Comorbid Major Depressive Disorder in Schizophrenia: A Systematic Review and Meta-Analysis.
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SUBMITTER: Etchecopar-Etchart D
PROVIDER: S-EPMC8451068 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:IntroductionThe kynurenine pathway has been attracting attention as a relevant pathway in schizophrenia (SZ), bipolar disorder (BD), and major depressive disorder (MDD). We conducted a systematic review and meta-analysis of the kynurenine pathway metabolites from cerebrospinal fluid (CSF) samples in SZ, BD, and MDD.MethodsPubMed and Scopus databases were systematically searched to identify peer-reviewed case-control studies until April 2022 that assessed kynurenine metabolites, namely, tryptophan (TRP), kynurenine (KYN), kynurenic acid (KA), quinolinic acid (QA), and 3- hydroxykynurenine (3-HK) in SZ, BD, or MDD subjects compared with healthy controls (HC). The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were followed. The random effects model method was selected when comparing the standardized mean differences (SMD) between two groups.ResultsThere were 23 articles that met the inclusion criteria (k=8, k=8, k=11, for SZ, BD, and MDD, respectively). In SZ, KA levels were increased [SMD=2.64, confidence interval (CI) =1.16 to 4.13, p=0.0005, I2=96%, k=6, n=384 subjects]. TRP (k=5) and KYN (k=4) did not differ significantly. In BD, TRP levels (k=7) did not differ significantly. The level of KA was increased in MDD (k=2), but the small number of studies made not possible for statistical significance evaluation. Finally, in MDD, although some studies tended to have an increased level of KYN in those with remission versus decreased levels in those with current depression, no significant difference was found in any of the kynurenine metabolite levels. Similarly, there was an increased level of QA (k=2) but the number of studies (k= 2) was small.ConclusionKA, which has possibly neuroprotective effects, is increased in SZ. QA, which has neurotoxic effects, may be increased in MDD. There were no alterations in BD. There may be alterations in this pathway based on population characteristics and mood states. Future studies should explore the utility of these metabolites as biomarkers.
| S-EPMC10668321 | biostudies-literature
Project description:Leading biological hypotheses propose that biological changes may underlie major depressive disorder onset and relapse/recurrence. Here, we investigate if there is prospective evidence for biomarkers derived from leading theories. We focus on neuroimaging, gastrointestinal factors, immunology, neurotrophic factors, neurotransmitters, hormones, and oxidative stress. Searches were performed in Pubmed, Embase and PsychInfo for articles published up to 06/2019. References and citations of included articles were screened to identify additional articles. Inclusion criteria were having an MDD diagnosis as outcome, a biomarker as predictor, and prospective design search terms were formulated accordingly. PRISMA guidelines were applied. Meta-analyses were performed using a random effect model when three or more comparable studies were identified, using a random effect model. Our search resulted in 67,464 articles, of which 75 prospective articles were identified on: Neuroimaging (N = 24), Gastrointestinal factors (N = 1), Immunology (N = 8), Neurotrophic (N = 2), Neurotransmitters (N = 1), Hormones (N = 39), Oxidative stress (N = 1). Meta-analyses on brain volumes and immunology markers were not significant. Only cortisol (N = 19, OR = 1.294, p = 0.024) showed a predictive effect on onset/relapse/recurrence of MDD, but not on time until MDD onset/relapse/recurrence. However, this effect disappeared when studies including participants with a baseline clinical diagnosis were removed from the analyses. Other studies were too heterogeneous to compare. Thus, there is a lack of evidence for leading biological theories for onset and maintenance of depression. Only cortisol was identified as potential predictor for MDD, but results are influenced by the disease state. High-quality (prospective) studies on MDD are needed to disentangle the etiology and maintenance of MDD.
| S-EPMC6974432 | biostudies-literature
Project description:EPIC array data were generated from 2 MDD case control cohorts. EWAS was performed in each cohort, followed by meta-analysis between the 2 cohort. Cohort 1: A total of 191 blood samples from 112 patients with MDD was collected up till the interim analysis (wave 1 samples) from an observational clinical study OBSERVEMDD0001 (ClinicalTrials.gov Identifier: NCT02489305) compared to 32 healthy controls; Cohort 2: The MDD cases (N = 359) were drawn from the Molecular Biomarkers of Antidepressant Response study compared to 68 healthy controls.
