Psychological Medicine最新文献

Background: Girls with predispositions for disordered eating (DE) may select into weight-conscious peer groups (i.e. peer groups that emphasize body weight/shape). However, factors driving selection into these peer groups remain unknown, as genetic and/or environmental predisposition to DE may lead girls to select weight-conscious peers. To explore what may drive selection, the present study investigated whether genetic or shared environmental influences underlie associations between DE and exposure to weight-conscious peers and whether effects differ by pubertal status.

Methods: Participants included 833 female twins (ages 8-15) from the Michigan State University Twin Registry. Bivariate twin models were conducted to explore etiologic overlap between DE and exposure to weight-conscious peers. Separate models were run for pre-early pubertal girls and mid-late pubertal girls given past research demonstrates differences in genetic and environmental contributions underlying eating pathology by pubertal status.

Results: During pre-early puberty, shared and non-shared environmental correlations accounted for the overlap between DE and weight-conscious peer group exposure. Furthermore, shared environmental and non-shared environmental influences underlying DE contributed to 33.3% and 20.0% of the individual differences in weight-conscious peer group membership, respectively. In mid-late puberty, the genetic and non-shared environmental correlations accounted for the overlap between DE and weight-conscious peer group exposure. Genetic and non-shared environmental influences underlying DE contributed to 37.5% and 19.4% of the variance in weight-conscious peer group membership, respectively.

Conclusions: While selection effects may exist across development, these effects may be driven by variance in DE due to shared environment in pre-early puberty and genes in mid-late puberty.

Background: Cumulative stress exposure is extensively involved in carcinogenesis. However, cancer risk associated with allostatic load (AL), a valid measure of chronic stress, has not been comprehensively evaluated in large cohorts, and the combined effect of AL and personality trait on cancer risk remains unknown.

Methods: This prospective cohort study was conducted based on 245,683 participants from the UK Biobank, with a median follow-up of 13.5 years. The AL score was calculated based on 11 biomarkers. Personality traits were constructed and categorized into two clusters. Multivariable Cox regression model was used to assess the risk of incident cancer according to AL and personality clusters, and multiplicative and additive interactions were evaluated.

Results: High AL was associated with an increased cancer risk compared to low AL (hazard ratio [HR] = 1.06, 95% confidence interval [CI]: 1.04-1.09), particularly for cancers of stomach, liver, kidney, esophageal, lung, colorectal, breast, and leukemia (HR ranged from 1.08 to 1.43). Personality clusters was associated with risk of lung cancer (HR = 1.14, 95% CI: 1.05-1.23), but not overall cancer. Significant synergistic interaction was observed between high AL and 'nervous-dominant' personality for overall cancer risk, with the strongest association observed for liver cancer (HR = 1.58, 95% CI: 1.24-2.02).

Conclusions: High AL was related to higher risks of overall cancer and site-specific cancers, particularly when combined with nervous-dominant personality, highlighting the interplay between chronic physiological stress and psychological factors in cancer development.

Background: 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.

Methods: 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.

Results: 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.

Conclusions: 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.

Background: Evidence regarding the effects of antipsychotic medication on cognitive functioning after a first-episode psychosis (FEP) remains inconclusive. This study examined whether dopamine D₂ receptor occupancy, affinity, and antipsychotic dose are related to cognitive functioning in people in remission from FEP.

Methods: 278 remitted FEP participants from the HAMLETT-trial were included. Cognitive functioning was assessed with the Brief Assessment of Cognition in Schizophrenia, 3-6 months after remission. D₂ receptor occupancy was estimated based on antipsychotic type and dose. Antipsychotics were categorized into partial agonists, or antagonists with high or low D₂ receptor affinity. Linear regression analyses were performed with inverse probability of treatment weighting to control for differences in characteristics between groups.

Results: D₂ receptor occupancy was negatively related to global cognition (β = -0.18), verbal fluency (β = -0.22), and attention and processing speed (β = -0.17, all p < 0.003). The interaction between daily dose and D₂ receptor affinity category was significant for global cognition (p = 0.0046) and working memory (p = 0.0019), but not for verbal fluency after correction for multiple testing (p = 0.029). Interactions showed that higher daily dose was related to lower cognitive functioning, with significantly stronger negative effects in high-affinity antagonists compared to other antipsychotics.

Conclusions: The current findings underscore the importance of antipsychotic D₂ receptor occupancy and affinity for cognitive functioning and suggest better cognitive functioning in users of partial agonists and low D₂ receptor affinity antipsychotics. This can be important when selecting antipsychotics for individuals with FEP.

Background: While prenatal exposure to tobacco has been associated with adolescent suicide attempt, little is known about the mechanisms explaining this association. This study aims to explore the mediating roles of internalizing symptoms, externalizing behaviors, and peer problems across childhood in the association between prenatal exposure to tobacco and adolescent suicide attempt.

Methods: We analyzed data from N = 8,861 participants from the Millennium Cohort Study followed from ages 9 months to 17 years. Binary logistic regression models were used to investigate the total association between exposure to tobacco in pregnancy and suicide attempt, and mediation analyses were conducted using structural equation models to investigate the direct and indirect associations.

Results: In models adjusted for key covariates, we found a significant association between prenatal tobacco exposure and increased risk of adolescent suicide attempts (odds ratio = 2.08, 95% confidence interval = [1.68, 2.56]), partly mediated through internalizing problems, externalizing behaviors, and peer problems from ages 3 to 14 years (accounting for 37% of the total association, that is, 16%, 12%, and 9%, respectively).

