Adverse childhood experiences (ACEs) are associated with increased long-term mental and physical health risk, yet inter-individual variation indicates that resilience is possible. Distinct trajectories of sustained mental well-being have been observed among individuals exposed to ACEs, predicting favorable long-term outcomes. However, the biopsychosocial markers underpinning sustained trajectories of resilience remain poorly understood. This study aimed to identify factors that predict higher well-being (‘resilient’) trajectories over time in individuals with and without ACE exposure.

Previously identified 12-year well-being trajectory classes (higher vs. lower well-being) were examined in participants with no ACE history (n = 779) and those exposed to ACEs (n = 889). Logistic regression models were used to identify factors differentiating higher versus lower well-being trajectories in the non-ACE sample, and resilience versus risk trajectories in the ACE sample. Predictors included childhood adversity characteristics, genetic predisposition, demographic and environmental factors, social and occupational factors, health and lifestyle factors, and psychological functioning.

Across both samples, higher well-being was predicted by higher education, better subjective physical health, greater social engagement, stronger work performance, and adaptive personality traits (lower neuroticism and higher extraversion). In the non-ACE sample, polygenic well-being scores and family history of mental illness further differentiated trajectories. In contrast, resilience following ACEs was additionally characterized by modifiable factors, including parenting style, relationship status, BMI, and conscientiousness.

Resilience in the context of childhood adversity is defined by identifiable, largely modifiable social, health, and personality factors, highlighting potential targets for interventions to enhance long-term well-being.

This review highlights 10 recent advances in climate change research with high policy relevance, spanning diverse topics: (1) the global temperature jump of 2023–2024; (2) sea surface warming and marine heatwaves; (3) land carbon sinks; (4) interactions between climate change and biodiversity loss; (5) accelerated groundwater decline; (6) global dengue incidence; (7) income and labour productivity loss; (8) strategic considerations for scaling carbon dioxide removal (CDR); (9) integrity of carbon credit markets; and (10) policy mixes for climate change mitigation.

Interdisciplinary understanding is vital for delivering sound climate policy advice. However, navigating the ever-growing and increasingly diverse scholarly literature on climate change is challenging for any individual researcher. This annual synthesis highlights and explains recent advances across a variety of fields of climate change research. This year, the 10 insights focus on: (1) the record-warmth of 2023/2024 and the elevated Earth energy imbalance; (2) acceleration of ocean warming and intensifying marine heatwaves; (3) northern land carbon sinks under strain; (4) reinforcing feedback between biodiversity loss and climate change; (5) accelerated depletion of groundwater; (6) global dengue incidence; (7) global income losses and labour productivity declines; (8) strategic scaling of CDR; (9) integrity challenges in carbon credit markets and emerging responses; and (10) effective policy mixes for emissions reductions. The insights have been written to be accessible to researchers from different fields, serving as entry-points to specific topics, as well as providing an overview of the evolving landscape of climate change research. In the final section, the insights are used to develop overarching policy-relevant messages. This paper provides the basis for a science-policy report that was shared with all Party delegations ahead of COP30 in Belém, Brazil.

Highlights of climate change research in 2024–2025: 10insightsclimate.science

Patients with posttraumatic stress disorder (PTSD) exhibit smaller regional brain volumes in commonly reported regions including the amygdala and hippocampus, regions associated with fear and memory processing. In the current study, we have conducted a voxel-based morphometry (VBM) meta-analysis using whole-brain statistical maps with neuroimaging data from the ENIGMA-PGC PTSD working group.

T1-weighted structural neuroimaging scans from 36 cohorts (PTSD n = 1309; controls n = 2198) were processed using a standardized VBM pipeline (ENIGMA-VBM tool). We meta-analyzed the resulting statistical maps for voxel-wise differences in gray matter (GM) and white matter (WM) volumes between PTSD patients and controls, performed subgroup analyses considering the trauma exposure of the controls, and examined associations between regional brain volumes and clinical variables including PTSD (CAPS-4/5, PCL-5) and depression severity (BDI-II, PHQ-9).

