Disorder- and emotional context-specific neurofunctional alterations during inhibitory control in generalized anxiety and major depressive disorder.
Ontology highlight
ABSTRACT:
SUBMITTER: Liu C
PROVIDER: S-EPMC8060548 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
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: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: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:OBJECTIVE:Experiential avoidance (EA) is a transdiagnostic construct that may underlie the high comorbidity between major depressive disorder (MDD) and generalized anxiety disorder (GAD). This analysis used data from a longitudinal study (conducted September 2010-April 2016) to examine whether adolescent EA varies by MDD and GAD symptomatology trajectory and predicts said trajectories. Longitudinal associations between EA, anxiety, and depression symptoms were also examined. METHODS:Adolescents aged 15 to 20 years (N = 183) were followed for 2 years using a comprehensive assessment battery. Symptom trajectory modeling, using weekly symptom ratings, identified 4 MDD and 4 GAD trajectories that were collapsed to form combined MDD/GAD trajectory groups: Persistent (n = 81), High-Decreasing (n = 44), Normal-Increasing (n = 37), and Minimal (n = 21). Group-based trajectory modeling, analyses of covariance, structural equation modeling, and linear regression analyses were performed. DSM-IV-TR criteria were used for MDD and GAD diagnoses. RESULTS:The Persistent adolescents had higher EA than other groups (P values ? .001), with greater EA stability versus High-Decreasing adolescents (P = .008). EA predicted anxiety and depressive symptoms alike (P values ? .005), which in turn did not predict EA (P values ? .188). EA, at both time points, predicted combined MDD/GAD trajectories after adjustment for depressive and anxiety symptoms and other confounders (P values < .001). CONCLUSIONS:EA appears to be an important predictor of MDD and GAD symptomatology in older adolescents, potentially serving as a treatment target. Findings suggest a possible trait-like nature for EA, perhaps increasing risk for the emergence and persistence of MDD and/or GAD. TRIAL REGISTRATION:ClinicalTrials.gov identifier: NCT02147184?.
| S-EPMC6854672 | biostudies-literature
Project description:BackgroundAbout half of patients with major depressive disorder (MDD) have clinically meaningful levels of anxiety. Greater severity of depressive illness and functional impairment has been reported in patients with high levels of anxiety accompanying depression. The pathogenesis for the comorbidity was still unsure.AimThis study aimed to determine whether there would be molecular link for overlapped pathogenesis between MDD and anxiety disorder.Materials and methodsUsing long noncoding RNA (lncRNA) microarray profiling and reverse transcription polymerase chain reaction, six downregulated lncRNAs and three upregulated lncRNAs had been identified to be the potential biomarkers for MDD and generalized anxiety disorder (GAD), respectively. Then, the lncRNAs were cross-checked in forty MDD patients, forty GAD patients, and forty normal controls.ResultsCompared with normal controls, six downregulated MDD lncRNAs also had a significantly lower expression in GAD (P < 0.01), and there was no significant difference between GAD and MDD (P > 0.05). In addition, three upregulated GAD lncRNAs had no different expression in MDD (P > 0.05), but there was remarkable difference between MDD and GAD (P < 0.01).ConclusionsThese results indicated that lncRNAs in peripheral blood mononuclear cells could be potential molecular link between MDD and GAD, which added new evidence to the overlapped pathogenesis and suggested that anxious depression could be a valid diagnostic subtype of MDD.
