Alpha psychiatry最新文献

{"title":"Shielding the First 24 Postnatal Months of Life: A Proposal for a Prospective Cohort Study of Early-Life Electromagnetic Exposure and Autism Risk.","authors":"Alberto Garoli, Alessandro Greco","doi":"10.31083/AP53282","DOIUrl":"10.31083/AP53282","url":null,"abstract":"<p><strong>Background: </strong>Autism Spectrum Disorder (ASD) involves Mirror Neuron System (MNS) dysfunction, driving core social and imitative impairments. Systemic physiological alterations such as autonomic dysregulation, mitochondrial dysfunction and neuroinflammation are known to impair synchronization and plasticity of neuronal clusters. A less-evident environmental cofactor, coinciding with rising ASD prevalence, is the considerable world-wide increase in electromagnetic radiation (EMR) overall exposure among children. Experimental evidence shows how low-intensity EMR influences cellular processes, via voltage-gated calcium channels (VGCCs), oxidative stress, and mitochondrial metabolism. The Resonant Convergence framework, allow to predict how chronic EMR exposure during the first 24 postnatal months of life can act as a factor in ASD pathogenesis. The best candidate mechanism is chronic Ion Cyclotron Resonance (ICR) detuning the Ca<sup>2+</sup>-calmodulin pathway, thus disrupting MNS synchronization.</p><p><strong>Methods and analysis: </strong>A prospective observational pilot cohort study (24-month follow-up) proposes to enroll 1000 full-term newborns into two arms: an EMR-reduced cohort (n = 500, rest and sleep-phase Faraday shielding) and a standard exposure cohort (n = 500). Exposure is quantified via radiofrequency (RF)/extremely low frequency(ELF) measurements, proximity analysis, device inventories and wearable dosimetry. The primary endpoint is a continuous neurodevelopmental trajectory score (joint attention, language, electroencephalogram (EEG) mu-rhythm); binary ASD diagnosis (Autism Diagnostic Observation Schedule, Second Edition (ADOS-2), Autism Diagnostic Interview-Revised (ADI-R)) is a secondary, exploratory endpoint. Moreover, an optional genomic screening will evaluate gene-environment interactions within extremely low-frequency electromagnetic field (ELF-EMF) vulnerable pathways, including ASD-associated genes upregulated by RF via bromodomain and extraterminal protein (BET)-mediated epigenetic mechanisms. Analyses will employ risk ratios, Fisher's exact tests and logistic regression adjusted for confounders; mixed-effects and Bayesian modeling will evaluate longitudinal outcomes and exposure reduction effects. Given a 2-3% baseline prevalence, approximately 20-30 ASD cases are expected. The study is therefore powered for exploratory signal detection rather than definitive causal inference, providing the critical baseline data required to justify and design future confirmatory trials. Sex-stratified modeling will address the 4:1 male-to-female prevalence ratio.</p><p><strong>Ethics and dissemination: </strong>Ethics committee approval is not yet sought; full protocol review and approval will be obtained prior to the study initiation, in strict accordance with the Declaration of Helsinki. Written parental informed consent will be mandatory for all participants prior to enrollment. Study findings and methodological mil","PeriodicalId":72151,"journal":{"name":"Alpha psychiatry","volume":"27 4","pages":"53282"},"PeriodicalIF":2.9,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13539998/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148889419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low Dose Ketamine Preconditions Astrocyte Mitochondria to Achieve Antidepressant Efficacy via Adenosine, Humanin, and Melatonin Upregulation and Efflux.","authors":"George Anderson","doi":"10.31083/AP54760","DOIUrl":"10.31083/AP54760","url":null,"abstract":"<p><p>Understanding the physiological changes induced by ketamine in mood disorders, while reducing its side effects, is likely to contribute to a more comprehensive understanding of the physiology underlying mood disorders, as well as to the development of faster-acting and more efficacious antidepressant treatments. An extensive review of the literature on ketamine and the pathophysiology of depression indicates that ketamine's antidepressant efficacy has classically been attributed to noncompetitive antagonism of the n-methyl-d-aspartate receptor (NMDAR) on the neuronal postsynaptic membrane, thereby reducing excessive Ca²⁺ influx through the NMDAR channel. However, recent evidence suggests that ketamine's antidepressant efficacy is mediated not by synaptic NMDAR antagonism but rather by its direct effects on mitochondrial function, arising from its amphiphilic structure. It is proposed that astrocyte mitochondria