There are 117.3 million people forcibly displaced because of war, conflict and natural disasters: 40% are children. With growing numbers, many high-income countries have adopted or are considering increasingly restrictive policies of immigration detention. Research on the impact of detention on mental health has focused on adults, although recent studies report on children.

To synthesise data on the impact of immigration detention on children’s mental health.

Systematic searches were conducted in PsycINFO, MEDLINE and Embase databases and grey literature and studies assessed using PRISMA guidelines (PROSPERO registration CRD42023369680). Included studies were quantitative, assessed children younger than 18 years who had been in immigration detention and reported mental health symptoms or diagnoses. Methodological quality was assessed using the Appraisal Tool for Cross-Sectional Studies. Meta-analyses estimated prevalence for major depression and post-traumatic stress disorder (PTSD).

Twenty-one studies reported data on 9620 children. Most studies were cross-sectional, had small sample sizes and used convenience sampling. A profoundly detrimental impact on children’s mental health across a variety of countries and detention settings was demonstrated. Meta-analysis found pooled prevalence of 42.2% for depression [95% CI 22.9, 64.3] and 32.0% for PTSD [95% CI 19.4, 48.0]. Severity of mental health impact increased with exposure to indefinite or protracted held detention.

Immigration detention harms children. No period of detention can be deemed safe, as all immigration detention is associated with adverse impacts on mental health. Our review highlights the urgency of alternative immigration policies that end the practice of detaining children and families.

Previous studies identified clusters of first-episode psychosis (FEP) patients based on cognition and premorbid adjustment. This study examined a range of socio-environmental risk factors associated with clusters of FEP, aiming a) to compare clusters of FEP and community controls using the Maudsley Environmental Risk Score for psychosis (ERS), a weighted sum of the following risks: paternal age, childhood adversities, cannabis use, and ethnic minority membership; b) to explore the putative differences in specific environmental risk factors in distinguishing within patient clusters and from controls.

A univariable general linear model (GLS) compared the ERS between 1,263 community controls and clusters derived from 802 FEP patients, namely, low (n = 223) and high-cognitive-functioning (n = 205), intermediate (n = 224) and deteriorating (n = 150), from the EU-GEI study. A multivariable GLS compared clusters and controls by different exposures included in the ERS.

The ERS was higher in all clusters compared to controls, mostly in the deteriorating (β=2.8, 95% CI 2.3 3.4, η2 = 0.049) and the low-cognitive-functioning cluster (β=2.4, 95% CI 1.9 2.8, η2 = 0.049) and distinguished them from the cluster with high-cognitive-functioning. The deteriorating cluster had higher cannabis exposure (meandifference = 0.48, 95% CI 0.49 0.91) than the intermediate having identical IQ, and more people from an ethnic minority (meandifference = 0.77, 95% CI 0.24 1.29) compared to the high-cognitive-functioning cluster.

High exposure to environmental risk factors might result in cognitive impairment and lower-than-expected functioning in individuals at the onset of psychosis. Some patients’ trajectories involved risk factors that could be modified by tailored interventions.

This study explored the association among dissociative experiences, recovery from psychosis and a range of factors relevant to psychosis and analysed whether dissociative experiences (compartmentalisation, detachment and absorption) could be used to predict specific stages of recovery. A cross-sectional design was used, and 75 individuals with psychosis were recruited from the recovery services of the Gloucestershire Health and Care NHS Foundation Trust. Five questionnaires were used – the Dissociative Experiences Scale – II (DES), Detachment and Compartmentalisation Inventory (DCI), Questionnaire about the Process of Recovery, Stages of Recovery Instrument (STORI), and Positive and Negative Syndrome Scale – and a proforma was used to collect demographic data.

Our findings indicated that compartmentalisation, detachment and absorption, as measured by DES and DCI, do not predict stages of recovery as measured by the STORI.

