Psychiatry Research最新文献

This critical analysis of the study by Narine et al. (2026) investigates the effectiveness of a non-culturally adapted partial hospital program (PHP) using Cognitive Behavioral Therapy (CBT) and Dialectical Behavior Therapy (DBT) across ethnoracial groups. The study found that Asian participants reported better relationship functioning post-treatment, although the effect size was small. Black participants showed greater perceived improvements in symptoms, including anxiety and depression, potentially due to the PHP's intensive approach. The study also revealed that Black participants reported the highest levels of respect and dignity in treatment, highlighting the importance of interpersonal dynamics in therapeutic success. The findings underscore the need for further exploration into culturally sensitive approaches to therapy, particularly for marginalized ethnoracial groups who may face unique challenges in mental health treatment. The analysis suggests that culturally adapted CBT and DBT may further enhance outcomes for these groups, ensuring more inclusive and effective care in acute psychiatric settings.

As a central hub of emotional processing, alterations in amygdala functional connectivity (FC) have garnered significant attention in both major depressive disorder (MDD) and bipolar disorder (BD), which holds promise in identifying differential biomarkers and highlighting their similarities. However, current findings are limited by inconsistency. To address this, we conducted a comparative and conjunction analysis using the Seed-based d Mapping (SDM) toolbox to examine amygdala FC alterations in MDD and BD patients. Our results revealed distinct amygdala FC alterations between MDD and BD were primarily identified in the left temporal pole, cingulate cortex, and left supramarginal gyrus, while shared amygdala FC abnormalities were particularly observed in the fronto-limbic regions and occipitotemporal gyrus. These findings highlight both commonalities and differences in amygdala FC alterations across MDD and BD, providing insights into the underlying pathophysiology of mood disorders and offering potential neural biomarkers for differential diagnosis, thereby aiding in the improvement of treatment strategies.

Introduction: The global prevalence of autism spectrum disorder (ASD) is increasing, yet effective strategies for early prediction and prevention are still limited. This umbrella review aims to synthesize available evidence on the association between maternal pregnancy complications and offspring ASD.

Methods: Following PRISMA guidelines, we systematically searched all published literature from PubMed, Embase, Web of Science, and Cochrane Library up to July 16, 2025, for systematic reviews on pregnancy complications and ASD. Only systematic reviews published in English were considered. Observational studies were included, while those on other neurodevelopmental disorders or teratogens were excluded. Study selection, data extraction, and quality assessment (using AMSTAR 2 and ROBIS) were conducted independently by two reviewers. Statistical analyses included random-effects meta-analysis, excess significance bias, Egger's test for publication bias, and sensitivity analysis.

Results: Among 596 identified records, 43 systematic reviews were assessed, with 2 (4.65%) moderate quality, 7 (16.28%) low quality, and 34 (79.07%) critically low quality. Fourteen meta-analyses (10 complication types, 30 studies) were included. Significant associations with increased ASD risk were found for gestational diabetes (OR = 1.29, 95% CI:1.14-1.45), preconception obesity (OR = 1.42, 95%CI:1.22-1.65), excessive gestational weight gain (OR = 1.18, 95%CI:1.08-1.29), polycystic ovary syndrome (OR = 1.64, 95%CI:1.50-1.82), gestational hypertension (OR = 1.37, 95%CI:1.22-1.55), pre-eclampsia (OR = 1.50, 95%CI:1.26-1.78), unclassified pregnancy infections (OR = 1.13, 95%CI:1.03-1.23), maternal autoimmune diseases (OR = 1.30, 95%CI:1.20-1.42), and asthma (OR = 1.36, 95%CI:1.28-1.44). All analyses had a high risk of bias; no convincing evidence was identified.

Conclusions: In conclusion, this umbrella review provides a stratified assessment of evidence linking pregnancy complications to offspring ASD. No associations were supported by convincing evidence; most were based on suggestive or weak evidence, with only a limited number reaching highly suggestive levels. These findings underscore the need for more robust primary studies to clarify these associations and their effect sizes.

