Mapping the Presence of Anxiety Symptoms in Adults With Major Depressive Disorder.
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ABSTRACT:
SUBMITTER: Ge F
PROVIDER: S-EPMC8169985 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BACKGROUND:We used network analyses to examine symptoms that may play a role in the co-occurrence of social anxiety disorder (SAD) and major depressive disorder (MDD). Whereas latent variable models examine relations among latent constructs, network analyses have the advantage of characterizing direct relations among the symptoms themselves. METHOD:We conducted network modeling on symptoms of social anxiety and depression in a clinical sample of 130 women who met criteria for SAD, MDD, both disorders, or had no lifetime history of mental illness. RESULTS:In the resulting network, the core symptoms of social fear and depressed mood appeared at opposite ends of the network and were weakly related; so-called "bridges" between these symptoms appeared to occur via intervening variables. In particular, the worthless variable appeared to play a central role in the network. LIMITATIONS:Because our data were cross-sectional, we are unable to draw conclusions about the direction of these effects or whether these variables are related to each other prospectively. CONCLUSIONS:Continued testing of these pathways using longitudinal data will help facilitate the development of more effective clinical interventions for these disorders.
| S-EPMC6202058 | biostudies-literature
Project description:This study examines the relationships between neuroticism (higher-order vulnerability factor), the cognitive styles of worry, brooding and reflection (second-order vulnerability factors) and symptoms of anxiety and depression in three groups of patients: patients with Generalized Anxiety Disorder (GAD), with Major Depressive Disorder (MDD) and with Mixed Anxiety-Depressive Disorder (MADD). One hundred and thirty four patients completed a battery of questionnaires including measures of neuroticism, worry, rumination (brooding and reflection), anxiety and depression. Multiple mediation analyses indicate that worry may act as a mediating mechanism linking neuroticism and anxiety symptoms in the three diagnostic groups, whereas brooding-rumination may play a mediating role between neuroticism and depressive symptoms in patients with MDD and MADD and, with less certainty, in patients with GAD. Overall, our findings suggest that neuroticism may increase the risk of anxious and depressive symptoms via specific links involving either worry or brooding, respectively, and that both worry and brooding may operate in the three groups examined, irrespectively of whether anxiety or depression are the main emotions or whether they coexist without any clear predominance; consequently, we hypothesize the existence of "specific transdiagnostic" mechanisms.
| S-EPMC4886972 | biostudies-other
Project description:Anxiety symptoms are prevalent in patients with major depressive disorder. A post-hoc analysis of two phase III trials was conducted to evaluate the efficacy of vilazodone on depression-related anxiety. Using the 17-item Hamilton Depression Rating Scale (HAMD17) Anxiety/Somatization subscale, patients were classified as anxious or nonanxious. Improvements in depressive symptoms were based on least squares mean changes in HAMD17 and Montgomery-Asberg Depression Rating Scale total scores. Anxiety symptoms in the anxious subgroup were evaluated using Hamilton Anxiety Rating Scale (HAMA) total and subscale (Psychic Anxiety, Somatic Anxiety) scores, HAMD17 Anxiety/Somatization subscale and item (Psychic Anxiety, Somatic Anxiety) scores, and the Montgomery-Asberg Depression Rating Scale Inner Tension item score. Most of the pooled study population [82.0% (708/863)] was classified with anxious depression. After 8 weeks of treatment, least squares mean differences between vilazodone and placebo for changes in HAMA total and HAMD17 Anxiety/Somatization subscale scores were -1.82 (95% confidence interval -2.81 to -0.83; P<0.001) and -0.75 (95% confidence interval -1.17 to -0.32; P<0.001), respectively. Statistically significant improvements with vilazodone were also found on all other anxiety-related measures, except the HAMA Somatic Anxiety subscale. Vilazodone may be effective in treating patients with major depressive disorder who exhibit somatic and/or psychic symptoms of anxiety.
