Social interaction is a primary aspect of communicating how others judge us. It allows us to update ourselves and our expectations about others. While humans generally exhibit self-related positive biases in their updating behavior, theoretical accounts propose that this biased processing is attenuated, absent, or negatively biased in participants with depressive symptoms. The process of aligning and integrating social evaluative feedback in realistic interaction scenarios that would test this assumption is, however, lacking. We provide an event-related potential (ERP) study that combines neuronal (feedback-related negativity [FRN] and late positive potential [LPP]) and behavioral measures of evaluative feedback processing and updating behavior.

We selected healthy adults (N = 62) with depression scores spanning a range of low to high values, as measured by the Beck Depression Inventory (BDI). Participants received feedback from supposed experts and peer senders, with the feedback being manipulated to be worse, congruent, or better than the participants’ self-ratings.

Participants with higher depression scores exhibited more negative initial self-ratings and developed a more negative feedback expectation across the experiment. In addition, we found that higher depression scores led to more negative updating toward worse expert feedback and less positive updating after better peer feedback. Concerning ERPs, unexpected but not self-incongruent feedback increased the FRN, while both types of incongruence increased the LPP. Finally, BDI scores correlated with LPP amplitudes for all feedback.

The results contribute to a deeper understanding of how individuals process and integrate social evaluative feedback and its relation to depressive symptoms.

Insight into psychosis is a multidimensional construct involving awareness of illness, attribution of symptoms, and perceived need for treatment. Despite extensive research, substantial variability in how insight is conceptualized and measured continues to hinder clinical assessment and cross-study comparisons.

Following Preferred Reporting Items for Systematic Review and Meta-Analysis Protocols guidelines and a registered International Prospective Register of Systematic Reviews protocol (CRD42024558386), we conducted a systematic search across five databases (n = 2,184). Twenty-nine studies met the inclusion criteria, comprising 15 primary scale development papers and 10 independent validation studies. We included instruments explicitly designed to assess insight in schizophrenia-spectrum, and evaluated them using the COnsensus-based Standards for the selection of health Measurement INstruments Risk of Bias checklist. Psychometric domains assessed included content validity, structural validity, construct validity, criterion validity, internal consistency, reliability, responsiveness, and interpretability.

Fifteen distinct insight scales were identified, comprising nine clinician-rated instruments, five self-report tools, and one hybrid format. Most demonstrated adequate content and structural validity, with 11 achieving ‘very good’ reliability ratings. Four scales showed the strongest overall psychometric support. However, responsiveness to clinical change was rarely tested, and cross-cultural validation remained limited. Earlier instruments primarily emphasized clinician-rated illness awareness, whereas more recent tools incorporated cognitive, neurocognitive, and subjective dimensions. Discrepancies between self-report and clinician ratings were common and often clinically meaningful. These findings underscore the need for multidimensional, psychometrically robust, and context-sensitive tools to advance both clinical assessment and research on insight in psychotic disorders.

Psychomotor disturbance has long been observed in major depressive disorder (MDD) and is thought to be a key indicator of illness course. However, dominant methods of measuring psychomotor disturbance, via self-report and clinician ratings, often lack objectivity and may be less sensitive to subtle psychomotor disturbances. Furthermore, the neural mechanisms of psychomotor disturbance in MDD remain unclear.

To address these gaps, we measured psychomotor agitation via a force variability paradigm and collected resting fMRI in 47 individuals with current MDD (cMDD) and 93 individuals with remitted MDD (rMDD). We then characterized whether resting-state cortico-cortical and cortico-subcortical connectivity related to force variability and depressive symptoms.

Behaviorally, individuals with cMDD exhibited greater force variability than rMDD individuals (t(138) = 3.01, p = 0.003, Cohen’s d = 0.25). Furthermore, greater force variability was associated with less visuomotor connectivity (r(130) = −0.23, p = 0.009, 95% CI [−0.38, −0.06]). Visuomotor connectivity was significantly reduced in cMDD relative to rMDD (t(130) = −2.77, p = 0.006, Cohen’s d = −0.24) and mediated the group difference in force variability (ACME β = −0.06, 95% CI [−0.16, −0.01], p = 0.04).

