scholarly journals A Prospective 12-Year Study of Subsyndromal and Syndromal Depressive Symptoms in Unipolar Major Depressive Disorders

1998 ◽  
Vol 55 (8) ◽  
pp. 694 ◽  
Author(s):  
Lewis L. Judd ◽  
Hagop S. Akiskal ◽  
Jack D. Maser ◽  
Pamela J. Zeller ◽  
Jean Endicott ◽  
...  
Keyword(s):  
Depressive Symptoms ◽  
Depressive Disorders ◽  
Major Depressive ◽  
Major Depressive Disorders

scholarly journals Systematic review and meta-analysis of the prevalence of depressive symptoms, dysthymia and major depressive disorders among homeless people

BMJ Open ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. e040061
Author(s):  
Getinet Ayano ◽  
Asmare Belete ◽  
Bereket Duko ◽  
Light Tsegay ◽  
Berihun Assefa Dachew
Keyword(s):  
Systematic Review ◽  
Depressive Symptoms ◽  
Depressive Disorders ◽  
Meta Analysis ◽  
Random Effect ◽  
Homeless People ◽  
Sensitivity Analyses ◽  
Prevalence Rates ◽  
Major Depressive ◽  
Major Depressive Disorders

ObjectivesTo assess the global prevalence estimates of depressive symptoms, dysthymia and major depressive disorders (MDDs) among homeless people.DesignSystematic review and meta-analysis.Data sourcesDatabases including PubMed, Scopus and Web of Science were systematically searched up to February 2020 to identify relevant studies that have reported data on the prevalence of depressive symptoms, dysthymia and MDDs among homeless people.Eligibility criteriaOriginal epidemiological studies written in English that addressed the prevalence of depressive problems among homeless people.Data extraction and synthesisA random-effect meta-analysis was performed to pool the prevalence estimated from individual studies. Subgroup and sensitivity analyses were employed to compare the prevalence across the groups as well as to identify the source of heterogeneities. The Joanna Briggs Institute’s quality assessment checklist was used to measure the study quality. Cochran’s Q and the I2 test were used to assess heterogeneity between the studies.ResultsForty publications, including 17 215 participants, were included in the final analysis. This meta-analysis demonstrated considerably higher prevalence rates of depressive symptoms 46.72% (95% CI 37.77% to 55.90%), dysthymia 8.25% (95% CI 4.79% to 11.86%), as well as MDDs 26.24% (95% CI 21.02% to 32.22%) among homeless people. Our subgroup analysis showed that the prevalence of depressive symptoms was high among younger homeless people (<25 years of age), whereas the prevalence of MDD was high among older homeless people (>50 years of age) when compared with adults (25–50 years).ConclusionThis review showed that nearly half, one-fourth and one-tenth of homeless people are suffering from depressive symptoms, dysthymia and MDDs, respectively, which are notably higher than the reported prevalence rates in the general population. The findings suggest the need for appropriate mental health prevention and treatment strategies for this population group.

scholarly journals Genetic correlations between pain phenotypes and depression and neuroticism

2019 ◽  
Vol 28 (3) ◽  
pp. 358-366 ◽  
Author(s):  
Weihua Meng ◽  
Mark J. Adams ◽  
Parminder Reel ◽  
Aravind Rajendrakumar ◽  
Yu Huang ◽  
...  
Keyword(s):  
Depressive Symptoms ◽  
Depressive Disorders ◽  
Genetic Correlations ◽  
The Body ◽  
Uk Biobank ◽  
Major Depressive ◽  
Genetic Mechanisms ◽  
Major Depressive Disorders ◽  
The Uk ◽  
Shared Genetic

Abstract Correlations between pain phenotypes and psychiatric traits such as depression and the personality trait of neuroticism are not fully understood. In this study, we estimated the genetic correlations of eight pain phenotypes (defined by the UK Biobank, n = 151,922–226,683) with depressive symptoms, major depressive disorders and neuroticism using the the cross-trait linkage disequilibrium score regression (LDSC) method integrated in the LD Hub. We also used the LDSC software to calculate the genetic correlations among pain phenotypes. All pain phenotypes, except hip pain and knee pain, had significant and positive genetic correlations with depressive symptoms, major depressive disorders and neuroticism. All pain phenotypes were heritable, with pain all over the body showing the highest heritability (h2 = 0.31, standard error = 0.072). Many pain phenotypes had positive and significant genetic correlations with each other indicating shared genetic mechanisms. Our results suggest that pain, neuroticism and depression share partially overlapping genetic risk factors.

scholarly journals Ramadan Fasting Improves Body Composition without Exacerbating Depression in Males with Diagnosed Major Depressive Disorders

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2718
Author(s):  
Haitham Jahrami ◽  
Ahmed S. BaHammam ◽  
Eman Ahmed Haji ◽  
Nicola L. Bragazzi ◽  
Ihab Rakha ◽  
...  
Keyword(s):  
Body Composition ◽  
Depressive Symptoms ◽  
Body Mass ◽  
Depressive Disorders ◽  
Depressive Symptomatology ◽  
Intermittent Fasting ◽  
Adult Males ◽  
Major Depressive ◽  
Ramadan Fasting ◽  
Major Depressive Disorders