represent the primary target of ketamine, with the broader effects induced by ketamine occurring downstream of the optimization of astrocyte mitochondrial function and, consequently, astrocyte function. Developmental stress and trauma are proposed to differentially prime specific regions of the central nervous system, rendering them more susceptible to subsequent stressors through the epigenetic regulation of astrocytes. This process increases astrocyte reactivity and dysregulates astrocyte mitochondrial function in response to subsequent stressors, while also increasing blood-brain barrier permeability within these regions. At stress-vulnerable sites, ketamine may upregulate adenosine, humanin, and melatonin, thereby restoring astrocyte function and attenuating inflammatory activity within the local astrocytic microenvironment, including microglia, neurons, and oligodendrocytes. Ketamine's modulation of mitochondrial function is proposed to be mediated via NMDARs located on the inner mitochondrial membrane, leading to alterations in mitochondrial ionic regulation that enhance astrocyte mitochondrial resilience to stress, possibly through a preconditioning mechanism. Ketamine-induced increases in melatonin and humanin are proposed to suppress microglial activation, promote white matter remyelination, and restore neuronal activity, as well as patterned intercellular and interregional communication. This hypothesis-driven overview evaluates ketamine's capacity to restore astrocyte mitochondrial function and thereby counteract the consequences of developmental stress and trauma that underlie vulnerability to subsequent stress-induced depression.</p>","PeriodicalId":72151,"journal":{"name":"Alpha psychiatry","volume":"27 4","pages":"54760"},"PeriodicalIF":2.9,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540058/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148889279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Effect of Acute Psychotic Period on Physiological Values Measured in Blood in Male Patients With Schizophrenia.","authors":"Guler Celikel, Suat Yalcin, Tevfik Kalelioglu, Nesrin Karamustafalioglu","doi":"10.31083/AP53389","DOIUrl":"10.31083/AP53389","url":null,"abstract":"<p><strong>Background: </strong>There is increasing evidence that plasma osmolarity is an independent prognostic factor associated with mortality in patients with cardiovascular disease. Whole blood viscosity (WBV) is also associated with established cardiometabolic risk factors for cardiovascular disease. The present study aimed to investigate the effects of the acute phase of schizophrenia on physiological parameters, including WBV and plasma osmolarity, in male patients with schizophrenia.</p><p><strong>Methods: </strong>A total of 121 male patients with schizophrenia were included in this study. Routine blood test results were obtained from hospital records, and the laboratory values required for the calculation of viscosity and osmolarity were recorded. Laboratory data from the patients' most recent acute exacerbation were retrieved from hospital records and used as the acute-phase data.</p><p><strong>Results: </strong>There was no statistically significant difference in serum osmolarity between the acute and remission phases (<i>p</i> = 0.360). Blood urea nitrogen (BUN) and glucose levels were significantly higher during the remission phase, whereas sodium levels were significantly higher during the acute phase. No significant differences were observed in WBV values between the acute and remission phases (<i>p</i> > 0.05). Furthermore, there were no significant differences in WBV-related parameters, including hematocrit (HCT) and total protein, between the two phases. Low-density lipoprotein (LDL), high-density lipoprotein (HDL), total cholesterol, and triglyceride levels were significantly higher during the remission phase.</p><p><strong>Conclusions: </strong>Although differences were observed in osmolarity-related parameters and viscosity-associated metabolic variables between the acute and remission phases in male patients with schizophrenia, no statistically significant differences were found in serum osmolarity or WBV between the two phases.