Our findings represent a crucial step toward clarifying the pathophysiology of psychomotor agitation in MDD. Specifically, altered visuomotor functional connectivity emerged as a candidate neural mechanism, highlighting a promising direction for future research on dysfunctional visually guided movements in MDD.

Severe mental disorders (SMDs) impose profound suffering on patients and heavy burdens on family caregivers, often resulting in abusive behaviors. This study aimed to examine the association between psychiatric symptom severity and caregiver abuse, and to assess whether caregiver tobacco dependence moderates this relationship.

A cross-sectional study included 763 patient–caregiver dyads in rural Shandong, China. Psychiatric symptom severity was measured using the 18-item Brief Psychiatric Rating Scale. Caregiver tobacco dependence was assessed using the Fagerström Test for Nicotine Dependence. Patients reported caregivers’ verbal/physical abuse in the past year. Ordered logistic regression and interaction terms tested associations and moderation.

Overall, 25.7% of caregivers engaged in verbal abuse and 14.9% in physical abuse. Psychiatric symptom severity was significantly associated with both verbal (OR = 1.018, 95% CI: 1.010–1.026) and physical abuse (OR = 1.015, 95% CI: 1.005–1.025). Caregivers with moderate to severe tobacco dependence were more likely to commit verbal (OR = 1.851, 95% CI: 1.136–3.016) and physical abuse (OR = 2.292, 95% CI: 1.287–4.079) than non-smokers. Moderate to severe tobacco dependence significantly amplified the association between psychiatric symptom severity and verbal abuse (interaction OR = 1.024, 95% CI: 1.002–1.046), but not physical abuse.

In rural China, greater psychiatric symptom severity among patients with SMDs is associated with increased frequency of both verbal and physical abuse by caregivers, particularly verbal abuse among those with moderate to severe tobacco dependence, underscoring the need for caregiver-targeted psychological support and tobacco cessation interventions.

Alterations in the central and peripheral energy metabolism are increasingly recognized as key pathophysiological processes in psychiatric disorders. We investigated mitochondrial respiration and density linked to cellular energy metabolism and oxidative DNA damage in borderline personality disorder (BPD).

This cross-sectional case–control study compared three groups matched for age and body mass index: women with acute BPD, remitted BPD, and female healthy controls (n = 32, 15, 29). Peripheral blood mononuclear cells were investigated for differences in mitochondrial respiration, density, and markers of oxidative DNA damage.

Participants with acute BPD showed significantly reduced and less efficient mitochondrial ATP production compared to both remitted individuals and controls. Mitochondrial coupling and respiration were inversely associated with oxidative DNA damage, although DNA damage levels did not differ significantly across diagnostic groups. Sensitivity analyses indicated that comorbid major depressive episodes and antidepressant use did not account for the results.

These findings indicate mitochondrial alterations accompany acute symptom severity in BPD and may improve with remission. Unraveling causes and consequences of mitochondrial downregulation and its interplay with DNA maintenance in the context of stress and psychopathology could contribute to novel models and treatment strategies in BPD and related severe psychiatric disorders.

The distinction between passive and active suicidal ideation (SI) and their underlying etiologies remains poorly understood. The Interpersonal Theory of Suicide implicates guilt, loneliness, and hopelessness in these SI subtypes, but there is minimal work testing these relationships in real time, capturing clinically meaningful fluctuations in SI. We conducted the first ecological momentary assessment (EMA) study to distinguish between passive and active SI in adolescents, and the first study to evaluate moment-to-moment etiological factors and mediators of passive and active SI in this age group.

Participants (N = 104) were adolescent psychiatric inpatients (Mage = 15.1; 72.12% female). They completed an EMA protocol including measures of guilt, loneliness, hopelessness, and passive and active SI for four weeks post-discharge. Multilevel modeling was used to evaluate guilt and loneliness, respectively, as predictors of prospective passive and active SI, respectively. We also evaluated whether hopelessness mediated the interaction between guilt and loneliness in predicting future SI. Hopelessness was also evaluated as a mediator between passive and active SI.

Guilt predicted prospective passive and active SI, respectively, whereas loneliness only predicted prospective passive SI. The interaction between guilt and loneliness did not predict active SI, and hopelessness did not mediate the association between guilt and active SI. Passive SI prospectively predicted active SI, but hopelessness did not mediate this association.