Background: Ramadan fasting (RF) is a form of intermittent fasting that generally improves body composition and related metabolic profiles. Whether RF exacerbates depressive symptomatology in individuals diagnosed with major depressive disorder (MDD) is undetermined. Methods: 100 men, who lived in Bahrain and were between the ages of 18 and 64 years with an established diagnosis of MDD, participated in this 4-week study. Based on preference, participants were assigned to a fasting group (FG, n = 50) and a non-fasting group (NFG, n = 50). The FG engaged in fasting from 03:40 to 18:10 (dawn and dusk timings). Changes in depressive symptoms, body mass, body composition, and components of metabolic syndrome were measured. Results: There were no significant changes in depressive symptoms within the FG vs. NFG after controlling for baseline covariates: mean difference 0.49 (SE = 0.63), p = 0.43. No adverse effects were reported in either group. The FG experienced significant reductions in body mass, 1.87 kg, p = 0.001; body mass index, 0.69 kg/m2, p = 0.001; body fat, 0.87%, p = 0.001; body surface area, 0.03 m2, p = 0.001; and lean mass, 0.77 kg, p = 0.001. Conclusions: RF did not negatively affect depressive symptoms and improved body composition, suggesting short-term intermittent fasting may be a safe dietary practice for adult males with MDD.

scholarly journals Genetic correlations between pain phenotypes and depression and neuroticism

2018 ◽  
Author(s):  
Weihua Meng ◽  
Mark J Adams ◽  
Ian J Deary ◽  
Colin NA Palmer ◽  
Andrew M McIntosh ◽  
...  
Keyword(s):  
Depressive Symptoms ◽  
Knee Pain ◽  
Depressive Disorders ◽  
Genetic Correlations ◽  
Hip Pain ◽  
The Body ◽  
Major Depressive ◽  
Major Depressive Disorders ◽  
The Uk ◽  
Shared Genetic

AbstractCorrelations between pain phenotypes and psychiatric traits such as depression and the personality trait of neuroticism are not fully understood. The purpose of this study was to identify whether eight pain phenotypes, depressive symptoms, major depressive disorders, and neuroticism are correlated for genetic reasons. Eight pain phenotypes were defined by a specific pain-related question in the UK Biobank questionnaire. First we generated genome-wide association summary statistics on each pain phenotype, and estimated the common SNP-based heritability of each trait using GCTA. We then estimated the genetic correlation of each pain phenotype with depressive symptoms, major depressive disorders and neuroticism using the the cross-trait linkage disequilibrium score regression (LDSC) method integrated in the LD Hub. Third, we used the LDSC software to calculate genetic correlations among pain phenotypes. All pain phenotypes were heritable, with pain all over the body showing the highest heritability (h2=0.31, standard error=0.072). All pain phenotypes, except hip pain and knee pain, had significant and positive genetic correlations with depressive symptoms, major depressive disorders and neuroticism. The largest genetic correlations occurred between neuroticism and stomach or abdominal pain (rg=0.70, P=2.4 x 10−9). In contrast, hip pain and knee pain showed weaker evidence of shared genetic architecture with these negative emotional traits. In addition, many pain phenotypes had positive and significant genetic correlations with each other indicating shared genetic mechanisms. Pain at a variety of body sites is heritable and genetically correlated with depression and neuroticism. This suggests that pain, neuroticism and depression share partially overlapping genetic risk factors.

scholarly journals The Role of HPA Axis and Allopregnanolone on the Neurobiology of Major Depressive Disorders and PTSD

2021 ◽  
Vol 22 (11) ◽  
pp. 5495
Author(s):  
Felipe Borges Almeida ◽  
Graziano Pinna ◽  
Helena Maria Tannhauser Barros
Keyword(s):  
Hpa Axis ◽  
Depressive Disorders ◽  
Post Traumatic Stress ◽  
Major Depressive ◽  
Physiological Adaptations ◽  
Suppression Test ◽  
Post Traumatic ◽  
Major Depressive Disorders ◽  
Cortisol Release

Under stressful conditions, the hypothalamic-pituitary-adrenal (HPA) axis acts to promote transitory physiological adaptations that are often resolved after the stressful stimulus is no longer present. In addition to corticosteroids (e.g., cortisol), the neurosteroid allopregnanolone (3α,5α-tetrahydroprogesterone, 3α-hydroxy-5α-pregnan-20-one) participates in negative feedback mechanisms that restore homeostasis. Chronic, repeated exposure to stress impairs the responsivity of the HPA axis and dampens allopregnanolone levels, participating in the etiopathology of psychiatric disorders, such as major depressive disorder (MDD) and post-traumatic stress disorder (PTSD). MDD and PTSD patients present abnormalities in the HPA axis regulation, such as altered cortisol levels or failure to suppress cortisol release in the dexamethasone suppression test. Herein, we review the neurophysiological role of allopregnanolone both as a potent and positive GABAergic neuromodulator but also in its capacity of inhibiting the HPA axis. The allopregnanolone function in the mechanisms that recapitulate stress-induced pathophysiology, including MDD and PTSD, and its potential as both a treatment target and as a biomarker for these disorders is discussed.

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