The results of this study suggest that there is no simple relationship between dissociative and psychotic symptoms. They also suggest a need to assess these symptoms separately in practice and indicate that special approaches to treatment of psychosis may be needed in cases where such symptoms have a significant role.

Accurate diagnosis of bipolar disorder (BPD) is difficult in clinical practice, with an average delay between symptom onset and diagnosis of about 7 years. A depressive episode often precedes the first manic episode, making it difficult to distinguish BPD from unipolar major depressive disorder (MDD).

We use genome-wide association analyses (GWAS) to identify differential genetic factors and to develop predictors based on polygenic risk scores (PRS) that may aid early differential diagnosis.

Based on individual genotypes from case–control cohorts of BPD and MDD shared through the Psychiatric Genomics Consortium, we compile case–case–control cohorts, applying a careful quality control procedure. In a resulting cohort of 51 149 individuals (15 532 BPD patients, 12 920 MDD patients and 22 697 controls), we perform a variety of GWAS and PRS analyses.

Although our GWAS is not well powered to identify genome-wide significant loci, we find significant chip heritability and demonstrate the ability of the resulting PRS to distinguish BPD from MDD, including BPD cases with depressive onset (BPD-D). We replicate our PRS findings in an independent Danish cohort (iPSYCH 2015, N = 25 966). We observe strong genetic correlation between our case–case GWAS and that of case–control BPD.

We find that MDD and BPD, including BPD-D are genetically distinct. Our findings support that controls, MDD and BPD patients primarily lie on a continuum of genetic risk. Future studies with larger and richer samples will likely yield a better understanding of these findings and enable the development of better genetic predictors distinguishing BPD and, importantly, BPD-D from MDD.

Celiac disease (CD), an autoimmune disorder triggered by gluten, impacts about one percent of the population. Only one-third receive a diagnosis, leaving the majority unaware of their condition. Untreated CD can lead to gut lining damage, resulting in malnutrition, anemia, and osteoporosis. Our primary goal was to identify at-risk groups and assess the cost-effectiveness of active case finding in primary care.

Our methodology involved systematic reviews and meta-analyses focusing on the accuracy of CD risk factors (chronic conditions and symptoms) and diagnostic tests (serological and genetic). Prediction models, based on identified risk factors, were developed for identifying individuals who would benefit from CD testing in routine primary care. Additionally, an online survey gauged individuals’ preferences regarding diagnostic certainty before initiating a gluten-free diet. This information informed the development of economic models evaluating the cost-effectiveness of various active case finding strategies.

Individuals with dermatitis herpetiformis, a family history of CD, migraine, anemia, type 1 diabetes, osteoporosis, or chronic liver disease showed one and a half to two times higher risk of having CD. IgA tTG, and EMA demonstrated good diagnostic accuracy. Genetic tests showed high sensitivity but low specificity. Survey results indicated substantial variation in preference for certainty from a blood test before initiating a gluten-free diet. Cost-effectiveness analyses showed that, in adults, IgA tTG at a one percent pre-test probability (equivalent to population screening) was the most cost effective. For non-population screening strategies, IgA EMA plus HLA was most cost effective. There was substantial uncertainty in economic model results.

While population-based screening with IgA tTG appears the most cost effective in adults, decisions for implementation should not solely rely on economic analyses. Future research should explore whether population-based CD screening aligns with UK National Screening Committee criteria and requires a long-term randomized controlled trial of screening strategies.

Stigma of mental health conditions hinders recovery and well-being. The Honest, Open, Proud (HOP) program shows promise in reducing stigma but there is uncertainty about the feasibility of a randomized trial to evaluate a peer-delivered, individual adaptation of HOP for psychosis (Let's Talk).

A multi-site, Prospective Randomized Open Blinded Evaluation (PROBE) design, feasibility randomised controlled trial (RCT) comparing the peer-delivered intervention (Let's Talk) to treatment as usual (TAU). Follow-up was 2.5 and 6 months. Randomization was via a web-based system, with permuted blocks of random size. Up to 10 sessions of the intervention over 10 weeks were offered. The primary outcome was feasibility data (recruitment, retention, intervention attendance). Primary outcomes were analyzed by intention to treat. Safety outcomes were reported by as treated status. The study was prospectively registered: https://doi.org/10.1186/ISRCTN17197043.