Findings suggest that passive and active SI may share overlap but also differences in their etiologies. Their relationship with etiological factors and mediators may differ as a function of temporal scale.

One of the challenges of psychological research is obtaining a sample representative of the general population. One largely overlooked participant characteristic is sub-clinical levels of psychiatric symptoms.

A series of studies were conducted to assess (i) whether typical psychology study participants had more psychiatric symptoms than the general population, (ii) whether there are sub-groups defined by psychiatric symptoms within the no-diagnosis, no-medication participant pool, and (iii) whether sub-clinical levels of psychiatric symptoms have an effect on standard behavioral tasks. Five UK national datasets (N > 10,000) were compared to data from psychology study participants (Study 1: n = 872; Study 2: n = 43,094; Study 3: n = 267).

Psychology study participants showed significantly higher levels of anxiety and depression and lower well-being, according to four commonly used mental health measures (GHQ-12, PHQ-8, WEMWBS, and WHO-5). Five sub-groups within the psychology study participant group were identified based on symptom levels, ranging from none to significant psychiatric symptoms. These groupings predicted performance on tests of executive function, including the Stroop task and the n-back task, as well as measures of intelligence.

This study demonstrates that standard psychology participant pools are unrepresentative and suggests that a failure to account for psychiatric symptoms when recruiting for any psychological study is likely to negatively impact the reproducibility and generalizability of psychological science.

Alterations in reward responsiveness represent a key mechanism implicated in youth depression risk. However, not all youth with these alterations develop depression, suggesting the presence of factors that may moderate risk patterns. As socioeconomic disadvantage is also related to youth depression risk, particularly for youth exhibiting altered reward function, this study examined whether indices of family- and neighborhood-level disadvantage interacted with electrocortical reward responsivity to predict depression symptom trajectories across childhood and adolescence.

Participants included 76 youth (ages 9–16 years) at low and high risk for depression based on maternal history of depression. At baseline, youth completed a monetary reward-guessing task while electroencephalography was recorded to measure the reward positivity (RewP), an event-related potential indexing reward responsiveness. Family and neighborhood disadvantage were assessed using the income-to-needs (ITN) ratio and Area Deprivation Index (ADI), respectively. Self-reported and clinician-rated depression symptoms were assessed across a multiwave, 18-month follow-up.

RewP interacted with family- and neighborhood-level disadvantage to predict self-reported depression symptom trajectories. Specifically, blunted RewP predicted self-reported depression symptom increases for youth with a lower ITN ratio and higher ADI score. A blunted RewP also predicted clinician-rated depression symptom increases for youth living in neighborhoods with higher ADI scores.

Findings suggest that reduced reward responsiveness is a mechanism implicated in future depression risk among youth, specifically in the context of family- and neighborhood-level socioeconomic disadvantage. Interventions that enhance reward response among youth exposed to higher levels of socioeconomic disadvantage may be particularly effective in preventing depression emergence.

Major depressive disorder (MDD) is closely associated with suicide, which often begins with suicidal ideation (SI). However, the underlying neural mechanisms remain unclear.

We included 73 MDD patients with SI (MDD-SI), 44 MDD patients without SI (MDD-NSI) and 78 healthy controls (HCs), then compared the amplitude of low-frequency fluctuations (ALFF), functional connectivity (FC), and effective connectivity (EC) differences across groups and analyzed their relationship with SI severity. FC and EC analyses used brain regions with ALFF differences between MDD-SI and MDD-NSI as seed points. ALFF findings were validated using the REST-meta-MDD consortium dataset (N = 1 596, 24 sites). Additionally, we explored the trend of changes in abnormal activity and connectivity of SI and suicidal behavior (SB) in MDD-SI.

Compared to MDD-NSI, MDD-SI showed increased ALFF in the right anterior cingulate cortex (ACC), validated by the REST-meta-MDD consortium dataset. MDD-SI also exhibited reduced FC between the right ACC and the left inferior frontal gyrus and decreased EC from the right ACC to the right fusiform gyrus, which were negatively correlated with the Hamilton Depression Rating Scale (HAMD)-suicidality item scores. Increased EC was observed in MDD-SI from the right ACC to the right cerebellar tonsil and from the left inferior parietal lobule (IPL) to the right ACC, following a progressive increase pattern (HC < MDD-NSI < MDD-SI without SB < MDD-SI with SB).

