ◽  
Dan-Mircea Mirea ◽  
Nayra A. Martin-Key ◽  
...  

AbstractThe vast personal and economic burden of mood disorders is largely caused by their under- and misdiagnosis, which is associated with ineffective treatment and worsening of outcomes. Here, we aimed to develop a diagnostic algorithm, based on an online questionnaire and blood biomarker data, to reduce the misdiagnosis of bipolar disorder (BD) as major depressive disorder (MDD). Individuals with depressive symptoms (Patient Health Questionnaire-9 score ≥5) aged 18–45 years were recruited online. After completing a purpose-built online mental health questionnaire, eligible participants provided dried blood spot samples for biomarker analysis and underwent the World Health Organization World Mental Health Composite International Diagnostic Interview via telephone, to establish their mental health diagnosis. Extreme Gradient Boosting and nested cross-validation were used to train and validate diagnostic models differentiating BD from MDD in participants who self-reported a current MDD diagnosis. Mean test area under the receiver operating characteristic curve (AUROC) for separating participants with BD diagnosed as MDD (N = 126) from those with correct MDD diagnosis (N = 187) was 0.92 (95% CI: 0.86–0.97). Core predictors included elevated mood, grandiosity, talkativeness, recklessness and risky behaviour. Additional validation in participants with no previous mood disorder diagnosis showed AUROCs of 0.89 (0.86–0.91) and 0.90 (0.87–0.91) for separating newly diagnosed BD (N = 98) from MDD (N = 112) and subclinical low mood (N = 120), respectively. Validation in participants with a previous diagnosis of BD (N = 45) demonstrated sensitivity of 0.86 (0.57–0.96). The diagnostic algorithm accurately identified patients with BD in various clinical scenarios, and could help expedite accurate clinical diagnosis and treatment of BD.


2021 ◽  
pp. 000486742199879
Author(s):  
Pavitra Aran ◽  
Andrew J Lewis ◽  
Stuart J Watson ◽  
Thinh Nguyen ◽  
Megan Galbally

Objective: Poorer mother–infant interaction quality has been identified among women with major depression; however, there is a dearth of research examining the impact of bipolar disorder. This study sought to compare mother–infant emotional availability at 6 months postpartum among women with perinatal major depressive disorder, bipolar disorder and no disorder (control). Methods: Data were obtained for 127 mother–infant dyads from an Australian pregnancy cohort. The Structured Clinical Interview for the DSM-5 was used to diagnose major depressive disorder ( n = 60) and bipolar disorder ( n = 12) in early pregnancy (less than 20 weeks) and review diagnosis at 6 months postpartum. Prenatal and postnatal depressive symptoms were measured using the Edinburgh Postnatal Depression Scale, along with self-report psychotropic medication use. Mother and infant’s interaction quality was measured using the Emotional Availability Scales when infants reached 6 months of age. Multivariate analyses of covariance examining the effects of major depressive disorder and bipolar disorder on maternal emotional availability (sensitivity, structuring, non-intrusiveness, non-hostility) and child emotional availability (responsiveness, involvement) were conducted. Results: After controlling for maternal age and postpartum depressive symptoms, perinatal disorder (major depressive disorder, bipolar disorder) accounted for 17% of the variance in maternal and child emotional availability combined. Compared to women with major depressive disorder and their infants, women with bipolar disorder and their infants displayed lower ratings across all maternal and child emotional availability qualities, with the greatest mean difference seen in non-intrusiveness scores. Conclusions: Findings suggest that perinatal bipolar disorder may be associated with additional risk, beyond major depressive disorder alone, to a mother and her offspring’s emotional availability at 6 months postpartum, particularly in maternal intrusiveness.


Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1728
Author(s):  
Dinyadarshini Johnson ◽  
Sivakumar Thurairajasingam ◽  
Vengadesh Letchumanan ◽  
Kok-Gan Chan ◽  
Learn-Han Lee

The field of probiotic has been exponentially expanding over the recent decades with a more therapeutic-centered research. Probiotics mediated microbiota modulation within the microbiota–gut–brain axis (MGBA) have been proven to be beneficial in various health domains through pre-clinical and clinical studies. In the context of mental health, although probiotic research is still in its infancy stage, the promising role and potential of probiotics in various mental disorders demonstrated via in-vivo and in-vitro studies have laid a strong foundation for translating preclinical models to humans. The exploration of the therapeutic role and potential of probiotics in major depressive disorder (MDD) is an extremely noteworthy field of research. The possible etio-pathological mechanisms of depression involving inflammation, neurotransmitters, the hypothalamic–pituitary–adrenal (HPA) axis and epigenetic mechanisms potentially benefit from probiotic intervention. Probiotics, both as an adjunct to antidepressants or a stand-alone intervention, have a beneficial role and potential in mitigating anti-depressive effects, and confers some advantages compared to conventional treatments of depression using anti-depressants.