149 patients were referred to the study and 70 were recruited. 35 were randomly assigned to intervention + TAU and 35 to TAU. Recruitment was 93% of the target sample size. Retention rate was high (81% at 2.5 months primary endpoint), and intervention attendance rate was high (83%). 21% of 33 patients in Let's talk + TAU had an adverse event and 16% of 37 patients in TAU. One serious adverse event (pre-randomization) was partially related and expected.

This is the first trial to show that it is feasible and safe to conduct a RCT of HOP adapted for people with psychosis and individual delivery. An adequately powered trial is required to provide robust evidence.

The association between cannabis and psychosis is established, but the role of underlying genetics is unclear. We used data from the EU-GEI case-control study and UK Biobank to examine the independent and combined effect of heavy cannabis use and schizophrenia polygenic risk score (PRS) on risk for psychosis.

Genome-wide association study summary statistics from the Psychiatric Genomics Consortium and the Genomic Psychiatry Cohort were used to calculate schizophrenia and cannabis use disorder (CUD) PRS for 1098 participants from the EU-GEI study and 143600 from the UK Biobank. Both datasets had information on cannabis use.

In both samples, schizophrenia PRS and cannabis use independently increased risk of psychosis. Schizophrenia PRS was not associated with patterns of cannabis use in the EU-GEI cases or controls or UK Biobank cases. It was associated with lifetime and daily cannabis use among UK Biobank participants without psychosis, but the effect was substantially reduced when CUD PRS was included in the model. In the EU-GEI sample, regular users of high-potency cannabis had the highest odds of being a case independently of schizophrenia PRS (OR daily use high-potency cannabis adjusted for PRS = 5.09, 95% CI 3.08–8.43, p = 3.21 × 10−10). We found no evidence of interaction between schizophrenia PRS and patterns of cannabis use.

Regular use of high-potency cannabis remains a strong predictor of psychotic disorder independently of schizophrenia PRS, which does not seem to be associated with heavy cannabis use. These are important findings at a time of increasing use and potency of cannabis worldwide.

Associations between childhood trauma, neurodevelopment, alcohol use disorder (AUD), and posttraumatic stress disorder (PTSD) are understudied during adolescence.

Using 1652 participants (51.75% female, baseline Mage = 14.3) from the Collaborative Study of the Genetics of Alcoholism, we employed latent growth curve models to (1) examine associations of childhood physical, sexual, and non-assaultive trauma (CPAT, CSAT, and CNAT) with repeated measures of alpha band EEG coherence (EEGc), and (2) assess whether EEGc trajectories were associated with AUD and PTSD symptoms. Sex-specific models accommodated sex differences in trauma exposure, AUD prevalence, and neural development.

In females, CSAT was associated with higher mean levels of EEGc in left frontocentral (LFC, ß = 0.13, p = 0.01) and interhemispheric prefrontal (PFI, ß = 0.16, p < 0.01) regions, but diminished growth in LFC (ß = −0.07, p = 0.02) and PFI (ß = −0.07, p = 0.02). In males, CPAT was associated with lower mean levels (ß = −0.17, p = 0.01) and increased growth (ß = 0.11, p = 0.01) of LFC EEGc. Slope of LFC EEGc was inversely associated with AUD symptoms in females (ß = −1.81, p = 0.01). Intercept of right frontocentral and PFI EEGc were associated with AUD symptoms in males, but in opposite directions. Significant associations between EEGc and PTSD symptoms were also observed in trauma-exposed individuals.

Childhood assaultive trauma is associated with changes in frontal alpha EEGc and subsequent AUD and PTSD symptoms, though patterns differ by sex and trauma type. EEGc findings may inform emerging treatments for PTSD and AUD.