</p>","PeriodicalId":72151,"journal":{"name":"Alpha psychiatry","volume":"27 4","pages":"53389"},"PeriodicalIF":2.9,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540002/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148889381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Artificial Intelligence Chatbot Dependence, Anxiety, and Depressive Symptoms in University Students: Initial Psychometric Evaluation of the Artificial Intelligence Chatbot Dependence Scale (AICDS) in Spanish.","authors":"Iván Barrios, Julio Torales, Sandra Blanco, Carlos Manuel Giménez-Barboza, Brenda Mikaela Monges-Guerrero, Axel Verón-Otero, Gladys Mercedes Estigarribia Sanabria, Eva Natalia Giménez-Legal, João Mauricio Castaldelli-Maia, Antonio Ventriglio","doi":"10.31083/AP53298","DOIUrl":"10.31083/AP53298","url":null,"abstract":"<p><strong>Background: </strong>Artificial intelligence (AI) chatbots are rapidly becoming integrated into higher education, supporting human-computer interaction, knowledge explanation, rapid access to information, access to online learning resources, and personalized learning pathways. However, little is known about potential patterns of dependence on these technologies and their relationship with anxiety and depressive symptoms. This study aimed to conduct an initial psychometric evaluation of the Spanish version of the Artificial Intelligence Chatbot Dependence Scale (AICDS) and to explore its association with anxiety and depressive symptoms among university students.</p><p><strong>Methods: </strong>A cross-sectional study was conducted among 200 university students from Santa Rosa del Aguaray, Paraguay. Participants completed the AICDS together with screening measures of anxiety and depressive symptoms. Data were analyzed using R version 4.5.3. Confirmatory factor analysis using diagonally weighted least squares estimation with robust standard errors was performed to examine the scale's factor structure, and multiple linear regression models were used to evaluate associations between AICDS scores and anxiety and depressive symptoms.</p><p><strong>Results: </strong>The findings supported a unidimensional factor structure with acceptable-to-good model fit and high internal consistency (Cronbach's α = 0.833; McDonald's ω = 0.903). Fully standardized factor loadings ranged from 0.538 to 0.873. In bivariate analyses, students who screened positive for anxiety symptoms had higher AICDS scores than those who screened negative, although the effect size was small. However, this association was not maintained after adjustment for sociodemographic and academic covariates in multiple regression models. No significant association was observed between AICDS scores and depressive symptoms under two-tailed testing.</p><p><strong>Conclusions: </strong>These findings provide preliminary evidence supporting the internal consistency and factorial validity of the Spanish version of the AICDS in this sample. However, associations between AI chatbot dependence and anxiety or depressive symptoms were weak and not robust after adjustment. Further longitudinal and psychometric research is needed before broader conclusions can be drawn about the mental health implications of AI chatbot dependence among university students.</p>","PeriodicalId":72151,"journal":{"name":"Alpha psychiatry","volume":"27 4","pages":"53298"},"PeriodicalIF":2.9,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540032/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148889700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Longer Duration of Drug Elimination and Withdrawal Symptoms in Overweight Patients Undergoing Detoxification for Benzodiazepine Dependence.","authors":"Anna Basińska-Szafrańska","doi":"10.31083/AP51895","DOIUrl":"10.31083/AP51895","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;In patients undergoing detoxification for benzodiazepine (BZD) dependence, withdrawal symptoms frequently persist into the low-concentration phase following drug discontinuation. Prolonged drug elimination may extend the duration of required medical supervision. Because lipophilic BZDs can accumulate in adipose tissue and be released gradually during detoxification, overweight patients may experience delayed elimination. This study quantitatively examined whether BZD elimination and the duration of withdrawal symptoms are prolonged in overweight patients.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;From 508 records of concentration-monitored detoxification, a retrospective sample of 290 inpatients matched for diet and physical activity was selected. All patients underwent detoxification according to the SAER protocol (Satiation, Anti-accumulation paradigm, Elimination, and Readaptation). Following (S) satiation with diazepam, further unnecessary (A) accumulation was prevented through aggressive day-by-day dose reductions guided by serum concentration monitoring. Subsequent tapering, leading to effective (E) elimination, was adjusted according to the evolving intensity of withdrawal symptoms, characterized by episodes of peak severity (withdrawal crises) interspersed with periods of relative relief. Completion of (R) readaptation was defined by the cessation of withdrawal symptoms after elimination. The duration of effective elimination, from peak serum concentration to undetectable levels, with particular attention to the post-discontinuation phase, was recorded. Concomitant medications known to influence BZD elimination were identified. Elimination parameters and the timing of clinically significant withdrawal crises were analyzed in relation to patients' body mass index (BMI).