2022-11-03 | GSE198904 | GEO
Project description:ObjectiveTo provide an estimate of the effect of interventions on comorbid depressive disorder (MDD) or subthreshold depression in type 1 and type 2 diabetes.MethodsSystematic review and meta-analysis. We searched PubMed, PsycINFO, Embase, and the Cochrane Library for randomized controlled trials evaluating the outcome of depression treatments in diabetes and comorbid MDD or subthreshold symptoms published before August 2019 compared to care as usual (CAU), placebo, waiting list (WL), or active comparator treatment as in a comparative effectiveness trial (CET). Primary outcomes were depressive symptom severity and glycemic control. Cohen's d is reported.ResultsForty-three randomized controlled trials (RCTs) were selected, and 32 RCTs comprising 3,543 patients were included in the meta-analysis. Our meta-analysis showed that, compared to CAU, placebo or WL, all interventions showed a significant effect on combined outcome 0,485 (95% CI 0.360; 0.609). All interventions showed a significant effect on depression. Pharmacological treatment, group therapy, psychotherapy, and collaborative care had a significant effect on glycemic control. High baseline depression score was associated with a greater reduction in HbA1 c and depressive outcome. High baseline HbA1 c was associated with a greater reduction in HbA1 c.ConclusionAll treatments are effective for comorbid depression in type 1 diabetes and type 2 diabetes. Over the last decade, new interventions with large effect sizes have been introduced, such as group-based therapy, online treatment, and exercise. Although all interventions were effective for depression, not all treatments were effective for glycemic control. Effective interventions in comorbid depressive disorder may not be as effective in comorbid subthreshold depression. Baseline depression and HbA1 c scores modify the treatment effect. Based on the findings, we provide guidance for treatment depending on patient profile and desired outcome, and discuss possible avenues for further research.
| S-EPMC7882189 | biostudies-literature
Project description:BackgroundAlthough its effect has not been verified, family therapy - such as family psychoeducation (FPE) - is a widely used intervention for treating major depressive disorder (MDD). To our knowledge, no systematic review and meta-analysis exists that examines the effect of FPE on MDD.AimsTo assess evidence on the effectiveness of FPE on depressive symptoms in people with MDD.MethodWe searched several databases - including PubMed, MEDLINE and Web of Science, among others - to identify eligible studies on the topic published up to March 2022. Our criteria included studies on participants with a primary MDD diagnosis and their family members and excluded studies on people with bipolar disorders and other mental illnesses. In the included studies, family members in the control groups did not receive FPE. Participants in both the intervention and control groups received standard treatment. Two researchers independently selected relevant publications, extracted data and evaluated methodological quality using the Cochrane risk of bias assessment tool and GRADE evaluation. The protocol was registered with PROSPERO (no. CRD42020185884).ResultsThe meta-analysis included five studies with 301 patients with MDD and their family members. The effect of FPE on patients' symptom severity, compared with the control condition, at 16 weeks was available for five comparisons of four randomised control trials (RCTs); a final follow-up was available for six comparisons of five RCTs. The meta-analysis showed a statistically significant improvement in patients' symptoms, compared with control, at 16 weeks (s.m.d. = -0.52, 95% CI -1.03 to -0.01) and at a final follow-up (s.m.d. = -0.53, 95% CI -0.98 to -0.08). The meta-analysis on the effect of FPE on family functioning showed a non-significant improvement both at 16 weeks and at final follow-up.ConclusionsFPE had a small but statistically significant effect on depressive symptoms in people with MDD, in both the short and long term. However, according to the GRADE framework, all outcomes are graded very low on certainty; therefore, more high-quality research is needed.
