Attenuated positive symptom syndrome (APSS), characterized by ‘putatively prodromal’ attenuated psychotic-like pathology, indicates increased risk for psychosis. Poor premorbid social adjustment predicts severity of APSS symptoms and predicts subsequent psychosis in APSS-diagnosed individuals, suggesting application for improving detection of ‘true’ prodromal youth who will transition to psychosis. However, these predictive associations have not been tested in controls and therefore may be independent of the APSS diagnosis, negating utility for improving prediction in APSS-diagnosed individuals.

Association between premorbid social maladjustment and severity of positive, negative, disorganized, and general APSS symptoms was tested in 156 individuals diagnosed with APSS and 76 help-seeking (non-APSS) controls enrolled in the Enhancing the Prospective Prediction of Psychosis (PREDICT) study using prediction analysis.

Premorbid social maladjustment was associated with social anhedonia, reduced expression of emotion, restricted ideational richness, and deficits in occupational functioning, independent of the APSS diagnosis. Associations between social maladjustment and suspiciousness, unusual thought content, avolition, dysphoric mood, and impaired tolerance to normal stress were uniquely present in participants meeting APSS criteria. Social maladjustment was associated with odd behavior/appearance and diminished experience of emotions and self only in participants who did not meet APSS criteria.

Predictive associations between poor premorbid social adjustment and attenuated psychotic-like pathology were identified, a subset of which were indicative of high risk for psychosis. This study offers a method for improving risk identification while ruling out low-risk individuals.

Antisaccade tasks can be used to index cognitive control processes, e.g. attention, behavioral inhibition, working memory, and goal maintenance in people with brain disorders. Though diagnoses of schizophrenia (SZ), schizoaffective (SAD), and bipolar I with psychosis (BDP) are typically considered to be distinct entities, previous work shows patterns of cognitive deficits differing in degree, rather than in kind, across these syndromes.

Large samples of individuals with psychotic disorders were recruited through the Bipolar-Schizophrenia Network on Intermediate Phenotypes 2 (B-SNIP2) study. Anti- and pro-saccade task performances were evaluated in 189 people with SZ, 185 people with SAD, 96 people with BDP, and 279 healthy comparison participants. Logistic functions were fitted to each group's antisaccade speed-performance tradeoff patterns.

Psychosis groups had higher antisaccade error rates than the healthy group, with SZ and SAD participants committing 2 times as many errors, and BDP participants committing 1.5 times as many errors. Latencies on correctly performed antisaccade trials in SZ and SAD were longer than in healthy participants, although error trial latencies were preserved. Parameters of speed-performance tradeoff functions indicated that compared to the healthy group, SZ and SAD groups had optimal performance characterized by more errors, as well as less benefit from prolonged response latencies. Prosaccade metrics did not differ between groups.

With basic prosaccade mechanisms intact, the higher speed-performance tradeoff cost for antisaccade performance in psychosis cases indicates a deficit that is specific to the higher-order cognitive aspects of saccade generation.

The nosological status of generalized anxiety disorder (GAD) versus dysthymic disorder (DD) has been questioned. The aim of this study was to examine qualitative differences within (co-morbid) GAD and DD symptomatology.

Latent class analysis was applied to anxious and depressive symptomatology of respondents from three population-based studies (2007 Australian National Survey of Mental Health and Wellbeing; National Comorbidity Survey Replication; and Netherlands Mental Health Survey and Incidence Study-2; together known as the Triple study) and respondents from a multi-site naturalistic cohort [Netherlands Study of Depression and Anxiety (NESDA)]. Sociodemographics and clinical characteristics of each class were examined.

A three-class (Triple study) and two-class (NESDA) model best fitted the data, reflecting mainly different levels of severity of symptoms. In the Triple study, no division into a predominantly GAD or DD co-morbidity subtype emerged. Likewise, in spite of the presence of pure GAD and DD cases in the NESDA sample, latent class analysis did not identify specific anxiety or depressive profiles in the NESDA study. Next, sociodemographics and clinical characteristics of each class were examined. Classes only differed in levels of severity.

The absence of qualitative differences in anxious or depressive symptomatology in empirically derived classes questions the differentiation between GAD and DD.

Psychological distress is common among women of childbearing age, and limited longitudinal research suggests prolonged exposure to maternal distress is linked to child mental health problems. Estimating effects of maternal distress over time is difficult due to potential influences of child mental health problems on maternal distress and time-varying confounding by family circumstances.