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Elimination duration was positively correlated with BMI (ρ = 0.39, &lt;i&gt;p&lt;/i&gt; &lt; 0.001). The timing of the strongest and/or the final crises also showed weak but significant positive correlations with BMI in the overall sample (ρ = 0.18 and 0.15, &lt;i&gt;p&lt;/i&gt; &lt; 0.01 and &lt; 0.05 cutoff, respectively), and within the identified co-medication subgroups, including the valproate, carbamazepine, and no-modifier groups (ρ = 0.19-0.26, all &lt;i&gt;p&lt;/i&gt; &lt; 0.05). These associations accounted for a small proportion of the variance in overall time to withdrawal crisis (R&lt;sup&gt;2&lt;/sup&gt; = 0.02-0.07). Nevertheless, they translated into an additional 8-11 days of necessary monitored care among obese patients. Elimination duration was further prolonged in patients receiving valproate. Extended elimination was not associated with reduced withdrawal symptom severity.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;Among patients undergoing detoxification for BZD dependence, higher BMI was associated with prolonged drug elimination and a longer duration of recurring withdrawal crises, without attenuation of symptom severity. Although the observed associations were m","PeriodicalId":72151,"journal":{"name":"Alpha psychiatry","volume":"27 4","pages":"51895"},"PeriodicalIF":2.9,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540023/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148889342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polysomnographic Parameters in Schizoaffective Disorder: A Systematic Review and Meta-Analysis.","authors":"Dario Morra, Gianluca Ficca, Giuseppe Barbato","doi":"10.31083/AP52900","DOIUrl":"10.31083/AP52900","url":null,"abstract":"<p><strong>Background: </strong>Schizoaffective disorder (SZA) is a severe psychiatric condition characterized by overlapping affective and psychotic features; however, its sleep architecture remains poorly characterized. This systematic review and meta-analysis compared polysomnographic findings in drug-free patients with SZA with those of healthy controls (HC), patients with schizophrenia (SCZ), and patients with major depressive disorder (MDD).</p><p><strong>Methods: </strong>An extensive database search identified 40 studies. Nine case-control studies including 79 patients with SZA, 88 patients with SCZ, 79 HC, and 131 patients with MDD were included in the meta-analyses. Total sleep time, sleep efficiency, sleep latency, wake after sleep onset, and rapid-eye-movement (REM) and non-REM (NREM) sleep variables were analyzed. The primary outcome measure was the standardized mean difference (SMD). Data were analyzed using a random-effects model. Publication bias was assessed using Egger's regression test and funnel plot asymmetry.</p><p><strong>Results: </strong>Compared with HC, patients with SZA showed reduced total sleep time, increased sleep latency and wakefulness after sleep onset, reduced REM sleep duration, shortened REM latency, and reduced stage 4 sleep duration and percentage. Patients with SZA differed from those with MDD only in exhibiting increased sleep latency, whereas no significant differences were observed between patients with SZA and those with SCZ.</p><p><strong>Conclusions: </strong>Polysomnographic abnormalities in SZA demonstrate a general pattern of sleep disruption compared with HC, without clear differentiation from SCZ or MDD. Overall, current evidence does not support sleep architecture as a reliable biomarker for distinguishing SZA from related psychotic or affective disorders. These findings should be considered exploratory, given the small sample sizes, limited number of available studies, and substantial heterogeneity across studies. Further research is needed to determine whether specific sleep measures may better distinguish SZA from other psychiatric conditions.