Psychological Medicine最新文献

Background: Irritable bowel syndrome (IBS) commonly co-occurs with psychological distress, including depression and anxiety, but the temporal and bidirectional nature of this relationship remains unclear. Dysregulation of the gut-brain-microbiota axis has been proposed as a shared mechanism.

Methods: We conducted two retrospective, population-based cohort studies using Taiwan's National Health Insurance Research Database (2000-2015). Cohort 1 assessed the risk of incident IBS among patients with newly diagnosed depression or anxiety, while Cohort 2 evaluated the risk of subsequent depression or anxiety among patients with newly diagnosed IBS. Propensity score matching, multivariable Cox regression, and Fine-Gray competing risk models were applied.

Results: IBS was associated with increased risks of depression (adjusted hazard ratio [aHR] = 1.55) and anxiety (aHR = 1.68). Conversely, depression and anxiety were associated with higher risks of developing IBS (aHR = 1.45 and 1.51, respectively). Associations were stronger among females and younger adults aged 18-39 years. Sleep disorders (SDs) showed the strongest modifying effect in both directions (sub-distribution HR ≈ 1.60). Results were consistent across sensitivity analyses.

Conclusions: This nationwide longitudinal study demonstrates a robust bidirectional association between IBS and psychological distress, supporting integrated screening and multidisciplinary care approaches targeting gut-brain interactions.

Background: Seeking to clarify the parent-offspring transmission of Major Depression (MD) and type I Bipolar Disorder (BD), we examined offspring MD and BD risk in five informative parental pairs: Unaffected x MD, Unaffected x BD, MDxMD, MDxBD and BDxBD.

Methods: We identified 289,637 individuals born in Sweden 1970-1990, followed through 2018, from parents with MD and/or BD identified from Swedish medical registers. We quantified the MD→MD, BD→BD, MD→BD and BD→MD parent-offspring transmission and explored effects of parental illness on MD→BD conversions.

Results: The risk for MD was modestly and similarly increased in offspring of Unaffected x MD (HR=1.64) and Unaffected x BD parents (HR=1.53), higher in MDxMD and MDxBD pairings (HRs=2.39 and 2.47) and slightly lower in BDxBD matings (HR=2.29). By contrast, risk for BD was much higher in Unaffected x BD versus Unaffected x MD matings (HRs = 5.59 vs. 1.70), further elevated modestly in MDxBD matings (HR=6.26) and very high in BDxBD matings (HR=13.61). The rate of offspring MD→BD conversions was substantially increased by parental BD but not parental MD. Offspring BD was equally predicted by paternal and maternal affective illness while offspring MD was more strongly predicted by maternal than paternal affective illness.

Conclusions: Examining risk for MD and BD in offspring of different parental mating types of MD and BD is an informative strategy for further clarifying the cross-generational transmission of these two partially related and partially distinct mood disorders.

Background: People with schizophrenia develop more chronic diseases at a younger age and die younger than people in the general population. It has been hypothesized that this excess morbidity and mortality could be partially due to accelerated aging in schizophrenia. If true, this would motivate the development of 'gero-protective' interventions to reduce chronic disease burden in schizophrenia. However, it has been difficult to test this hypothesis, in part, due to the limited ability to measure aging in samples of people with schizophrenia.

Methods: We utilized a novel neuroimaging biomarker of the longitudinal pace of aging, DunedinPACNI, to test for accelerated whole-body aging in schizophrenia across four neuroimaging datasets (total N = 2,096, 48% female) accessed through the Lieber Institute for Brain Development, the University of Bari Aldo Moro, and the North American Prodrome Longitudinal Study - 3.

Results: We found consistent evidence of faster DunedinPACNI in schizophrenia compared with controls. In contrast, youth at clinical-high risk for psychosis did not have faster DunedinPACNI compared to controls. Unaffected siblings of patients also did not have faster DunedinPACNI than controls. Faster DunedinPACNI in schizophrenia was not explained by tobacco smoking or antipsychotic medication use.