Author(s):  
Andreas Menke

Major depressive disorder (MDD) is a common, serious and in some cases life‐threatening condition and affects approximately 350 million people globally (Otte et al., 2016). The magnitude of the clinical burden reflects the limited effectiveness of current available therapies. The current prescribed antidepressants are based on modulating monoaminergic neurotransmission, i.e. they improve central availability of serotonin, norepinephrine and dopamine. However, they are associated with a high rate of partial or non-response, delayed response onset and limited duration. Actually more than 50% of the patients fail to respond to their first antidepressant they receive. Therefore there is a need of new treatment approaches targeting other systems than the monoaminergic pathway. One of the most robust findings in biological psychiatry is a dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis in major depression (Holsboer, 2000). Many studies observed an increased production of the corticotropin-releasing hormone (CRH) in the hypothalamus, leading to an increased release of adrenocorticotropic hormone (ACTH) from the pituitary and subsequently to an enhanced production of cortisol in the adrenal cortex. Due to an impaired sensitivity of the glucocorticoid receptor (GR) the negative feedback mechanisms usually restoring homeostasis after a stress triggered cortisol release are not functioning properly (Holsboer, 2000, Pariante and Miller, 2001). However, treatment strategies targeting the GR or the CRH receptors have not been successful for a general patient population. Selecting the right patients for these treatment alternatives may improve therapy outcome, since a dysregulation of the HPA axis affects only 40-60 % of the depressed patients. Thus, patients with a dysregulated HPA axis have first to be identified and then allocated to a specific treatment regime. Tests like the dexamethasone-suppression-test (DST) or the dex-CRH test have been shown to uncover GR sensitivity deficits, but are not routinely applied in the clinical setting. Recently, the dexamethasone-induced gene expression could uncover GR alterations in participants suffering from major depression and job-related exhaustion (Menke et al., 2012, Menke et al., 2013, Menke et al., 2014, Menke et al., 2016). Actually, by applying the dexamethasone-stimulation test we found a GR hyposensitivity in depressed patients (Menke et al., 2012) and a GR hypersensitivity in subjects with job-related exhaustion (Menke et al., 2014). These alterations normalized after clinical recovery (Menke et al., 2014). Interestingly, the dexamethasone-stimulation test also uncovered FKBP5 genotype dependent alterations in FKBP5 mRNA expression in depressed patients and healthy controls (Menke et al., 2013). FKBP5 is a co-chaperone which modulates the sensitivity of the GR (Binder, 2009). In addition, the dexamethasone-stimulation test provided evidence of common genetic variants that modulate the immediate transcriptional response to GR activation in peripheral human blood cells and increase the risk for depression and co-heritable psychiatric disorders (Arloth et al., 2015). In conclusion, the molecular dexamethasone-stimulation test may thus help to characterize subgroups of subjects suffering from stress-related conditions and in the long-run may be helpful to guide treatment regime as well as prevention strategies.   References: Arloth J, Bogdan R, Weber P, Frishman G, Menke A, Wagner KV, Balsevich G, Schmidt MV, Karbalai N, Czamara D, Altmann A, Trumbach D, Wurst W, Mehta D, Uhr M, Klengel T, Erhardt A, Carey CE, Conley ED, Major Depressive Disorder Working Group of the Psychiatric Genomics C, Ruepp A, Muller-Myhsok B, Hariri AR, Binder EB, Major Depressive Disorder Working Group of the Psychiatric Genomics Consortium PGC (2015) Genetic Differences in the Immediate Transcriptome Response to Stress Predict Risk-Related Brain Function and Psychiatric Disorders. Neuron 86:1189-1202. Binder EB (2009) The role of FKBP5, a co-chaperone of the glucocorticoid receptor in the pathogenesis and therapy of affective and anxiety disorders. Psychoneuroendocrinology 34 Suppl 1:S186-195. Holsboer F (2000) The corticosteroid receptor hypothesis of depression. Neuropsychopharmacology 23:477-501. Menke A, Arloth J, Best J, Namendorf C, Gerlach T, Czamara D, Lucae S, Dunlop BW, Crowe TM, Garlow SJ, Nemeroff CB, Ritchie JC, Craighead WE, Mayberg HS, Rex-Haffner M, Binder EB, Uhr M (2016) Time-dependent effects of dexamethasone plasma concentrations on glucocorticoid receptor challenge tests. Psychoneuroendocrinology 69:161-171. Menke A, Arloth J, Gerber M, Rex-Haffner M, Uhr M, Holsboer F, Binder EB, Holsboer-Trachsler E, Beck J (2014) Dexamethasone stimulated gene expression in peripheral blood indicates glucocorticoid-receptor hypersensitivity in job-related exhaustion. Psychoneuroendocrinology 44:35-46. Menke A, Arloth J, Putz B, Weber P, Klengel T, Mehta D, Gonik M, Rex-Haffner M, Rubel J, Uhr M, Lucae S, Deussing JM, Muller-Myhsok B, Holsboer F, Binder EB (2012) Dexamethasone Stimulated Gene Expression in Peripheral Blood is a Sensitive Marker for Glucocorticoid Receptor Resistance in Depressed Patients. Neuropsychopharmacology 37:1455-1464. Menke A, Klengel T, Rubel J, Bruckl T, Pfister H, Lucae S, Uhr M, Holsboer F, Binder EB (2013) Genetic variation in FKBP5 associated with the extent of stress hormone dysregulation in major depression. Genes Brain Behav  12:289-296. Otte C, Gold SM, Penninx BW, Pariante CM, Etkin A, Fava M, Mohr DC, Schatzberg AF (2016) Major depressive disorder. Nature reviews Disease primers 2:16065. Pariante CM, Miller AH (2001) Glucocorticoid receptors in major depression: relevance to pathophysiology and treatment. Biological psychiatry 49:391-404.