</p>","PeriodicalId":72151,"journal":{"name":"Alpha psychiatry","volume":"27 4","pages":"52900"},"PeriodicalIF":2.9,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540051/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148889388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Imatinib-Induced Changes in Anxiety-Like Behaviors are Associated With Prefrontal Cortical Metabolic Remodeling in Mice.","authors":"Jieyu Ji, You Wang, Shanglan Qu, Xin Peng, Ruixue Ma, Hanwei Li, Jinlong Chang, Lijuan Li, Yanjiao Li, Zhiting Gong","doi":"10.31083/AP51694","DOIUrl":"10.31083/AP51694","url":null,"abstract":"<p><strong>Background: </strong>Anxiety-related symptoms are frequently reported in patients with chronic myeloid leukemia (CML) receiving tyrosine kinase inhibitor (TKI) therapy. However, the role of TKIs, including imatinib, in development of anxiety remains unclear. The prefrontal cortex (PFC) is closely associated with anxiety-like behaviors, and its metabolic components, particularly lipid- and myelin-related metabolites, are involved in their regulation. Whether imatinib affects brain metabolism remains unknown. This study aimed to evaluate the effects of imatinib on anxiety-like behaviors and to investigate associated metabolic alterations in the PFC.</p><p><strong>Methods: </strong>Anxiety-like behaviors were assessed using a battery of behavioral assays in imatinib-treated mice. PFC tissues from imatinib-treated and control mice were subjected to untargeted metabolomic analysis.</p><p><strong>Results: </strong>Imatinib-treated mice exhibited selective alterations in anxiety-like behaviors. Metabolomic analysis revealed distinct metabolic profiles between the two groups, with significant changes in lipid-related pathways, particularly sphingolipid metabolism. These findings extend the current understanding of the metabolic basis of anxiety-like behaviors and suggest that TKI treatment may influence neuropsychiatric processes through metabolic remodeling of the PFC.</p><p><strong>Conclusions: </strong>This study highlights a potential link between TKI therapy and brain metabolism and provides a framework for understanding the neurobiological basis of anxiety-related effects. These findings may inform future research on the neuropsychiatric consequences of targeted cancer therapies.</p>","PeriodicalId":72151,"journal":{"name":"Alpha psychiatry","volume":"27 4","pages":"51694"},"PeriodicalIF":2.9,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540018/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148889325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Excitation/Inhibition Balance as a Mechanistic Link Between Sleep Disturbance and Autism Spectrum Disorder: A Bidirectional Framework.","authors":"Yuhan Wu, Di Wu, Wei Zhong, Jun Ma","doi":"10.31083/AP52264","DOIUrl":"10.31083/AP52264","url":null,"abstract":"<p><p>Sleep disturbances are highly prevalent in autism spectrum disorder (ASD), yet their significance may extend beyond that of a common co-occurring condition. Growing evidence suggests that excitation/inhibition (E/I)-related network dysregulation may provide a valuable framework for understanding the association between sleep disturbances and variability in core ASD symptom expression. This review synthesizes findings from polysomnography, actigraphy, circadian rhythm research, neuroimaging, electrophysiological studies, and animal models to examine how E/I-related vulnerability in ASD may contribute to impaired sleep initiation and maintenance. It further explores how sleep and circadian disruption may, in turn, influence daytime symptom expression through alterations in synaptic homeostasis and network rebalancing. By proposing a bidirectional framework, this review aims to integrate current evidence on sleep-related symptom variability in ASD and to inform future longitudinal, mechanistic, and biomarker-driven research.</p>","PeriodicalId":72151,"journal":{"name":"Alpha psychiatry","volume":"27 4","pages":"52264"},"PeriodicalIF":2.9,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540059/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148889057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy of Acupuncture Combined With Pharmacotherapy for Depression: A Randomized Controlled Clinical Trial.","authors":"Shuyun Huang, Sumiao Zhou, Lida Zhang, Fengchun Wu, Zhendong Zhang, Yuping Ning, Zixuan Liu, Jingping Wu, Bingxin Chen, Qiuling Lu, Li Gao, Zhimin Zhu, Wei Han, Yuanyuan Huang","doi":"10.31083/AP52350","DOIUrl":"10.31083/AP52350","url":null,"abstract":"<p><strong>Background: </strong>Depression is frequently accompanied by comorbid symptoms such as anxiety, insomnia, and cognitive impairment, which complicate treatment and adversely affect clinical outcomes. Acupuncture has shown promise as a complementary therapy; however, the efficacy of acupuncture combined with selective serotonin reuptake inhibitors (SSRIs) requires further investigation.</p><p><strong>Methods: </strong>This single-center, randomized clinical trial enrolled 213 inpatients with depression and comorbid symptoms. Participants were randomly assigned to receive either SSRIs treatment or antidepressant treatment combined with acupuncture for two weeks. Clinical outcomes were assessed using the Hamilton Depression Rating Scale (HAMD), Hamilton Anxiety Rating Scale (HAMA), Mini-Mental State Examination (MMSE), Pittsburgh Sleep Quality Index (PSQI), and Beck Scale for Suicide Ideation (BSI). The primary outcome was the change in the HAMD reduction rate.