Conclusions: The results support the hypothesis that schizophrenia is accompanied by accelerated aging. Results were inconsistent with some of the most obvious explanations for accelerated aging in schizophrenia (familial risk, smoking, and iatrogenic medication effects). Research should aim to uncover why people who have schizophrenia age rapidly, as well as the utility of early disease-risk monitoring and anti-aging interventions in schizophrenia.

Background: The co-occurrence of psychotic disorders and borderline personality disorder (BPD) complicates clinical management, with overlapping symptoms exacerbating morbidity and impairing therapeutic outcomes. This systematic review and meta-analysis aimed to estimate the prevalence of psychotic disorders and BPD co-occurrence, including with first-episode psychosis (FEP) and to describe associated sociodemographic and clinical characteristics.

Methods: Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, four databases were systematically searched from inception to June 2025. Eighteen studies met the inclusion criteria. Data extraction and quality appraisal (Effective Public Health Practice Project tool) were conducted independently by two reviewers. Random-effects meta-analyses estimated pooled prevalence rates.

Results: The pooled prevalence of BPD in people with psychotic disorders was 22.7% (95% CI: 14.2–34.3%), while 14.3% (95% CI: 5.5–32.1%) of individuals with BPD had a comorbid psychotic disorder. In FEP samples, 40.0% (95% CI: 21.9–61.3%) met the criteria for BPD. People with both conditions, often young women, showed greater emotional dysregulation, suicidality, psychotic symptoms, and social dysfunction. Trauma, dissociation and substance use emerged as frequent vulnerability factors. However, most studies were cross-sectional, with small samples and high heterogeneity (I² > 80%), limiting generalizability.

Conclusion: This co-occurrence constitutes a distinct clinical subgroup with complex needs. Categorical diagnostic approaches may fail to capture the dimensional nature of overlapping affective and psychotic symptoms. Integrative and personalized care pathways, especially in early intervention settings, are warranted. This review was registered in PROSPERO (CRD42024577525).

Background: Neurodevelopmental models regard impulsivity as a central risk factor for adolescent substance use. However, the practical utility of impulsivity in predicting substance use is complicated by variability among measures that encompass multiple methods and theoretical domains. Prior research has been constrained by cross-sectional designs, small sample sizes, and/or the use of a narrow subset of impulsivity measures.

Method: Leveraging the ABCD dataset (n = 11,868), we identified and replicated correlations among impulsivity measures and assessed their prospective longitudinal and concurrent predictive utility regarding adolescent substance use outcomes before 15 years old. We then used simulation to inform how associations between impulsivity and substance use vary across sampling strategies (population vs. high-risk cohorts) and sample sizes.

Findings: Correlations between questionnaire and behavioral measures of impulsivity were small, and questionnaires significantly outperformed behavioral measures in predicting substance use initiation, largely due to the contribution of the CBCL externalizing scale. Predictions of substance use based on impulsivity were statistically detectable but small according to clinical standards (AUCs 0.6-0.76), exhibiting sensitivity to sample size and base rate of substance use, and thus, poor absolute predictive performance. Large samples (n > 1,000) were needed to achieve adequate power for impulsivity measures to predict substance use initiation.

Conclusion: These results support a significant but small contribution of impulsivity in predicting the onset of early adolescent substance use, indicating that these factors alone are insufficient for clinically deployable prediction. In community samples, large sample sizes are needed for reproducible impulsivity prediction of adolescent substance use.

Background: Depression is a common comorbidity in neuropsychiatric disorders, affecting a significant proportion of patients with neurodegenerative diseases. Traditional antidepressants show limited efficacy, particularly in cases involving comorbid depressive symptoms, highlighting the need for alternative treatments.

Methods: Here we provide the first data on possible benefits of add-on therapy with transcranial pulse stimulation (TPS). Based on the largest patient sample in the emerging field of focused ultrasound (FUS) neuromodulation to date, a retrospective analysis was conducted on 88 patients with various neuropsychiatric diagnoses to evaluate the impact of TPS on depressive symptoms, measured by the Beck Depression Inventory (BDI-II).