Increased activity and aberrant connectivity of the ACC may be associated with SI in MDD patients and potentially serve as biomarkers for suicide risk.

Deficits in working memory (WM) and attention have a considerable functional impact on people with bipolar disorder (PBD). Understanding the neurocognitive underpinnings of these cognitive constructs might facilitate the discovery of more effective pro-cognitive interventions. Therefore, we employed a paradigm designed for jointly studying attentional control and WM encoding.

We used a visuospatial change-detection task using four Gabor Patches with differing orientations in 63 euthymic PBD and 76 healthy controls (HCS), which investigated attentional competition during WM encoding. To manipulate bottom-up attention using stimulus salience, two Gabor patches flickered, which were designated as either targets or distractors. To manipulate top-down attention, the Gabor patches were preceded by either a predictive or a non-predictive cue for the target locations.

Across all task conditions, PBD stored significantly less information in visual WM than HCS (significant effect of group). However, we observed no significant group-by-salience or group-by-cue interactions. This indicates that impaired WM was not caused by deficits in attentional control.

While WM was disturbed in PBD, attentional prioritization of salient targets and distractors, as well as the utilization of external top-down cues, were not compromised. Thus, the control of attentional selection appears to be intact at least for our specific manipulation of this cognitive construct. These findings provide valuable clues for models of WM dysfunction in PBD by suggesting that later stages of WM encoding, such as WM consolidation, are likely primarily impaired, while selective attention is not a main source of impairment.

Accurate and up-to-date epidemiological data on the prevalence and treatment of common mental disorders are essential for evidence-based healthcare policy and resource allocation. However, large-scale, representative epidemiological surveys on common mental disorders in China—particularly those incorporating insomnia disorder and applying the latest diagnostic criteria alongside validated assessment tools—remain notably lacking.

We conducted a population-based, cross-sectional epidemiological survey to assess the prevalence and treatment of common mental disorders among adults in Beijing, China, using a multistage clustered probability sampling design (n = 10,778). Licensed psychiatrists administered standardized diagnostic interviews based on DSM-5 criteria to assess both lifetime and current mental disorders through a single-stage assessment protocol.

Among all lifetime mental disorders assessed, depressive disorders constituted the most prevalent diagnostic category (7.7%), with major depressive disorder representing the most common specific diagnosis (5.4%). Individuals aged 65 years and older exhibited significantly higher 1-month prevalence of both depressive disorders and insomnia disorder compared with younger age groups. Alcohol-related disorder was more prevalent in men than in women, and in urban residents than in rural residents. Help-seeking patterns revealed a predominant reliance on informal support over professional services among individuals with lifetime mental disorders. Only 13.4% sought help from mental health professionals, and 12.7% received mental health professional treatment.

The improved access to treatment did not translate into a reduction in population-level mental disorder prevalence, which may be attributable to the low rate of professional mental health treatment. Governments must optimize mental healthcare access.

Avoidant/restrictive food intake disorder (ARFID) leads to faltering growth and psychosocial impairment. Three phenotypes can co-occur: fear of aversive consequences of eating (ARFID-fear phenotype), sensory sensitivity, and lack of interest in eating/food. We hypothesized that youth with ARFID, especially ARFID-fear phenotype, would show hyperactivation of fear-related regions in response to ARFID-specific fear images, compared to healthy controls (HC), and activation of these regions would positively correlate with ARFID fear severity.

Youth (N=103: 76 ARFID, including 20 ARFID-fear phenotype; 27 HC) underwent functional MRI scanning while viewing ARFID-specific fear (e.g. vomiting, choking) versus neutral images. We compared blood-oxygen-level-dependent (BOLD) response in fear-related region of interests (ROI; e.g. amygdala, hippocampus, insula) between ARFID and ARFID-fear phenotype versus HC. We evaluated the association between brain response and ARFID fear severity in ARFID-fear phenotype.

Across individuals, there was a robust bilateral amygdala response to ARFID-specific fear versus neutral images. Compared to HC, ARFID-fear phenotype showed a greater insula response to ARFID-specific fear versus neutral images (p=0.049). There were no other group differences and no significant relationships between BOLD response and ARFID fear severity in ARFID-fear phenotype.