We analysed the UK Millennium Cohort Study, a nationally representative sample with data collected throughout childhood. Adopting a marginal structural modelling framework, we investigated effects of exposure to medium/high levels of maternal psychological distress (Kessler-6 score 8+) on child mental health problems (Strengths and Difficulties Questionnaire borderline/abnormal behaviour cut-off) using maternal and child mental health data at 3, 5, 7 and 11 years, accounting for the influence of child mental health on subsequent maternal distress, and baseline and time-varying confounding.

Prior and concurrent exposures to maternal distress were associated with higher levels of child mental health problems at ages 3, 5, 7 and 11 years. For example, elevated risks of child mental health problems at 11 years were associated with exposure to maternal distress from 3 years [risk ratio (RR) 1.27 (95% confidence interval (CI) 1.08–1.49)] to 11 years [RR 2.15 (95% CI 1.89–2.45)]. Prolonged exposure to maternal distress at ages 3, 5, 7 and 11 resulted in an almost fivefold increased risk of child mental health problems.

Prior, concurrent and, particularly, prolonged exposure to maternal distress raises risks for child mental health problems. Greater support for mothers experiencing distress is likely to benefit the mental health of their children.

Timing of developmental milestones, such as age at first walking, is associated with later diagnoses of neurodevelopmental disorders. However, its relationship to genetic risk for neurodevelopmental disorders in the general population is unknown. Here, we investigate associations between attainment of early-life language and motor development milestones and genetic liability to autism, attention deficit hyperactivity disorder (ADHD), and schizophrenia.

We use data from a genotyped sub-set (N = 25699) of children in the Norwegian Mother, Father and Child Cohort Study (MoBa). We calculate polygenic scores (PGS) for autism, ADHD, and schizophrenia and predict maternal reports of children's age at first walking, first words, and first sentences, motor delays (18 months), and language delays and a generalised measure of concerns about development (3 years). We use linear and probit regression models in a multi-group framework to test for sex differences.

We found that ADHD PGS were associated with earlier walking age (β = −0.033, padj < 0.001) in both males and females. Additionally, autism PGS were associated with later walking (β = 0.039, padj = 0.006) in females only. No robust associations were observed for schizophrenia PGS or between any neurodevelopmental PGS and measures of language developmental milestone attainment.

Genetic liabilities for neurodevelopmental disorders show some specific associations with the age at which children first walk unsupported. Associations are small but robust and, in the case of autism PGS, differentiated by sex. These findings suggest that early-life motor developmental milestone attainment is associated with genetic liability to ADHD and autism in the general population.

Disruptive behavior disorders (DBD) are heterogeneous at the clinical and the biological level. Therefore, the aims were to dissect the heterogeneous neurodevelopmental deviations of the affective brain circuitry and provide an integration of these differences across modalities.

We combined two novel approaches. First, normative modeling to map deviations from the typical age-related pattern at the level of the individual of (i) activity during emotion matching and (ii) of anatomical images derived from DBD cases (n = 77) and controls (n = 52) aged 8–18 years from the EU-funded Aggressotype and MATRICS consortia. Second, linked independent component analysis to integrate subject-specific deviations from both modalities.

While cases exhibited on average a higher activity than would be expected for their age during face processing in regions such as the amygdala when compared to controls these positive deviations were widespread at the individual level. A multimodal integration of all functional and anatomical deviations explained 23% of the variance in the clinical DBD phenotype. Most notably, the top marker, encompassing the default mode network (DMN) and subcortical regions such as the amygdala and the striatum, was related to aggression across the whole sample.

Overall increased age-related deviations in the amygdala in DBD suggest a maturational delay, which has to be further validated in future studies. Further, the integration of individual deviation patterns from multiple imaging modalities allowed to dissect some of the heterogeneity of DBD and identified the DMN, the striatum and the amygdala as neural signatures that were associated with aggression.

A hospital built environment can affect patients’ treatment satisfaction, which is, in turn, associated with crucial clinical outcomes. However, little research has explored which elements are specifically important for psychiatric in-patients. This study aims to identify which elements of the hospital environment are associated with higher patient satisfaction with psychiatric in-patient care.

The study was conducted in Italy and the United Kingdom. Data was collected through hospital visits and patient interviews. All hospitals were assessed for general characteristics, aspects specific to psychiatry (patient safety, mixed/single-sex wards, smoking on/off wards), and quality of hospital environment. Patients’ treatment satisfaction was assessed using the Client Assessment of Treatment Scale (CAT). Multi-level modelling was used to explore the role of environment in predicting the CAT scores adjusted for age, gender, education, diagnosis, and formal status.