| S-EPMC5419018 | biostudies-literature
Project description:To determine longitudinal associations between patterns of comorbid cigarette, alcohol, and marijuana use and Antisocial Personality Disorder (ASPD), Major Depressive Episode (MDE), and Generalized Anxiety Disorder (GAD) in adulthood.A random community-based sample [X? age=36.6 (SD=2.8)] from the Children and Adults in the Community Study, an on-going investigation of substance use and psychiatric disorders. Data were collected at six time waves. Conjoint trajectories of cigarette, alcohol, and marijuana use spanning adolescence to adulthood were determined; multivariable logistic regression analyses assessed associations between trajectory group membership and having ASPD, MDE, or GAD in adulthood.Five conjoint trajectory groups were obtained: HHH (chronic cigarette, alcohol, and marijuana use), DDD (delayed/late-starting cigarette, alcohol, and marijuana use), LML (low/no smoking, moderate alcohol use, occasional marijuana use), HMN (chronic smoking, moderate alcohol use, no marijuana use), and NON (occasional alcohol use only). Compared with members of the NON group, those in the HHH group had significantly greater odds for having ASPD (Adjusted Odds Ratio [AOR]=28.52, 95% Confidence Interval [CI]=9.44-86.17), MDE (AOR=2.67, 95% CI=1.14-6.26), and GAD (AOR=6.39, 95% CI=2.62-15.56). Members of the DDD, LML, and HMN groups had weaker and less consistent associations with the three psychiatric outcomes.In a large, community-based sample, long-term concurrent use of more than one substance was associated with both externalizing and internalizing psychiatric disorders in adulthood. Prevention and treatment programs might target individuals in the community and general clinical populations with comorbid substance use, even if they haven't been identified as having a substance use disorder.
| S-EPMC4955839 | biostudies-literature
Project description:BackgroundTrait anxiety is reliably associated with enhanced neural responses following errors: meta analyses have described how the electrophysiological response to errors known as the Error-Related Negativity (ERN) is increased in anxious individuals, particularly in relation to worry. The ERN has been related to a broader class of control signals, particularly via a common theta band denominator, but it is unknown whether worry relates to these alternative medial frontal metrics. Moreover, it is unclear if increased ERN in anxiety relates to altered cognitive control.MethodsIn this report we examine EEG activities in Generalized Anxiety Disorder (GAD, N=39) and control (CTL: N=52) participants during an executive control task. We leveraged a previously defined theta-band network to examine if an altered control signal in GAD underlies a differential implementation of cognitive control.ResultsGAD and CTL groups were reliably dissociated by both error- and conflict- related neural activity, in both the time and frequency (i.e. theta band) domains. Moreover, we demonstrate that ERN, error-related theta power, and the single trial correlation between theta and response time were unique predictors of GAD status. Overall, we were able to account for nearly 1/4 of the group variance and successfully classify GAD from control participants with 2/3 accuracy.ConclusionsCollectively, these findings suggest that multiple neural metrics of error processing may uniquely distinguish clinical anxiety from healthy individuals, and that mechanisms of control also differ in GAD; finally, these error-related neural measures have the potential to be sensitive and specific bio-signatures of anxiety.
| S-EPMC5580396 | biostudies-literature
Project description:BackgroundRecent studies have investigated the potential of treatments that modify the gut microbiome, such as fecal microbiota transplantation and probiotics, in individuals with psychiatric illnesses.ObjectiveThe aim of this study was to investigate the safety, tolerability, and efficacy of a novel gut microbiome therapeutic, Microbial Ecosystem Therapuetic-2 (MET-2), in people with depression and anxiety.MethodsIn this phase 1, open-label trial, 12 adults diagnosed with major depressive disorder, generalized anxiety disorder, or both were recruited. Over 8 weeks, participants consumed three capsules per day, orally, of an encapsulated microbial therapeutic (MET-2), which contained 40 strains of bacteria that were purified and lab-grown from the stool of a single healthy donor. Participants were assessed biweekly using clinical scales and questionnaires in order to evaluate the safety, efficacy, and tolerability of the therapeutic.ResultsThe therapeutic was found to be generally safe and tolerable, with limited adverse events and side effects and no serious adverse events. Of the 12 individuals included in this study, 9 (75%) responded to treatment (50% improvement in Montgomery-Asberg Depression Rating Scale [MADRS] scores, 7-item Generalized Anxiety Disorder scale [GAD-7] scores, or both, from baseline to the week-8 visit). Over the course of 10 weeks, MET-2 significantly decreased mean MADRS and GAD-7 scores (MADRS: F2.731, 30.05=8.784, P<.001; GAD-7: F2.778, 30.55= 9.638, P<.001). Multiple comparisons with Bonferroni adjustments showed a significant reduction in MADRS scores from baseline (mean 19.00, SD 4.843) to week 6 (mean 11.25, SD 8.001; P=.009), week 8 (mean 8.667, SD 8.732; P=.002), and week 10 (mean 8.250, SD 9.304; P=.006). Multiple comparisons showed a significant reduction in GAD-7 scores from baseline (mean 13.58, SD 4.010) to week 4 (mean 9.167, SD 5.096; P=.03), week 6 (mean 7.667, SD 4.539; P=.004), week 8 (mean 7.333, SD 6.583; P=.03), and week 10 (mean 7.500, SD 6.448; P=.03).ConclusionsThe findings from this study are the first to provide evidence for the role of microbial ecosystem therapy in treating depression and anxiety. However, a double-blind, randomized controlled trial with a larger sample size is needed for more conclusive results.Trial registrationClinicalTrials.gov NCT04052451; https://www.clinicaltrials.gov/ct2/show/NCT04052451.International registered report identifier (irrid)RR2-10.2196/17223.