| S-EPMC4186734 | biostudies-literature
Project description:Lead is a ubiquitous neurotoxicant, and adverse cognitive and behavioral effects are well-documented in children and occupationally exposed adults but not in adults with low environmental exposure.To investigate the association of current blood lead levels with 3 common psychiatric disorders-major depression, panic, and generalized anxiety-in young adults.Cross-sectional epidemiologic survey.Nationally representative sample of US adults.A total of 1987 adults aged 20 to 39 years who responded to the National Health and Nutrition Examination Survey (1999-2004).Twelve-month DSM-IV criteria-based diagnoses of major depressive disorder, panic disorder, and generalized anxiety disorder assessed using the Composite International Diagnostic Interview.The mean (SD) blood lead level was 1.61 (1.72) microg/dL (range, 0.3-37.3 microg/dL) (to convert to micromoles per liter, multiply by 0.0483). Increasing blood lead levels were associated with higher odds of major depression (P = .05 for trend) and panic disorder (P = .02 for trend) but not generalized anxiety disorder (P = .78 for trend) after adjustment for sex, age, race/ethnicity, education status, and poverty to income ratio. Persons with blood lead levels in the highest quintile had 2.3 times the odds of major depressive disorder (95% confidence interval [CI], 1.13-4.75) and 4.9 times the odds of panic disorder (1.32-18.48) as those in the lowest quintile. Cigarette smoking was associated with higher blood lead levels and outcome, but models that excluded current smokers also resulted in significantly increased odds of major depression (P = .03 for trend) and panic disorder (P = .01 for trend) with higher blood lead quintiles.In these young adults with low levels of lead exposure, higher blood lead levels were associated with increased odds of major depression and panic disorders. Exposure to lead at levels generally considered safe could result in adverse mental health outcomes.
| S-EPMC2917196 | biostudies-other
Project description:BACKGROUND:Major depressive disorder (MDD) with concurrent anxiety symptoms may signal a difficult-to-treat patient. Brexpiprazole is a serotonin-dopamine activity modulator: a partial agonist at 5-HT1A and dopamine D2 receptors at similar potency, and an antagonist at 5-HT2A and noradrenaline alpha1B/2C receptors. The objective of this Phase IIIb study was to explore effectiveness, safety, and tolerability of brexpiprazole adjunctive to antidepressant (ADT) monotherapy in patients with MDD and anxiety symptoms (NCT02013531). METHODS:Patients with MDD, Hamilton Anxiety Rating Scale (HAM-A) total score ? 20, and inadequate response to current ADT received open-label brexpiprazole 1-3 mg day-1 (target dose 2 mg day-1) + ADT for 6 weeks. Efficacy endpoints included change from baseline at Week 6 in Montgomery-Åsberg Depression Rating Scale (MADRS) total score, HAM-A total score, and Sheehan Disability Scale (SDS). Safety and tolerability assessments included adverse events (AEs). RESULTS:Of 37 participants enrolled, 32 (86.5%) completed the study. Baseline mean (SD) MADRS total score was 30.1 (5.1); mean HAM-A total score was 26.9 (5.0). Improvements from baseline were observed at Week 6 for least squares mean change in MADRS total score (-19.6, p < .0001 vs. baseline), HAM-A total score (-17.8, p < .0001) and mean (SD) SDS mean score [-3.6 (2.6)]. Brexpiprazole was well tolerated. The most frequent treatment-emergent AEs were increased appetite (13.5%) and diarrhea, dry mouth, and dizziness (all 10.8%). CONCLUSIONS:These open-label results support the anxiolytic effects of adjunctive brexpiprazole in the treatment of patients with MDD.