The study included 18 psychiatric hospitals (7 in Italy and 11 in the United Kingdom) and 2130 patients. Healthcare systems in these countries share key characteristics (e.g. National Health Service, care organised on a geographical basis) and differ in policy regulation and governance. Two elements were associated with higher patient treatment satisfaction: being hospitalised on a mixed-sex ward (p = 0.003) and the availability of rooms to meet family off wards (p = 0.020).

As hospitals are among the most expensive facilities to build, their design should be guided by research evidence. Two design features can potentially improve patient satisfaction: family rooms off wards and mixed-sex wards. This evidence should be considered when designing or renovating psychiatric facilities.

Common mental disorders (CMDs) including depression, anxiety, and stress are very common, but it is unclear whether the last decades of social, economic, and political change have impacted incidence of CMD. This study explored temporal trends in the recorded incidence of CMD in the United Kingdom.

We used data from general practices in the United Kingdom (Clinical Practice Research Datalink) to estimate the annual recorded incidence of CMD for 2000–2020, including symptoms, diagnosis, or pharmaceutical treatment. Trends were explored by sex, age, ethnicity, region, deprivation, and comorbidity.

We included 29 480 164 individuals who were followed up for 12.5 years on average (s.d. = 6.4 years). The recorded incidence of CMD episodes was 55.9 per 1000 person-years in 2000 [95% confidence interval (CI) 55.8–56.1], increasing to 79.6 per 1000 person-years in 2019 (95% CI 79.5–79.8). Females had higher recorded incidence rates, as did those living in more deprived areas. We observed striking patterns by age over time, with rates in ages 16–24 increasing from 40.2 per 1000 in 2000 (95% CI 39.8–40.5), to 107.8 per 1000 in 2019 (95% CI 107.0–108.6). In contrast, the rates in those aged ≥55 years decreased since 2014. There were differing patterns of incidence by ethnic group, with a steeper increase in Asian, Black, and mixed groups in recent years.

Overall, the incidence of recorded CMD in the UK general practice increased between 2000 and 2019 with a small decrease in 2020. The overall trends obscured important differences across population subgroups, which may have implications for prevention.

Emerging adulthood is a peak period of risk for alcohol and illicit drug use. Recent advances in psychiatric genetics suggest that the co-occurrence of substance use and psychopathology arises, in part, from a shared genetic etiology. We sought to extend this research by investigating the influence of genetic risk for schizophrenia on trajectories of four substance use behaviors as they occurred across emerging adulthood.

Young adult participants of non-Hispanic European descent provided DNA samples and completed daily reports of substance use for 1 month per year across 4 years (N = 30 085 observations of N = 342 participants). A schizophrenia polygenic score was included in two-level hierarchical linear models designed to test associations between genetic risk for schizophrenia, participant age, and four substance use phenotypes.

Participants with a greater schizophrenia polygenic score experienced greater age-related increases in the likelihood of using substances across emerging adulthood (p < 0.005). Additionally, our results suggest that the polygenic score was positively associated with participants’ overall likelihood to engage in illicit drug use but not alcohol-related substance use.

This study used a novel combination of polygenic prediction and intensive longitudinal methods to characterize the influence of genetic risk for schizophrenia on patterns of age-related change in substance use across emerging adulthood. Results suggest that genetic risk for schizophrenia has developmentally specific effects on substance use behaviors in a non-clinical population of young adults.

Studies have shown that specific cognitions and behaviours play a role in maintaining chronic fatigue syndrome (CFS). However, little research has investigated illness-specific cognitive processing in CFS. This study investigated whether CFS participants had an attentional bias for CFS-related stimuli and a tendency to interpret ambiguous information in a somatic way. It also determined whether cognitive processing biases were associated with co-morbidity, attentional control or self-reported unhelpful cognitions and behaviours.

A total of 52 CFS and 51 healthy participants completed self-report measures of symptoms, disability, mood, cognitions and behaviours. Participants also completed three experimental tasks, two designed specifically to tap into CFS salient cognitions: (i) visual-probe task measuring attentional bias to illness (somatic symptoms and disability) v. neutral words; (ii) interpretive bias task measuring positive v. somatic interpretations of ambiguous information; and (iii) the Attention Network Test measuring general attentional control.

Compared with controls, CFS participants showed a significant attentional bias for fatigue-related words and were significantly more likely to interpret ambiguous information in a somatic way, controlling for depression and anxiety. CFS participants had significantly poorer attentional control than healthy individuals. Attention and interpretation biases were associated with fear/avoidance beliefs. Somatic interpretations were also associated with all-or-nothing behaviour and catastrophizing.