Pharmacological treatments for attention-deficit/hyperactivity disorder (ADHD) are efficacious and safe; however, substantial interindividual variability in treatment response persists, with many patients experiencing suboptimal outcomes or early discontinuation. Although genetic factors have been proposed as contributors to this variability, clinically actionable predictors remain elusive. Here, we present the first meta-analysis evaluating whether polygenic liability for ADHD and related psychiatric and behavioral-cognitive phenotypes is associated with clinically meaningful response to methylphenidate in 1000 ADHD cases from Norway, Brazil, and Spain assessed in real-world settings. Polygenic scores (PGS) for ADHD, autism, bipolar disorder, educational attainment, major depressive disorder, neuroticism, and schizophrenia were calculated separately for each cohort. Treatment response was assessed using evaluations of global clinical improvement and harmonized by categorizing individuals as responders or non-responders. Cohort-specific associations were combined using fixed-effects meta-analysis. No PGS showed a significant association with treatment response. Effect sizes were small, consistent across cohorts, and characterized by minimal between-study heterogeneity. Sensitivity analyses incorporating clinical and treatment-related covariates yielded convergent results. As the first meta-analytic evaluation of polygenic predictors evaluating clinically meaningful ADHD stimulant response, these findings delineate the current limits of PGS in pharmacogenomic applications. Rather than supporting immediate clinical utility, our results highlight key methodological and conceptual constraints, including limited sample sizes, heterogeneous outcome definitions, and the indirect nature of susceptibility-based PGS for predicting treatment response. By mapping these boundaries, this study provides a framework to recalibrate research priorities and guide the next generation of ADHD pharmacogenomic studies toward larger, harmonized, and more informative definitions of treatment response.

Binge eating behavior and food craving are associated with altered reward sensitivity and impaired inhibitory control, contributing to physical and psychological consequences. Neurofeedback (NFB) has emerged as a promising non-invasive intervention for reducing binge eating behaviors, yet its overall efficacy remains unclear and warrants quantitative synthesis. A systematic search was conducted across MEDLINE, CENTRAL, EMBASE, ClinicalTrial.gov, and PubMed to identify randomized controlled trials (RCTs) of NFB interventions for binge eating behaviors or binge eating disorder (BED) in adults. The primary outcome was food craving. The secondary outcomes were binge eating severity, binge eating frequency, and self-efficacy. Data synthesis was performed using a random-effects meta-analysis. Seven RCTs with 251 participants were included. NFB was associated with improved food craving (standard mean difference, SMD = -0.45, 95 % confidence interval, CI = -0.78 to -0.12) and binge eating frequency (SMD = -0.54, 95 % CI = -1.00 to -0.08) with moderate effect sizes. However, NFB did not significantly affect binge eating severity and self-efficacy (SMD = -0.22, 95 % CI = -0.56 to 0.12; SMD = 0.21, 95 % CI = -0.33 to 0.75). For food craving severity, NFB was more effective in non-clinical populations (SMD = -0.58, 95 % CI = -0.98 to -0.17) than in participants with BED (SMD = -0.20, 95 % CI = -0.84 to 0.44). NFB shows promise as a non-invasive intervention to reduce binge eating and food craving. Despite protocol variability and limited generalizability, its favorable safety profile and potential efficacy suggest it may serve as an adjunctive option for individuals with binge eating behaviors; however, the evidence remains preliminary and hypothesis-generating.

Here, we present the first genome-wide association study and polygenic risk score analysis of obsessive-compulsive symptoms in a sample of 661 clinically diagnosed pediatric participants diagnosed with mental illness and healthy controls. Using a psychiatric questionnaire score as a quantitative trait we conducted a large-scale genetic analysis and ran multiple post-association analyses to investigate the mediating role of obsessive-compulsive symptoms in six comorbid mental disorders. Polygenic risk scores were computed for OCS using genome-wide summary statistics from obsessive-compulsive disorder, attention-deficit/hyperactivity disorder, anxiety disorders, depression, autism spectrum disorder, and tic disorders. Across all models, the PRS of OCS explained modest yet significant proportion of shared genetic risk across six mental disorders consistent with effect sizes typically observed in complex psychiatric traits. Furthermore, Mendelian randomization analysis suggested a potential causal pathway in which OCS mediates the genetic risk for anxiety. These findings highlight shared polygenic mechanisms between OCS and a range of neuropsychiatric conditions. We observed a potential causal pathway in which OCS mediates the genetic risk for anxiety, supporting the hypothesis that OCS may serve as a transdiagnostic mediator within the pediatric population. This study underscores the value of examining genetic risk across the symptom spectrum of mental illnesses, rather than relying solely on binary diagnostic categories.