| S-EPMC5064333 | biostudies-literature
Project description:BackgroundWe investigated the efficacy of electroconvulsive therapy in patients with major depressive disorder and concomitant anxiety symptoms and explored the relationships between depression symptoms and anxiety symptoms during acute electroconvulsive therapy.MethodsMajor depressive disorder inpatients (N = 130) requiring electroconvulsive therapy were recruited for a maximum of 12 treatments each. Depression symptoms, using the core factor subscale derived from the 17-item Hamilton Depression Rating Scale, and anxiety symptoms, using the anxiety/somatization subscale from the Hamilton Depression Rating Scale-17, were assessed before electroconvulsive therapy, after every 3 electroconvulsive therapy treatments, and after the final electroconvulsive therapy. Both core factor subscale and anxiety/somatization subscale scores were converted to T-score units to compare the degrees of changes between depression symptoms and anxiety symptoms after electroconvulsive therapy. The relationships between core factor subscale and anxiety/somatization subscale were analyzed using the cross-lagged longitudinal model during acute electroconvulsive therapy.ResultsA total 116 patients who completed at least the first 3 electroconvulsive therapy treatments were included in the analysis. Reduction of core factor scale T-scores was significantly greater than that of anxiety/somatization subscale T-scores. The model satisfied all indices of goodness-of-fit (chi-square = 30.204, df = 24, P = 0.178, Tucker-Lewis Index = 0.976, Comparative Fit Index = 0.989, Root Mean Square Error of Approximation = 0.047). Core factor subscale changes did not definitely predict subsequent anxiety/somatization subscale changes.ConclusionsElectroconvulsive therapy is effective in the acute treatment of major depressive disorder patients associated with anxiety symptoms. Anxiety symptoms improved less than depression symptoms during acute electroconvulsive therapy. However, earlier reduction in depression symptoms does not definitely drive subsequent relief in anxiety symptoms.
| S-EPMC6822139 | biostudies-literature
Project description:In this paper we examine the nature of automatic cognitive processing in anxiety disorders and Major Depressive Disorder (MDD). Rather than viewing automaticity as a unitary construct, we follow a social cognition perspective (Bargh, 1994) that argues for four theoretically independent features of automaticity: unconscious (processing of emotional stimuli occurs outside awareness), efficient (processing emotional meaning uses minimal attentional resources), unintentional (no goal is needed to engage in processing emotional meaning), and uncontrollable (limited ability to avoid, alter or terminate processing emotional stimuli). Our review of the literature suggests that most anxiety disorders are characterized by uncontrollable, and likely also unconscious and unintentional, biased processing of threat-relevant information. In contrast, MDD is most clearly typified by uncontrollable, but not unconscious or unintentional, processing of negative information. For the anxiety disorders and for MDD, there is no sufficient evidence to draw firm conclusions about efficiency of processing, though early indications are that neither anxiety disorders nor MDD are characterized by this feature. Clinical and theoretical implications of these findings are discussed and directions for future research are offered. In particular, it is clear that paradigms that more directly delineate the different features of automaticity are required to gain a more comprehensive and systematic understanding of the importance of automatic processing in emotion dysregulation.
| S-EPMC3419810 | biostudies-literature
Project description:Background: Major Depressive Disorder (MDD) is a moderately heritable disorder with a high lifetime prevalence. At present, laboratory blood tests to support MDD diagnosis are not available. Methods: We used a classifier approach on blood gene expression profiles of a unique set of non-medicated subjects (MDD patients and controls) to select genes of which expression is predictive for disease status. To reveal blood gene expression changes related to MDD disease, we applied a powerful ex vivo stimulus to the blood, i.e. incubation with lipopolysaccharide (LPS; 10 ng/ml blood). Results: Based on LPS-stimulated blood gene expression using whole-genome microarrays in 42 subjects (primary cohort; 21 MDD patients (mean age 42.3 years), 21 healthy controls (mean age 41.9 years)), we identified a set of genes (CAPRIN1, CLEC4A, KRT23, MLC1, PLSCR1, PROK2, ZBTB16) that serves as a molecular signature of MDD. These findings were validated for the primary cohort using an independent quantitative PCR method (P = 0.007). The difference between depressive patients and controls was confirmed (P = 0.019) in a replication cohort of 13 patients with MDD (mean age 42.8 years) and 14 controls (mean age 45.6 years). The MDD-signature score comprised of expression levels of 7 genes could discriminate depressive patients from controls with sensitivity of 76.9% and specificity of 71.8%. Conclusions: We show for the first time that molecular analysis of stimulated blood cells can be used as an endophenotype for MDD diagnosis, which is a milestone in establishing biomarkers for neuropsychiatric disorders with moderate heritability in general. Our results may provide a new entry point for following and predicting treatment outcome, as well as prediction of severity and recurrence of MDD. In total, 33 MDD patients and 34 healthy controls were analyzed using basal gene expression in whole blood, and gene expression from whole blood that was stimulated with LPS for 5-6 h, using microarrays. Patients were arbitrarily selected from all patients to serve as primary cohort (nMDD = 21 (MDD01-MDD21); nControls = 21 (Con01-Con21)), or replication cohort (nMDD = 12 (MDD22-MDD35); nControls = 13 (Con22-Con37)) using microarrays. This submission does not include Samples CON21_LPS or CON30_LPS.