</p><p><strong>Results: </strong>Both groups demonstrated significant clinical improvement after two weeks of treatment. However, analysis of covariance (ANCOVA) revealed that the acupuncture group achieved significantly greater reductions in HAMD, HAMA, and PSQI scores, as well as significantly higher MMSE scores, compared with the control group (all adjusted <i>p</i> < 0.05). Hierarchical regression analyses indicated that baseline symptom severity and duration of illness were significant predictors of treatment response.</p><p><strong>Conclusions: </strong>When used as an adjunct to antidepressant therapy, acupuncture provides rapid and broad therapeutic benefits for patients with depression. Compared with SSRI monotherapy, the combined treatment was associated with greater improvements in depressive and anxiety symptoms, sleep quality, and cognitive performance. These findings support the integration of acupuncture into multimodal treatment strategies for managing the complex symptom profile of major depressive disorder.</p><p><strong>Clinical trial registration: </strong>The study has been registered on https://itmctr.ccebtcm.org.cn/en/index.html (registration number: ITMCTR2025001802; registration link: https://trialsearch.who.int/Trial2.aspx?TrialID=ITMCTR2025001802).</p>","PeriodicalId":72151,"journal":{"name":"Alpha psychiatry","volume":"27 4","pages":"52350"},"PeriodicalIF":2.9,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13539995/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148889740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Global Burden and Inequalities in Mental Disorders Across Countries and Territories: 1990 to 2021.","authors":"Dongjun Zhang, Jiali Wu, Mingyue Wu, Xin Chen, Mengyao Jin, Jiahan Gao, Chenglin Zhang, Lina Wang","doi":"10.31083/AP51756","DOIUrl":"10.31083/AP51756","url":null,"abstract":"<p><strong>Background: </strong>Although the global burden of mental disorders has been extensively documented, systematic assessments of cross-country inequalities, particularly regarding how this burden varies across levels of socio-demographic development, remain limited.</p><p><strong>Methods: </strong>Data on disability-adjusted life-years (DALYs) attributable to mental disorders and the socio-demographic index (SDI) were obtained from the 2021 Global Burden of Disease Study. Absolute and relative inequalities were assessed using the slope index of inequality (SII) and concentration index (CI).</p><p><strong>Results: </strong>Between 1990 and 2021, the total number of DALYs attributable to mental disorders increased by 73.4%, with the largest increase observed among adults aged 30 to 54 years. Age-standardized DALY rates increased by 9.4%, primarily driven by anxiety disorders, eating disorders, and depressive disorders. Females exhibited higher age-standardized rates of depressive disorders, anxiety disorders, bipolar disorder, and eating disorders, whereas males had higher rates of schizophrenia, autism spectrum disorder, conduct disorder, attention-deficit/hyperactivity disorder (ADHD), and other mental disorders. Anxiety disorders and depressive disorders were the primary contributors to the increasing burden, particularly among women and adolescents. In 2021, the burden of mental disorders showed substantial geographical variation across countries and territories. Inequality analyses demonstrated that the SII for overall mental disorders increased from 69 to 243, whereas relative inequality remained stable over time. Across SDI strata, high-SDI countries experienced a greater burden of eating disorders, ADHD, schizophrenia, and anxiety disorders, while low-SDI countries experienced a greater burden of depressive disorders and idiopathic developmental intellectual disability.</p><p><strong>Conclusions: </strong>The burden of mental disorders remains substantial and unequally distributed worldwide. Persistent and widening disparities over the past three decades highlight the urgent need for strengthened global health policies and coordinated multilevel interventions aimed at reducing inequalities across countries with differing levels of socio-demographic development.</p>","PeriodicalId":72151,"journal":{"name":"Alpha psychiatry","volume":"27 4","pages":"51756"},"PeriodicalIF":2.9,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540006/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148889363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}