Results: The study revealed significant improvements in BDI-II scores posttreatment (N = 88), with the most substantial effects observed in more severely impacted patients: individuals with minimal to severe depression (BDI-II ≥9; N = 32) experienced an average reduction of 5.22 points (29.46%), while those with mild to severe depression (BDI-II ≥14; N = 15) showed an even greater mean improvement of 10.40 points (40.51%). These results surpassed established thresholds for clinical relevance and substantially exceeded placebo effect sizes observed in relevant brain stimulation studies. Moreover, depression score improvement was independent of diagnostic group (dementia, movement disorders, or other), improvement of the primary diagnosis, antidepressant medication, and baseline cognitive status, highlighting the potential of TPS as an effective therapeutic add-on intervention for patients receiving state-of-the-art treatments.

Conclusions: The study's findings indicate that TPS enhances depression outcomes in neuropsychiatric patients, particularly in those with more severe depressive symptoms.

This systematic review and meta-analyses provide the first synthesis of the literature on trait mindfulness and psychotic-like experiences (PLEs). Theoretical models suggest a protective function of mindfulness and it is important to understand any potential role of mindfulness in the prevention and treatment of PLEs. We examined the following: (1) What is the relationship between trait mindfulness and PLEs in nonclinical populations?; and (2) What is the effect of mindfulness-based interventions (MBIs) on PLEs in nonclinical populations? Five databases were searched, and effect sizes were extracted for each study. Seventeen papers were included in the review. Eleven papers explored the relationship between mindfulness and PLEs, and the meta-regression found a small negative association between PLEs and mindfulness (k = 8; pooled correlation r = -0.25; 95% confidence interval [CI]: -0.37, -0.13, p < .001). Eight studies investigated the effect of MBIs on PLEs and the summary effect was not significant in the meta-analysis (k = 5; pooled standard mean difference = .09; 95% CI: -0.61, 0.79, p = 0.80). Overall, the findings suggest that higher levels of mindfulness are associated with reduced PLEs, with no evidence for the effectiveness of MBIs in reducing PLEs. Findings should be interpreted cautiously given the small number of studies and high heterogeneity in the meta-analyses. Future studies are needed to determine whether MBIs might prevent the transition to psychosis or an at-risk mental state and might usefully measure a broader range of clinically relevant outcomes.

Background: Extensive evidence links air pollution exposure to cognitive decline; however, it remains unclear whether cognitive reserve and brain reserve modify this association. We examined the moderating roles of cognitive reserve contributors and brain reserve in the association between air pollution and cognitive function in dementia-free adults.

Methods: Cross-sectional data were obtained from 650 participants who underwent 3T brain magnetic resonance imaging and completed the Montreal Cognitive Assessment (MoCA). Cognitive reserve contributors were assessed based on education, occupation, and social engagement. Brain reserve was quantified using the ventricle-to-brain ratio derived from brain scans. Five-year average concentrations of particulate matter with diameters ≤10 and ≤2.5 μm and nitrogen dioxide were estimated based on residential addresses. Partial least squares structural equation modeling was applied to construct latent variables representing the air pollution mixture and composite cognitive reserve (contributors). Analyses examined whether cognitive reserve contributors and brain reserve modified associations of air pollution with MoCA scores and suspected mild cognitive impairment.

Results: In individuals with an average level of cognitive reserve, a 1-standard deviation increase in air pollution mixture was associated with a 0.24-point decrease in MoCA scores (95% confidence interval [CI]: -0.31 to -0.16). This association was attenuated in individuals with higher cognitive reserve (β = -0.12; 95% CI: -0.25 to 0.02) and intensified in those with lower cognitive reserve (β = -0.36; 95% CI: -0.37 to -0.35). The moderating effect of brain reserve was not significant.

Conclusions: Higher cognitive reserve may mitigate the effects of air pollution on cognitive function.