People with CFS have illness-specific biases which may play a part in maintaining symptoms by reinforcing unhelpful illness beliefs and behaviours. Enhancing adaptive processing, such as positive interpretation biases and more flexible attention allocation, may provide beneficial intervention targets.

Social support has been shown to be associated with a reduced likelihood of developing psychotic experiences in the general population and even amongst those at high risk due to exposure to multiple forms of victimisation (poly-victimised). However, it is unclear whether this association is merely due to the confounding effects of shared environmental and genetic influences, or reverse causality. Therefore, we investigated whether social support has a unique environmentally mediated effect on adolescent psychotic experiences after accounting for familial factors, including genetic factors, and also prior psychopathology.

Participants were from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally-representative cohort of 2232 UK-born twins. Adolescents were interviewed at age 18 about psychotic experiences and victimisation exposure since age 12, and their perceptions of social support. Prior childhood mental health problems and psychotic symptoms were assessed at age 12. The discordant twin method was used to disentangle the relative family-wide and unique-environmental effects of social support on psychotic experiences in the general population and among poly-victimised adolescents.

Perceived social support, particularly from friends, was found to have a unique environmentally mediated buffering effect on adolescent psychotic experiences in the whole sample and in the high-risk poly-victimised group.

The protective effects of social support on adolescent psychotic experiences cannot be accounted for by shared environmental or genetic factors, nor by earlier psychopathology. Our findings suggest that early intervention programmes focused on increasing perceptions of social support have the potential to prevent the emergence of psychotic experiences amongst adolescents.

The treatment of depression in patients with somatic disorders is crucial, given its negative impact on quality of life (QoL), functioning, and even on the somatic disease prognosis. We aimed to examine the most updated evidence on the effects of psychotherapy in patients with depression and somatic disorders, including HIV, oncological, cardiometabolic, and neurological disorders.

We conducted a meta-analysis of 75 randomized trials (8209 participants) of psychotherapy for adults with somatic disorders and a diagnosis or elevated symptoms of depression. Outcomes included depression, QoL, somatic health-related outcomes, and mortality.

Psychotherapy significantly reduced the severity of depression at post-treatment across all categories of somatic disorders (Hedges'g = 0.65; 95% CI 0.52–0.79), with sustained effects at 6–11 months (g = 0.38; 95% CI 0.22–0.53) and at 12 months follow-up or longer (g = 0.13; 95% CI 0.04–0.21). Psychotherapy also showed significant effects on QoL (g = 0.26; 95% CI 0.17–0.35), maintained up to 11 months follow-up (g = 0.25; 95% CI 0.16–0.34). No significant effects were observed on the most frequently reported somatic health-related outcomes (glycemic control, pain), and neither on mortality. Heterogeneity in most analyses was very high, and only 29 (38%) trials were rated at low risk of bias (RoB).

Psychotherapy may be an effective treatment option for patients with depression and somatic disorders, with long-term effects on depression severity and QoL. However, these results should be interpreted with caution due to heterogeneity and RoB.

Experience of early-life socioeconomic deprivation (ELSD) may increase the risk of mental disorders in young adulthood. This association may be mediated by structural and functional alterations of the hippocampus.

We conducted a prospective cohort study on 122 participants of the European Longitudinal Study of Pregnancy and Childhood. Information about ELSD was collected via questionnaire from mothers during the first 18 months of participants’ lives. At age 23–24, participants underwent examination by structural magnetic resonance imaging, resting-state functional connectivity and assessment of depressive symptoms (Mood and Feelings Questionnaire) and anxiety (Spielberger State-Trait Anxiety Inventory). The association of ELSD with brain outcomes in young adulthood was assessed with correlations, linear regression (adjusting for sex, socioeconomic position and mother's mental health) and moderated mediation analysis.

Higher ELSD was associated with greater depressive symptoms (B = 0.22; p = 0.001), trait anxiety (B = 0.07; p = 0.02) and lower global connectivity of the right hippocampus (B = −0.01; p = 0.02). These associations persisted when adjusted for covariates. In women, lower global connectivity of the right hippocampus was associated with stronger trait anxiety (B = −4.14; p = 0.01). Global connectivity of the right hippocampus as well as connectivity between the right hippocampus and the left middle temporal gyrus mediated the association between ELSD and trait anxiety in women. Higher ELSD correlated with a lower volume of the right hippocampus in men, but the volume of the right hippocampus was not related to mental health.

Early preventive strategies targeted at children from socioeconomically deprived families may yield long-lasting benefits for the mental health of the population.