Conclusions: These findings suggest that interventions targeting mental health symptoms and peer problems may maximize suicide prevention efforts among children who were prenatally exposed to tobacco, thus potentially reducing the long-term risk of suicide attempt.

Background: Anhedonia is a multidimensional concept, and it is not known which aspects of it are linked to the heterogeneity of treatment responses in major depressive disorder (MDD). We examine the role of anhedonia dimensions in predicting response to antidepressant medication and adjunctive pharmacotherapy.

Methods: In CAN-BIND-1, 187 adults with MDD completed the Dimensional Anhedonia Rating Scale (DARS) and the Snaith-Hamilton Pleasure Scale (SHAPS) before undergoing 8 weeks of treatment with escitalopram. At week 8, 90 nonresponders received adjunctive treatment with aripiprazole for an additional 8 weeks. Mixed-effects models tested the hobbies, food, social, and sensory subscales and items of DARS and SHAPS as predictors of change in the Montgomery-Åsberg Depression Rating Scale (MADRS).

Results: Of the four DARS subscales, sensory anhedonia predicted a worse treatment outcome with escitalopram (b = 1.14, 95%CI 0.08 to 2.20, p = 0.034) as did a three-item SHAPS sensory anhedonia subscale (b = 1.50, 95%CI 0.43 to 2.57, p = 0.006). A combined DARS-SHAPS sensory anhedonia subscale complemented the previously reported interest-activity symptom dimension to improve treatment outcome prediction. In contrast, food and social anhedonia dimensions predicted worse outcomes with adjunctive aripiprazole (b = 2.52, 95%CI 1.25 to 3.80, p < 0.001; b = 2.56, 95%CI 1.16 to 3.96, p < 0.001). Corresponding SHAPS items showed similar results.

Conclusions: The inability to enjoy sensory experiences and the lack of interest in food and social activities distinctly predict outcomes with serotonergic versus dopaminergic pharmacotherapy. These findings require replication and extension to other treatments.

Over twenty years ago, an editorial in this journal called for further studies of the epidemiological and psychopathological characteristics of 'recurrent brief depression' in clinical samples in primary and secondary care settings. At that time, relatively little was known about the epidemiology or potential neuropsychobiology of the condition, and no evidence-based treatments had been identified. Two decades have passed, but there have been no substantial developments in understanding in the last ten years. The seeming withdrawal from research into recurrent brief depression is regrettable, given widespread concerns about the burden of depressive symptoms in young people. It seems reasonable to call once again for further investigations in clinical samples, this time with a focus on younger individuals.

Background: Adults with intellectual disability (ID) experience marked mental health inequities, yet population-wide estimates that capture both primary- and specialist-care diagnoses remain scarce.

Methods: Using nationwide Swedish registries, including primary care, specialist, inpatient, prescription drug, criminal, and suspicion registers, we included all individuals born in Sweden between 1958 and 1997 (N = 3,970,600), including 38,818 individuals with ID diagnoses (0.98%; 49.1% mild, 13.3% moderate, and 9.6% severe/profound). Hazard ratios (HR) were calculated using Cox proportional hazards regression to estimate the relative risk of lifetime diagnoses of major depression, anxiety disorders (ANX), obsessive-compulsive disorder (OCD), bipolar disorder (BD), attention-deficit/hyperactivity disorder (ADHD), drug use disorder, alcohol use disorder, schizophrenia, and other nonaffective psychosis. Additionally, cohort effects on psychiatric diagnosis risks in adults with intellectual disabilities versus the general population were evaluated.

Results: People with ID were at higher risk for all psychiatric and substance use disorders, with HRs ranging from 1.7-2.0 for major depression and anxiety, drug and alcohol use disorders, 3.5-5.8 for BD, OCD and ADHD, and 10.9-12.7 for schizophrenia and other nonaffective psychosis. Higher prevalence was consistently seen among those with mild versus moderate or severe/profound intellectual disability. Relative risks narrowed modestly in successive birth cohorts, although absolute differences remained substantial.

Conclusions: Across six decades of follow-up, adults with ID faced markedly higher psychiatric and substance-use morbidity - most pronounced for psychotic disorders - than the general population. Whole-system mental-health screening and tailored interventions are required to address this persistent disparity.

Background: Impaired social functioning is commonly observed in youth at clinical high risk (CHR) for psychosis. Interpersonal synchrony, defined as the temporal alignment of movement between interacting partners, is a key component of successful social interactions. This study aimed to investigate interpersonal head synchrony in naturalistic virtual settings among CHR individuals using automated video analysis tools.

Methods: We analyzed short video recordings from virtual clinical interviews involving 116 participants including 50 CHR participants, 36 individuals with sub-threshold positive symptoms (SUB), and 30 healthy controls (HC). Vertical head movement time series were extracted using an open-access video-based head-tracking tool. Interpersonal head synchrony was computed using Windowed Cross-Correlation to assess group differences and associations with clinical symptoms and functioning.

Results: CHR participants showed significantly reduced strength of synchrony compared to HC (β = -0.05, 95% CI [-0.09, -0.02], p = .004), although 14% of variance in strength of synchrony was attributable to assessor identity. No significant group differences were found for delay of synchrony. Within the CHR group, delay of synchrony was positively associated with social anhedonia (r = 0.29). Strength of synchrony correlated with better social (r = 0.33) and role (r = 0.28) functioning.

Conclusion: Our findings suggest that impaired interpersonal head synchrony is already present in the psychosis-risk state and relates to negative symptoms and social and role functioning. These findings support the utility of nonverbal synchrony as a potential biomarker and demonstrate the feasibility of automated tools and virtual assessments to study social processes in at-risk populations.