Psychological Medicine最新文献

Background: Cannabis is one of the most commonly used drugs globally, although its legal status varies across regions. Public support for its decriminalization has increased, but gaps in our understanding of the health consequences of cannabis use remain, particularly related to its impact on mental health. This article provides an updated systematic review and meta-analysis (previous being Lev-Ran et al., ) looking at the relationship between cannabis and depression.

Methods: Literature available before March 2023 was screened for longitudinal studies that included cannabis use and depression. Cross-sectional studies and those only looking at special populations were excluded. Studies must have also controlled for depression at baseline to allow for investigation of a temporal relationship. Extracted data included cannabis measures, depression outcomes, adjusted odds ratios, and study settings. Meta-analysis employed a random effects model with multilevel meta-regression for effect size moderators.

Results: The search yielded 1,599 titles from various databases, resulting in 22 studies for meta-analysis, including 14 from Lev-Ran et al. Eleven studies were US-based, with participants mostly under 18. Meta-analysis showed a higher risk of depression among cannabis users (OR: 1.29, 95% CI: 1.13-1.46). Risk of bias assessment showed medium risk across studies with exposure measurement being a key bias area. The funnel plot and Egger's Sandwich test did not suggest publication bias.

Conclusions: This study underscores the association between cannabis use and depression but also emphasizes the need for further research, especially in understanding usage patterns, heavy use definitions, and long-term effects on depression risk amidst changing cannabis trends.

Background: Previous research has shown abnormal functional network gradients in Alzheimer's disease (AD). Structural network gradient is capable of capturing continuous changes in brain morphology and has the ability to elucidate the underlying processes of neurodevelopment. However, it remains unclear whether structural network gradients are altered in AD and what associations exist between these changes and cognitive function, and gene expression profiles.

Methods: By constructing an individualized structural network gradient decomposition framework, we calculated the morphological similarity network (MSN) gradients for 404 subjects (186 AD patients and 218 normal controls). We investigated AD-related alterations in MSN gradients, along with the associations between MSN gradients and cognitive function, MSN topological properties, and gene expression profiles.

Results: Our findings indicated that the principal MSN gradient alterations in AD were primarily characterized by an increase in the primary and secondary sensory cortices and a decrease in the association cortex 1. The primary and higher-order cortices exhibited opposite associations with cognition, including executive function, language skills, and memory processes. Moreover, the principal MSN gradients were found to significantly predict cognitive function in AD. The altered gradient pattern was 14.8% attributable to gene expression profiles, and the genes demonstrating the highest correlation are involved in metabolic activity and synaptic signaling.

Conclusions: Our results offered novel insights into the underlying mechanisms of structural brain network impairment in AD patients, enhancing our understanding of the neurobiological processes responsible for impaired cognition in patients with AD, and offering a new dimensional structural biomarker for AD.

Background: Maternal perinatal mental health is essential for optimal brain development and mental health of the offspring. We evaluated whether maternal depression during the perinatal period and early life of the offspring might be selectively associated with altered brain function during emotion regulation and whether those may further correlate with physiological responses and the typical use of emotion regulation strategies.

Methods: Participants included 163 young adults (49% female, 28-30 years) from the ELSPAC prenatal birth cohort who took part in its neuroimaging follow-up and had complete mental health data from the perinatal period and early life. Maternal depressive symptoms were measured mid-pregnancy, 2 weeks, 6 months, and 18 months after birth. Regulation of negative affect was studied using functional magnetic resonance imaging, concurrent skin conductance response (SCR) and heart rate variability (HRV), and assessment of typical emotion regulation strategy.

Results: Maternal depression 2 weeks after birth interacted with sex and showed a relationship with greater brain response during emotion regulation in a right frontal cluster in women. Moreover, this brain response mediated the relationship between greater maternal depression 2 weeks after birth and greater suppression of emotions in young adult women (ab = 0.11, SE = 0.05, 95% CI [0.016; 0.226]). The altered brain response during emotion regulation and the typical emotion regulation strategy were also as sociated with SCR and HRV.

Conclusions: These findings suggest that maternal depression 2 weeks after birth predisposes female offspring to maladaptive emotion regulation skills and particularly to emotion suppression in young adulthood.