| S-EPMC9380172 | biostudies-literature
Project description:The objective of this study was to assess the benefits and potential risks associated with different physical exercise modalities for managing symptoms in adults with major depressive disorder who were not receiving second-generation antidepressants or cognitive behavioral therapy. A systematic review and meta-analysis of randomized controlled trials (RCTs) were conducted. The search included multiple databases: Medline, Cochrane Central Register of Controlled Trials (CENTRAL), Embase, PsycInfo, Web of Science, Clinical Trials repository, gray literature, and manual search. No language restrictions were applied. Eligible studies involved RCTs of adults with major depressive disorder who were not on antidepressants or receiving psychological therapy, comparing various exercise modalities with second-generation antidepressants or cognitive behavioral therapy, body-mind exercise, or no exercise interventions. Nine RCTs involving 678 adults were analyzed. The pooled results indicated a small clinical effect favoring exercise in reducing depressive symptoms, although the difference was not statistically significant (SMD = 0.27, 95% CI [- 0.58, 0.04], P = 0.09). Subgroup analyses suggested that intervention duration, frequency, intensity, supervision, age, overweight/obesity status, and diagnosis of depression could influence treatment outcomes. A sensitivity analysis was conducted for studies with controls without exercise interventions and a low risk of bias in the domains related to the randomization process and deviations from the intended interventions. The results showed that there are no statistically significant differences when interventions are compared with medication and body-mind exercise (p = 0.12, I2 = 78%). Furthermore, the analysis showed a moderate effect size favoring exercise, but no statistically significant difference between groups (p = 0.05), with high heterogeneity (I2 = 85%). The evidence quality was generally low to very low, and methodological limitations compromised the certainty of the findings. Adverse events associated with exercise were manageable. The study emphasizes the need for well-designed RCTs to provide clearer insights into the potential benefits of exercise in managing major depressive disorder symptoms. Caution is warranted in interpreting these results due to the limitations of the included studies.Systematic review registration: PROSPERO CRD42022356741.
| S-EPMC10425328 | biostudies-literature
Project description:ObjectiveMajor depressive disorder (MDD) has a relapse rate that cannot be ignored and places a tremendous burden on the patient in the prevention and treatment process. Yoga, a combination of physical and mental exercises, is effective and acceptable for the adjunctive treatment of MDD. This study aimed to explore further the evidence of yoga's efficacy for patients with MDD.MethodsPubMed, Embase, Cochrane library, PsycINFO, SinoMed, CNKI, Wanfang, and VIP databases from their inception to 13 October 2022 were searched by a pre-defined search strategy. RCTs of patients with MDD who met diagnostic criteria for yoga treatment were included. RoB2.0 was used to evaluate the quality of the literature. Improvement in depressive symptoms was assessed by the Beck Depression Inventory (BDI), Hamilton Depression Rating Scale (HAMD), or other scales were used as primary outcome indicators, and improvement in anxiety was assessed by the Hamilton Anxiety Scale (HAMA) and State-Trait Anxiety Inventory (STAI) scale as secondary outcome indicators. RR and Cohen's d at 95% CI were used as effect size estimates, and Q and I2 were used to evaluate the size of heterogeneity, with a p-value less than 0.05 indicating statistical significance.ResultsThirty-four RCT studies, including 1,269 patients in the treatment group and 1,072 patients in the control group, 48.4% of whom were women, were included in the study. Compared to the control group, the BDI-II results yielded a moderate effect of yoga on the improvement of depressive symptoms (Cohen's d = -0.60; 95% CI: -1.00 to -0.21; p < 0.01), the HAMD results yielded a moderate improvement of yoga on the severity of depressive symptoms (Cohen's d = -0.64; 95% CI: -0.98 to -0.30; p < 0.01), and the STAI results can be concluded that yoga had a negligible effect on the improvement of the level of anxiety (Cohen's d = -0.26; 95% CI: -0.48 to -0.04; p = 0.02). No adverse events occurred in the yoga group during the treatment.ConclusionYoga can improve depressive symptoms and anxiety in patients with MDD and has a safe and wide patient acceptance.Systematic review registration[https://www.crd.york.ac.uk/prospero/], identifier [PROSPERO, CRD42022373282].
| S-EPMC10077871 | biostudies-literature
Project description:BackgroundHippocampal disturbances are important in the pathophysiology of both schizophrenia and major depressive disorder (MDD). Imaging studies have shown selective volume deficits across hippocampal subfields in both disorders. We aimed to investigate whether these volumetric alterations in hippocampal subfields are shared or divergent across disorders.MethodsWe searched PubMed and Embase from database inception to May 8, 2021. We identified MRI studies in patients with schizophrenia, MDD or both, in which hippocampal subfield volumes were measured. We excluded nonoriginal, animal or postmortem studies, and studies that used other imaging modalities or overlapping data. We conducted a network meta-analysis to estimate and contrast alterations in subfield volumes in the 2 disorders.ResultsWe identified 45 studies that met the initial criteria for systematic review, of which 15 were eligible for network metaanalysis. Compared to healthy controls, patients with schizophrenia had reduced volumes in the bilateral cornu ammonis (CA) 1, granule cell layer of the dentate gyrus, subiculum, parasubiculum, molecular layer, hippocampal tail and hippocampus-amygdala transition area (HATA); in the left CA4 and presubiculum; and in the right fimbria. Patients with MDD had decreased volumes in the left CA3 and CA4 and increased volumes in the right HATA compared to healthy controls. The bilateral parasubiculum and right HATA were smaller in patients with schizophrenia than in patients with MDD.LimitationsWe did not investigate medication effects because of limited information. Study heterogeneity was noteworthy in direct comparisons between patients with MDD and healthy controls.ConclusionThe volumes of multiple hippocampal subfields are selectively altered in patients with schizophrenia and MDD, with overlap and differentiation in subfield alterations across disorders. Rigorous head-to-head studies are needed to validate our findings.