ARFID-specific fear images elicit amygdala responses across individuals, with greater activation in the insula only in ARFID-fear phenotype versus HC. These findings validate the ARFID-specific fear paradigm and highlight the intriguing possibility that, in the ARFID-fear phenotype, universally feared experiences such as choking and vomiting serve as the unconditioned stimulus in developing ARFID and may partially be mediated by the insular cortex.

People with severe mental illness (SMI) (schizophrenia-spectrum and bipolar disorders) experience a 15–20-year reduction in life expectancy. The role of social determinants, including that of social exclusion, in contributing to excess mortality in SMI remains underexplored.

Retrospective cohort study, comprising 8098 people with clinician-diagnosed SMI, matched to 581,209 population controls, followed for 5.7 years using person-level linked health/ census records. A social exclusion index was derived from census indicators: marital status, social isolation, economic inactivity, education, tenure, housing stability, and material assets.

Social exclusion was more common in SMI than in controls and strongly associated with higher mortality. Relative to the least socially excluded controls, adjusted hazard ratios (aHR) for mortality in SMI were: 16–44 years: aHR 7.58 (95% CI: 2.75–20.86) in the least socially excluded, increasing to 12.34 (7.92–19.24) in the most excluded; 45–64 years: 3.34 (1.98–5.64) [least excluded] increasing to 6.58 (5.32–8.14) [most excluded]; 65+ years: 2.71 (1.90–3.86) [least excluded], increasing to 3.07 (2.48–3.80)[most excluded]. Excess mortality among those with SMI was pronounced at younger ages if never married; by mid-life if living alone or economically inactive; and at 65+ years in those with SMI living alone, renting, or with no car ownership. Economic inactivity and lack of qualifications accounted for 16–35% of SMI mortality.

Social exclusion is an under-recognized contributor to premature mortality in SMI. Targeting social determinants through novel socially-focused interventions could improve survival in people with SMI.

Machine learning (ML) models show promise in predicting post-traumatic stress disorder (PTSD) treatment outcomes, but it is unknown how their predictions compare to those of clinicians. This study directly compared the accuracy of clinicians’ predictions of patient treatment outcomes with those of three ML models.

Twenty clinicians providing cognitive processing therapy repeatedly predicted outcomes for 194 veterans. We compared their accuracy against three ML models on two key endpoints: clinically meaningful symptom reduction (≥10-point PCL-5 decrease) and posttreatment severity (final PCL-5 < 33). Clinician predictions were compared against a recurrent neural network, a mixed-effects random forest, and a generalized linear mixed-effects model. We analyzed prediction accuracy and the association between clinician confidence and accuracy using logistic mixed-effects models.

ML models were significantly more accurate than clinicians at predicting whether a patient’s posttreatment PCL-5 score would be below 33 (p < .001). However, no significant difference in accuracy was found for predicting a ≥10-point symptom reduction (p = .734). Clinician confidence increased throughout treatment and was significantly associated with greater prediction accuracy for both outcomes (ORs = 1.06, ps < .001).

ML models can outperform clinicians in predicting posttreatment symptom severity, particularly early in treatment, suggesting they could be a useful tool for identifying patients at risk for suboptimal outcomes. However, ML models were not superior in predicting symptom reduction, where clinicians also performed at a high level. Findings support the selective use of ML to enhance, rather than replace, clinical judgment in PTSD treatment.

High uncertainty in recent global health, geopolitical, and climate crises has been proposed as one important driver of the rise in youth mental health problems. This makes intolerance of uncertainty – a transdiagnostic risk factor for mental health problems – a promising target for intervention.

This study presents a novel single-session online training that took a synergistic mindset approach to promote uncertainty-as-adaptive and growth mindsets. The novel Uncertainty-Mindset Training was compared with Psychoeducation and No-Training control groups in 259 older adolescents/emerging adults (18-to-24-year-olds).

The Uncertainty-Mindset Training reduced intolerance of uncertainty, anxiety symptoms, and depression symptoms 1 month later. Importantly, the clinical gains were mediated by reductions in intolerance of uncertainty.

Given that this ultra-brief training can be delivered at scale globally and at no cost to the users, it shows promise for significant public health impacts.