Background: Refugee experiences of trauma and displacement can significantly disrupt established social networks. While social functioning has been routinely associated with mental health, to our knowledge, no study has tested the direction of influence between social and psychological functioning within displaced refugee communities. This study investigated the temporal association between psychological symptoms (PTSD, depression, anger) and multiple facets of social functioning (including community connectedness, perceived social responsibility, positive social support and negative social support).

Method: A culturally diverse sample of refugees (N = 1,235) displaced in Indonesia completed an online survey at four time-points, six months apart. Longitudinal structural equation modelling was used to investigate the temporal ordering between psychological symptoms and social functioning.

Results: Findings revealed that greater psychological symptoms were associated with a subsequent deterioration in social functioning (decreased positive social support and community connectedness and increased negative social support and perceived social responsibility). Greater perceived social responsibility was also associated with subsequent increases in psychological symptoms, while positive social support and community connectedness were bi-directionally associated over-time.

Conclusions: These findings highlight the potential utility of mental health interventions for displaced refugees as a means to improve social functioning and inclusion with host communities. Findings have important implications in guiding the development of interventions and allocation of resources to support refugee engagement and wellbeing in displacement contexts.

Background: Post-traumatic stress disorder (PTSD) is a mental health condition caused by the dysregulation or overgeneralization of memories related to traumatic events. Investigating the interplay between explicit narrative and implicit emotional memory contributes to a better understanding of the mechanisms underlying PTSD.

Methods: This case-control study focused on two groups: unmedicated patients with PTSD and a trauma-exposed control (TEC) group who did not develop PTSD. Experiments included real-time measurements of blood oxygenation changes using functional near-infrared spectroscopy during trauma narration and processing of emotional and linguistic data through natural language processing (NLP).

Results: Real-time fNIRS monitoring showed that PTSD patients (mean [SD] Oxy-Hb activation, 0.153 [0.084], 95% CI 0.124 to 0.182) had significantly higher brain activity in the left anterior medial prefrontal cortex (L-amPFC) within 10 s after expressing negative emotional words compared with the control group (0.047 [0.026], 95% CI 0.038 to 0.056; p < 0.001). In the control group, there was a significant time-series correlation between the use of negative emotional memory words and activation of the L-amPFC (latency 3.82 s, slope = 0.0067, peak value = 0.184, difference = 0.273; Spearman's r = 0.727, p < 0.001). In contrast, the left anterior cingulate prefrontal cortex of PTSD patients remained in a state of high activation (peak value = 0.153, difference = 0.084) with no apparent latency period.

Conclusions: PTSD patients display overactivity in pathways associated with rapid emotional responses and diminished regulation in cognitive processing areas. Interventions targeting these pathways may alleviate symptoms of PTSD.

Background: Adverse childhood experiences (ACEs) have been associated with increased risks of autoimmune diseases. However, data are scarce on the role of specific ACEs as well as the potential mediating role of adverse mental health symptoms in this association.

Methods: A cohort study using the nationwide Icelandic Stress-And-Gene-Analysis (SAGA, 22,423 women) cohort and the UK Biobank (UKB, 86,492 women) was conducted. Participants self-reported on five ACEs. Twelve autoimmune diseases were self-reported in SAGA and identified via hospital records in UKB. Poisson regression was used to assess the cross-sectional association between ACEs and autoimmune diseases in both cohorts. Using longitudinal data on self-reported mental health symptoms in the UKB, we used causal mediation analyses to study potential mediation by depressive, anxiety, and PTSD symptoms in the association between ACEs and autoimmune diseases.

Results: The prevalence of ACEs was 50% in SAGA and 35% in UKB, while the prevalence of autoimmune diseases was 29% (self-reported) and 14% (clinically confirmed), respectively. In both cohorts, ACEs were associated with an increased prevalence ratio (PR) of any studied autoimmune disease in a dose-response manner (PR = 1.10 (95%CI = 1.08-1.12) per ACE), particularly for Sjögrens (PR = 1.34), polymyalgia rheumatica (PR = 1.20), rheumatoid arthritis (PR = 1.14), systemic lupus erythematosus (PR = 1.13), and thyroid disease (PR = 1.11). Sexual abuse and physical and emotional neglect were consistently associated with an elevated prevalence of autoimmune diseases when including all ACEs in the model. Approximately one fourth of the association was mediated through depression, anxiety, and PTSD.

Conclusions: These findings based on two large cohorts indicate a role of ACEs and corresponding mental health distress in autoimmune diseases among adult women.