PTSD patients exhibited smaller GM volumes across the frontal and temporal lobes, and cerebellum, with the most significant effect in the left cerebellum (Hedges’ g = 0.22, pcorrected = .001), and smaller cerebellar WM volume (peak Hedges’ g = 0.14, pcorrected = .008). We observed similar regional differences when comparing patients to trauma-exposed controls, suggesting these structural abnormalities may be specific to PTSD. Regression analyses revealed PTSD severity was negatively associated with GM volumes within the cerebellum (pcorrected = .003), while depression severity was negatively associated with GM volumes within the cerebellum and superior frontal gyrus in patients (pcorrected = .001).

PTSD patients exhibited widespread, regional differences in brain volumes where greater regional deficits appeared to reflect more severe symptoms. Our findings add to the growing literature implicating the cerebellum in PTSD psychopathology.

Interprofessional teams in the pediatric cardiac ICU consolidate their management plans in pre-family meeting huddles, a process that affects the course of family meetings but often lacks optimal communication and teamwork.

Cardiac ICU clinicians participated in an interprofessional intervention to improve how they prepared for and conducted family meetings. We conducted a pretest–posttest study with clinicians participating in huddles before family meetings. We assessed feasibility of clinician enrollment, assessed clinician perception of acceptability of the intervention via questionnaire and semi-structured interviews, and impact on team performance using a validated tool. Wilcoxon rank sum test assessed intervention impact on team performance at meeting level comparing pre- and post-intervention data.

Totally, 24 clinicians enrolled in the intervention (92% retention) with 100% completion of training. All participants recommend cardiac ICU Teams and Loved ones Communicating to others and 96% believe it improved their participation in family meetings. We exceeded an acceptable level of protocol fidelity (>75%). Team performance was significantly (p < 0.001) higher in post-intervention huddles (n = 30) than in pre-intervention (n = 28) in all domains. Median comparisons: Team structure [2 vs. 5], Leadership [3 vs. 5], Situation Monitoring [3 vs. 5], Mutual Support [ 3 vs. 5], and Communication [3 vs. 5].

Implementing an interprofessional team intervention to improve team performance in pre-family meeting huddles is feasible, acceptable, and improves team function. Future research should further assess impact on clinicians, patients, and families.

Major depressive disorder (MDD) is the leading cause of disability globally, with moderate heritability and well-established socio-environmental risk factors. Genetic studies have been mostly restricted to European settings, with polygenic scores (PGS) demonstrating low portability across diverse global populations.

This study examines genetic architecture, polygenic prediction, and socio-environmental correlates of MDD in a family-based sample of 10 032 individuals from Nepal with array genotyping data. We used genome-based restricted maximum likelihood to estimate heritability, applied S-LDXR to estimate the cross-ancestry genetic correlation between Nepalese and European samples, and modeled PGS trained on a GWAS meta-analysis of European and East Asian ancestry samples.

We estimated the narrow-sense heritability of lifetime MDD in Nepal to be 0.26 (95% CI 0.18–0.34, p = 8.5 × 10−6). Our analysis was underpowered to estimate the cross-ancestry genetic correlation (rg = 0.26, 95% CI −0.29 to 0.81). MDD risk was associated with higher age (beta = 0.071, 95% CI 0.06–0.08), female sex (beta = 0.160, 95% CI 0.15–0.17), and childhood exposure to potentially traumatic events (beta = 0.050, 95% CI 0.03–0.07), while neither the depression PGS (beta = 0.004, 95% CI −0.004 to 0.01) or its interaction with childhood trauma (beta = 0.007, 95% CI −0.01 to 0.03) were strongly associated with MDD.

Estimates of lifetime MDD heritability in this Nepalese sample were similar to previous European ancestry samples, but PGS trained on European data did not predict MDD in this sample. This may be due to differences in ancestry-linked causal variants, differences in depression phenotyping between the training and target data, or setting-specific environmental factors that modulate genetic effects. Additional research among under-represented global populations will ensure equitable translation of genomic findings.

This study aimed to examine the clinical risk factors for cephalosporin resistance in patients with Gram-negative bacteremia caused by Escherichia coli (EC), Klebsiella pneumoniae (KP), Enterobacter cloacae (ENC), and Pseudomonas aeruginosa (PS).