1994 ◽  
Vol 165 (3) ◽  
pp. 363-369 ◽  
Author(s):  
Laura Andrade ◽  
William W. Eaton ◽  
Howard Chilcoat

BackgroundThe co-occurrence of panic disorder and major depression in the same individual is common. A question to be answered is whether the comorbid disorder is a distinct one or may resemble one or other disorder. In this paper we examine whether the comorbid disorder is a distinct condition.MethodWe examined the symptom profiles and rates of comorbidity of panic attacks and DIS/DSM–III major depressive disorder in a population-based sample from four sites of the National Institute of Mental Health (NIMH) Epidemiologic Catchment Area Program (n= 12 668).ResultsThe co-occurrence of panic attacks and major depression over the lifetime was 11 times higher than expected by chance (OR = 11.4, 95% CI 9.5 to 13.6). Subjects with both panic and depression had worse symptoms than those who had only one disorder. However, the pattern of symptoms was remarkably similar, after overall severity was taken into account. Depressive symptoms associated with more severe forms of depression (e.g. guilt, suicidal thoughts or attempts, and motor disturbance) were more frequent in the comorbid group.ConclusionsThese findings may indicate a worse severity when the two disorders occur in the same individual.


2021 ◽  
Vol 30 ◽  
Author(s):  
Annelieke M. Roest ◽  
Ymkje Anna de Vries ◽  
Ali Al-Hamzawi ◽  
Jordi Alonso ◽  
Olatunde O. Ayinde ◽  
...  

Abstract Aims Major depressive disorder (MDD) is characterised by a recurrent course and high comorbidity rates. A lifespan perspective may therefore provide important information regarding health outcomes. The aim of the present study is to examine mental disorders that preceded 12-month MDD diagnosis and the impact of these disorders on depression outcomes. Methods Data came from 29 cross-sectional community epidemiological surveys of adults in 27 countries (n = 80 190). The Composite International Diagnostic Interview (CIDI) was used to assess 12-month MDD and lifetime DSM-IV disorders with onset prior to the respondent's age at interview. Disorders were grouped into depressive distress disorders, non-depressive distress disorders, fear disorders and externalising disorders. Depression outcomes included 12-month suicidality, days out of role and impairment in role functioning. Results Among respondents with 12-month MDD, 94.9% (s.e. = 0.4) had at least one prior disorder (including previous MDD), and 64.6% (s.e. = 0.9) had at least one prior, non-MDD disorder. Previous non-depressive distress, fear and externalising disorders, but not depressive distress disorders, predicted higher impairment (OR = 1.4–1.6) and suicidality (OR = 1.5–2.5), after adjustment for sociodemographic variables. Further adjustment for MDD characteristics weakened, but did not eliminate, these associations. Associations were largely driven by current comorbidities, but both remitted and current externalising disorders predicted suicidality among respondents with 12-month MDD. Conclusions These results illustrate the importance of careful psychiatric history taking regarding current anxiety disorders and lifetime externalising disorders in individuals with MDD.


2014 ◽  
Vol 205 (4) ◽  
pp. 268-274 ◽  
Author(s):  
Pim Cuijpers ◽  
Sander L. Koole ◽  
Annemiek van Dijke ◽  
Miquel Roca ◽  
Juan Li ◽  
...  

BackgroundThere is controversy about whether psychotherapies are effective in the treatment of subclinical depression, defined by clinically relevant depressive symptoms in the absence of a major depressive disorder.AimsTo examine whether psychotherapies are effective in reducing depressive symptoms, reduce the risk of developing major depressive disorder and have comparable effects to psychological treatment of major depression.MethodWe conducted a meta-analysis of 18 studies comparing a psychological treatment of subclinical depression with a control group.ResultsThe target groups, therapies and characteristics of the included studies differed considerably from each other, and the quality of many studies was not optimal. Psychotherapies did have a small to moderate effect on depressive symptoms against care as usual at the post-test assessment (g = 0.35, 95% CI 0.23–0.47; NNT = 5, 95% CI 4–8) and significantly reduced the incidence of major depressive episodes at 6 months (RR = 0.61) and possibly at 12 months (RR = 0.74). The effects were significantly smaller than those of psychotherapy for major depressive disorder and could be accounted for by non-specific effects of treatment.ConclusionsPsychotherapy may be effective in the treatment of subclinical depression and reduce the incidence of major depression, but more high-quality research is needed.


Sign in / Sign up

Export Citation Format

Share Document