| S-EPMC9911126 | biostudies-literature
Project description:Exposure to traumatic stress is associated with increased risk for posttraumatic stress disorder (PTSD) and alterations of hypothalamic-pituitary-adrenocortical (HPA) function. Research linking traumatic stress with HPA function in PTSD has been inconsistent, however, in part due to (a) the inclusion of trauma-exposed individuals without PTSD (TE) in control groups and (b) a failure to consider comorbid major depressive disorder (MDD) and moderating variables. This meta-analysis of 47 studies (123 effect sizes, N=6008 individuals) revealed that daily cortisol output was lower for PTSD (d=-.36, SE=.15, p=.008) and PTSD+MDD (d=-.65, SE=.25, p=.008) groups relative to no trauma controls (NTC); TE and NTC groups did not differ significantly from each other. Afternoon/evening cortisol was lower in TE (d=-.25, SE=.09, p=.007) and PTSD (d=-.27, SE=.12, p=.021) groups and higher in PTSD+MDD groups (d=.49, SE=.24, p=.041) relative to NTC. Post-DST cortisol levels were lower in PTSD (d=-.40, SE=.12, p<.001), PTSD+MDD (d=-.65, SE=.14, p<.001), and TE groups (d=-.53, SE=.14, p<.001) relative to NTC. HPA effect sizes were moderated by age, sex, time since index event, and developmental timing of trauma exposure. These findings suggest that enhanced HPA feedback function may be a marker of trauma-exposure rather than a specific mechanism of vulnerability for PTSD, whereas lower daily cortisol output may be associated with PTSD in particular.
| S-EPMC3340453 | biostudies-literature
Project description:BackgroundThe burden of depressive disorder is large and new treatment approaches are required. Repurposing widely available drugs such as statins may be a time- and cost-effective solution. Statins have anti-inflammatory and anti-oxidant properties which have been shown to be relevant to the pathophysiology of depression. This study assesses the efficacy, acceptability, tolerability, and safety of statins in major depressive disorder.MethodsOur study is an update and extension of a previous meta-analysis published in 2016 by Salagre et al. We performed a systematic review (PubMed/MEDLINE, Cochrane CENTRAL, ISI Web of Science, CINAHL, and ClinicalTrials.gov until the 1st September 2020) and meta-analysis of randomized controlled trials using any statin against placebo or any other statin in the treatment of major depressive disorder. Our primary efficacy outcome measure was the mean value on any standardized scale for depressive symptoms at 8 weeks of treatment. We also calculated outcomes for efficacy, response, and remission at 2, 4, and 12 weeks, as well as acceptability (dropouts for any cause), tolerability (dropouts due to any adverse event), and safety (any adverse event) outcomes at the studies' endpoints. Furthermore, we conducted an exploratory network meta-analysis for the primary efficacy outcome to identify potential differences between statins.ResultsWe retrieved five randomized controlled trials meeting our inclusion criteria: four used a statin in addition to an antidepressant and compared it to placebo plus antidepressant, and one compared two statins alone. and one comparing one statin with another. Statins compared to placebo in addition to antidepressants were efficacious at 8 weeks (N = 255, SMD = -0.48, 95% CI = -0.74 to -0. 22) and 12 weeks (N = 134, SMD = -0.47, 95% CI = -0.89 to -0.05, moderate certainty) with no difference for acceptability, tolerability, and safety (low certainty). An exploratory network meta-analysis suggested that the most lipophilic statins, especially simvastatin, could be more efficacious than less lipophilic or hydrophilic molecules.ConclusionsThis systematic review suggests the efficacy, acceptability, tolerability, and safety of statins in addition to antidepressants in patients with major depressive disorder. Further clinical trials in different settings are required to test this result.Trial rgistrationPROSPERO registration: CRD42020170938.
| S-EPMC8009386 | biostudies-literature