Growing studies have reported an elevated risk of violence in patients with depression, yet the neurobiological underpinnings remain poorly understood. The present study explored the resting-state electroencephalogram (EEG) features in major depressive disorder (MDD) patients with violent offenses to identify potential neurological markers for violence prediction and intervention.

Twenty-nine MDD patients who committed violent offenses (violent depression [VD] group), 27 MDD patients without violent behaviors (nonviolent depression [NVD] group), and 25 healthy controls (HCs) were included. Resting-state EEGs were recorded for at least 5 min. EEG microstates, functional connectivity (FC), and graph theory metrics were analyzed and compared between groups.

First, the VD group had increased microstate A, more microstates A-B transition, but lower microstates B-D and C-D transition. Second, the VD group exhibited two enhanced functional brain networks compared to NVD and HCs, and three weakened functional brain networks compared to HCs, which were primarily distributed in the frontal and frontoparietal networks. Third, the VD group specifically exhibited reduced nodal efficiency (aNe) in the superior parietal lobe and increased aNe in the middle occipital gyrus.

MDD patients with violent offenses exhibited alterations in EEG microstates, FCs in the frontal lobe and frontoparietal network, and disrupted aNe in specific parietal and occipital lobes. These alternations are closely associated with deficits in emotional regulation, executive function, and inhibitory control, which may subserve as potential neurobiomarkers for violence risk assessment in patients with depression.

Although the short-term preventive effects of mHealth consultation intervention on postpartum depressive symptoms have been demonstrated, the long-term effects and role of alleviating loneliness on depressive symptoms remain unclear.

This follow-up study extended our previous trial, which ended at three months postpartum, by continuing observation to 12 months. Participants in the original trial were randomized to the mHealth group (n = 365) or the usual care group (n = 369). Women in the mHealth group had access to free, unlimited mHealth consultation services with healthcare professionals from enrollment through four months postpartum. The primary outcome of this study was the risk of elevated postpartum depressive symptoms at 12 months post-delivery (Edinburgh Postnatal Depression Scale score of ≥9). The mediation effect of alleviating loneliness on the primary outcome was also evaluated, using the UCLA loneliness scale at three months postpartum.

A total of 515 women completed the follow-up questionnaires (mHealth group, 253/365; usual care group, 262/369; 70.2% of the original participants). Compared to the usual care group, the mHealth group had a lower risk of elevated postpartum depressive symptoms at 12 months post-delivery (36/253 [14.2%] vs. 55/262 [21.0%], risk ratio: 0.68 [95% confidence interval: 0.46–0.99]). Mediation analysis showed that reducing loneliness at three months post-delivery mediated approximately 20% of the total effect of the intervention on depressive symptoms 12 months post-delivery.

mHealth consultation services provided during the early perinatal period may help alleviate depressive symptoms at 12 months postpartum.

Antidepressants are the primary treatment for major depressive disorder (MDD), yet their precise neurobiological mechanisms remain incompletely understood. This study aimed to elucidate neural differences between medicated and unmedicated MDD patients by analyzing resting-state functional magnetic resonance imaging data.

We conducted a coordinate-based meta-analysis, complemented by behavioral, genetic, and neurotransmitter-level evaluations to identify potential therapeutic targets and diagnostic biomarkers. Using seed-based d-mapping with permutation of subject images (SDM-PSI), we assessed brain activation changes associated with antidepressant treatment. The identified regions were further characterized using large-scale molecular and functional brain databases.

A total of 59 studies on unmedicated MDD (2,618 patients, 2,486 controls) and 15 studies on medicated MDD (541 patients, 483 controls) were included. The meta-analysis revealed significantly increased activation in the left striatum among medicated patients, a region linked to cognitive functions such as memory and perception. Gene expression analysis highlighted SLC5A7 and prolactin (PRL) as key genes in this region, while neurotransmitter mapping showed associations with serotonin (5-HT1a, 5-HT2a) and dopamine (D1, D2) receptors. Additionally, reduced activation in the left middle occipital gyrus (MOG) was observed across both medicated and unmedicated groups. This region, implicated in recognition and face processing, showed high expression of TFAP2B and PRL and was associated with serotonin and norepinephrine transporter distributions.

These findings suggest that the left striatum may represent a core neurofunctional target of antidepressant treatment, while the left MOG may serve as a stable neurobiological marker for MDD diagnosis, independent of pharmacological status.