| S-EPMC8817211 | biostudies-literature
Project description:The pattern of structural brain alterations associated with major depressive disorder (MDD) remains unresolved. This is in part due to small sample sizes of neuroimaging studies resulting in limited statistical power, disease heterogeneity and the complex interactions between clinical characteristics and brain morphology. To address this, we meta-analyzed three-dimensional brain magnetic resonance imaging data from 1728 MDD patients and 7199 controls from 15 research samples worldwide, to identify subcortical brain volumes that robustly discriminate MDD patients from healthy controls. Relative to controls, patients had significantly lower hippocampal volumes (Cohen's d=-0.14, % difference=-1.24). This effect was driven by patients with recurrent MDD (Cohen's d=-0.17, % difference=-1.44), and we detected no differences between first episode patients and controls. Age of onset ?21 was associated with a smaller hippocampus (Cohen's d=-0.20, % difference=-1.85) and a trend toward smaller amygdala (Cohen's d=-0.11, % difference=-1.23) and larger lateral ventricles (Cohen's d=0.12, % difference=5.11). Symptom severity at study inclusion was not associated with any regional brain volumes. Sample characteristics such as mean age, proportion of antidepressant users and proportion of remitted patients, and methodological characteristics did not significantly moderate alterations in brain volumes in MDD. Samples with a higher proportion of antipsychotic medication users showed larger caudate volumes in MDD patients compared with controls. This currently largest worldwide effort to identify subcortical brain alterations showed robust smaller hippocampal volumes in MDD patients, moderated by age of onset and first episode versus recurrent episode status.
| S-EPMC4879183 | biostudies-literature
Project description:Alterations in regional subcortical brain volumes have been investigated as part of the efforts of an international consortium, ENIGMA, to identify reliable neural correlates of major depressive disorder (MDD). Given that subcortical structures are comprised of distinct subfields, we sought to build significantly from prior work by precisely mapping localized MDD-related differences in subcortical regions using shape analysis. In this meta-analysis of subcortical shape from the ENIGMA-MDD working group, we compared 1,781 patients with MDD and 2,953 healthy controls (CTL) on individual measures of shape metrics (thickness and surface area) on the surface of seven bilateral subcortical structures: nucleus accumbens, amygdala, caudate, hippocampus, pallidum, putamen, and thalamus. Harmonized data processing and statistical analyses were conducted locally at each site, and findings were aggregated by meta-analysis. Relative to CTL, patients with adolescent-onset MDD (≤ 21 years) had lower thickness and surface area of the subiculum, cornu ammonis (CA) 1 of the hippocampus and basolateral amygdala (Cohen's d = -0.164 to -0.180). Relative to first-episode MDD, recurrent MDD patients had lower thickness and surface area in the CA1 of the hippocampus and the basolateral amygdala (Cohen's d = -0.173 to -0.184). Our results suggest that previously reported MDD-associated volumetric differences may be localized to specific subfields of these structures that have been shown to be sensitive to the effects of stress, with important implications for mapping treatments to patients based on specific neural targets and key clinical features.
| S-EPMC8675412 | biostudies-literature