2011-10-04 | E-GEOD-19738 | biostudies-arrayexpress
Project description:BACKGROUND:The predictors of onset of major depressive disorder (MDD) and generalized anxiety disorder (GAD) are well-characterized. However the factors that predict remission from these conditions are less clear, and the study of this area is further complicated by differing definitions of remission. METHODS:Data come from the National Comorbidity Survey - Replication, and analysis was limited to respondents with a lifetime history of GAD (n=621) or MDD (n=1299) assessed by the Composite International Diagnostic Interview. Predictors of remission included demographic factors, adverse childhood events, family history, and clinical characteristics. Multiple definitions of remission were explored to account for residual symptoms. RESULTS:Half (54.4%) of respondents with MDD and 41.1% of respondents with GAD experienced full remission. Older age and higher socioeconomic status were positively related to remission in a dose-response manner for both disorders. Adverse childhood experiences and family history of anxious/depressive symptoms were negatively associated with remission from MDD. Comorbid GAD was inversely associated with remission from MDD (Odds ratio (OR): 0.62, 95% Confidence interval (CI): 0.44-0.88), but comorbid MDD did not impact remission from GAD (OR: 0.93, 95% CI: 0.64-1.35). With the exception of the influence of comorbidity, these associations were robust across definitions of remission. LIMITATIONS:Cross-sectional analysis and retrospective recall of onset of MDD/GAD. CONCLUSIONS:Many individuals with MDD or GAD will experience full remission. Some predictors appear to have a general association with remission from both disorders, while others are uniquely associated with remission from MDD.
| S-EPMC5515235 | biostudies-literature
Project description:Glycogen synthase kinase-3? (GSK3?) may play an important role in the brain of patients with major depressive disorder (MDD); therefore, we investigated whether the GSK3? gene is involved in the etiology of MDD and whether it affects MDD endophenotypes. Three single-nucleotide polymorphisms (SNPs) (rs6438552, rs7633279, and rs334558) were genotyped in 559 MDD patients and 486 healthy controls. To explore quantitative traits of MDD, we analyzed the association of these SNPs with the factor scores of the 17-item Hamilton Depression Rating Scale (HAMD-17) and the Hamilton Anxiety Rating Scale (HAMA). We also determined the effects of these SNPs on the measurement of the P300 wave. Although no significant association between GSK3? SNPs and MDD was found, some genotypes and haplotypes were associated with anxiety symptoms in MDD. The three SNPs were associated with the HAMA total score and with the HAMD anxiety and somatization factor score (p<0.05). Three-locus haplotype analysis showed the C-T-G carriers to have a strong association with the HAMA total score (p=0.032). Moreover, the P300 latency and amplitude were also associated with GSK3? genotypes. The individuals with the T allele genotype, both in rs6438552 and rs7633279, have a longer P300 latency than those carrying the C/C (p=0.04) and A/A genotype (p=0.013). The individuals with the G/G genotype in rs334558 have a lower amplitude than those carrying the A allele genotype (p=0.007). Our findings show, for the first time, that GSK3? polymorphisms may play an important role in MDD endophenotypes, especially in anxiety symptoms.
| S-EPMC3501115 | biostudies-literature