This retrospective cohort study included 400 adults with Gram-negative bacteremia. The goal was to review 100 cases involving each species and approximately half resistant and half susceptible to first-line cephalosporins, ceftriaxone (EC or KP), or cefepime (ENC or PS). Logistic regression was used to identify factors predictive of resistance.

A total of 378 cases of Gram-negative bacteremia were included in the analysis. Multivariate analysis identified significant risk factors for resistance, including admission from a chronic care hospital, skilled nursing facility, or having a history of infection within the prior 6 months (OR 3.00, P < .0001), requirement for mechanical ventilation (OR 3.76, P < .0001), presence of hemiplegia (OR 3.54, P = .0304), and presence of a connective tissue disease (OR 3.77, P = .0291).

Patients without the identified risk factors should be strongly considered for receiving ceftriaxone or cefepime rather than carbapenems and newer broad-spectrum agents.

Extrapyramidal symptoms (EPS) affect 15% to 30% of patients with schizophrenia treated with antipsychotics and have been associated with poor patient outcomes.

To examine the incidence and economic burden of EPS in patients with schizophrenia initiating treatment with atypical antipsychotics (AAPs).

Patients with schizophrenia newly initiating AAPs with no prior EPS were identified in the MarketScan Commercial and Medicare Supplemental database from January 1, 2012 to December 31, 2018. Incidence of EPS (new diagnosis or medication) was assessed in the year following AAP initiation. Patients were classified as developing (EPS cohort) or not developing (non-EPS cohort) EPS. All-cause and schizophrenia-related healthcare resource use and costs were compared between cohorts over the year following the first EPS claim (EPS) or randomly assigned index date (non-EPS). Multivariate models were developed for total healthcare costs and inpatient admissions.

A total of 3558 patients qualified for the study; 22.1% developed EPS in the year following AAP initiation (incidence: 26.9 cases/100-person-years). Multivariate analyses demonstrated that EPS patients had a 34% higher odds of all-cause (OR:1.3361, 95% CI:1.0770-1.6575, P < .01) and 84% increased odds of schizophrenia-related (OR:1.8436, 95% CI:1.0434-2.4219, P < .0001) inpatient admissions, as well as significantly higher all-cause (EPS: $26,632 vs non-EPS: $21,273, P < .001) and schizophrenia-related (EPS: $9018 vs non-EPS: $4475, P < .0001) total costs compared to the non-EPS cohort.

Approximately 20% of patients developed EPS in the year following AAP initiation. The significant increases in healthcare resource utilization and costs in the EPS cohorts highlight the need for treatments that effectively target schizophrenia symptoms while reducing the risk of EPS.

Sunovion Pharmaceuticals

While previous studies have suggested that higher levels of cognitive performance may be related to greater wellbeing and resilience, little is known about the associations between neural circuits engaged by cognitive tasks and wellbeing and resilience, and whether genetics or environment contribute to these associations.

The current study consisted of 253 monozygotic and dizygotic adult twins, including a subsample of 187 early-life trauma-exposed twins, with functional Magnetic Resonance Imaging data from the TWIN-E study. Wellbeing was measured using the COMPAS-W Wellbeing Scale while resilience was defined as a higher level of positive adaptation (higher levels of wellbeing) in the presence of trauma exposure. We probed both sustained attention and working memory processes using a Continuous Performance Task in the scanner.

We found significant negative associations between resilience and activation in the bilateral anterior insula engaged during sustained attention. Multivariate twin modelling showed that the association between resilience and the left and right insula activation was mostly driven by common genetic factors, accounting for 71% and 87% of the total phenotypic correlation between these variables, respectively. There were no significant associations between wellbeing/resilience and neural activity engaged during working memory updating.

The findings suggest that greater resilience to trauma is associated with less activation of the anterior insula during a condition requiring sustained attention but not working memory updating. This possibly suggests a pattern of ‘neural efficiency’ (i.e. more efficient and/or attenuated activity) in people who may be more resilient to trauma.