Background: Based on facial expression experiments, childhood adversity may be associated with threat-related information processing bias. Yet, it is unclear whether this generalizes to other threat-related stimuli, such as social and non-social visual scenes.

Methods: We combined fast periodic visual stimulation with frequency-tagging electroencephalography (EEG) and eye-tracking to assess automatic and implicit neural discrimination, neural salience and preferential looking towards negative versus neutral social and non-social visual scenes in young adults aged 16-24 years (51 with childhood adversity and psychiatric symptoms and 43 controls).

Results: Controls showed enhanced negative-neutral neural discrimination within a social versus non-social context. However, this facilitating effect of social content was absent in those with adversity, suggesting a selective alteration in social threat processing. Moreover, individual differences in adversity severity, and more specifically threat experiences (but not neglect experiences), were associated with decreased neural discrimination of negative versus neutral social scenes, corresponding to similar findings in facial expression processing, indicating the robustness of adversity-related deficits in threat-safety discrimination across social visual stimuli.

Conclusions: The adversity-related decreased threat-safety discrimination might impact individuals' perception of social cues in daily life and relate to poor social functioning and future development of psychopathology.

Background: Previous findings in psychosis have revealed mixed findings on glutamate (Glu) levels in the dorsal anterior cingulate cortex (dACC). Factors such as illness chronicity, methodology, and medication status have impeded a more nuanced evaluation of Glu in psychosis. The goal of this longitudinal neuroimaging study was to investigate the role of antipsychotics on Glu in the dACC in antipsychotic-naïve first-episode psychosis (FEP) patients.

Methods: We enrolled 117 healthy controls (HCs) and 113 antipsychotic-naïve FEP patients for this study. 3T proton magnetic resonance spectroscopy (1H-MRS; PRESS; TE = 80 ms) data from a voxel prescribed in the dACC were collected from all participants at baseline, 6, and 16 weeks following antipsychotic treatment. Glutamate levels were quantified using the QUEST algorithm and analyzed longitudinally using linear mixed-effects models.

Results: We found that baseline dACC glutamate levels in FEP were not significantly different than those of HCs. Examining Glu levels in FEP revealed a decrease in Glu levels after 16 weeks of antipsychotic treatment; this effect was weaker in HC. Finally, baseline Glu levels were associated with decreases in positive symptomology.

Conclusions: We report a progressive decrease of Glu levels over a period of 16 weeks after initiation of treatment and a baseline Glu level association with a reduction in positive symptomology, suggestive of a potential mechanism of antipsychotic drug (APD) action. Overall, these findings suggest that APDs can influence Glu within a period of 16 weeks, which has been deemed as an optimal window for symptom alleviation using APDs.

Background: Post-traumatic stress disorder (PTSD) is characterized by severe distress and associated with cardiometabolic diseases. Studies in military and clinical populations suggest that dysregulated metabolomic processes may be a key mechanism. Prior work identified and validated a metabolite-based distress score (MDS) linked with depression and anxiety and subsequent cardiometabolic diseases. Here, we assessed whether PTSD shares metabolic alterations with depression and anxiety and if additional metabolites are related to PTSD.

Methods: We leveraged plasma metabolomics data from three subsamples nested within the Nurses' Health Study II, including 2835 women with 2950 blood samples collected across three time points (1996-2014) and 339 known metabolites assayed by mass spectrometry-based techniques. Trauma and PTSD exposures were assessed in 2008 and characterized as follows: lifetime trauma without PTSD, lifetime PTSD in remission, and persistent PTSD symptoms. Associations between the exposures and the MDS or individual metabolites were estimated within each subsample adjusting for potential confounders and combined in random-effects meta-analyses.

Results: Persistent PTSD symptoms were associated with higher levels of the previously developed MDS. Out of 339 metabolites, we identified 29 metabolites (primarily elevated glycerophospholipids and glycerolipids) associated with persistent symptoms (false discovery rate < 0.05; adjusting for technical covariates). No metabolite associations were found with the other PTSD-related exposures.

Conclusions: As the first large-scale, population-based metabolomics analysis of PTSD, our study highlighted shared and distinct metabolic differences linked to PTSD versus depression or anxiety. We identified novel metabolite markers associated with PTSD symptom persistence, suggesting further connections with metabolic dysregulation that may have downstream consequences for health.