The UK Biobank is a large middle-aged cohort recruited in 2006–2010. We used data from its participants to analyze mortality, survival, and causes of death associated with mental disorders.

Our exposures were mental disorders identified using (1) symptom-based outcomes derived from an online Mental Health Questionnaire (n = 157 329), including lifetime/current depression, lifetime/current generalized anxiety disorder, lifetime/recent psychotic experience, lifetime bipolar disorder, current alcohol use disorder, and current posttraumatic stress disorder and (2) hospital data linkage of diagnoses within the International Classification of Diseases, 10th revision (ICD-10) (n = 502 422), including (A) selected diagnoses or groups of diagnoses corresponding to symptom-based outcomes and (B) all psychiatric diagnoses, grouped by ICD-10 section. For all exposures, we estimated age-adjusted mortality rates and hazard ratios, as well as proportions of deaths by cause.

We found significantly increased mortality risk associated with all mental disorders identified by symptom-based outcomes, except for lifetime generalized anxiety disorder (with hazard ratios in the range of 1.08–3.0). We also found significantly increased mortality risk associated with all conditions identified by hospital data linkage, including selected ICD-10 diagnoses or groups of diagnoses (2.15–7.87) and ICD-10 diagnoses grouped by section (2.02–5.44). Causes of death associated with mental disorders were heterogeneous and mostly natural.

In a middle-aged cohort, we found a higher mortality risk associated with most mental disorders identified by symptom-based outcomes and with all disorders or groups of disorders identified by hospital data linkage of ICD-10 diagnoses. The majority of deaths associated with mental disorders were natural.

Racing thoughts have been found in several states of bipolar disorder (BD), but also in healthy populations with subclinical mood alterations. The evaluation of racing thoughts relies on subjective reports, and objective measures are sparse. The current study aims at finding an objective neuropsychological equivalent of racing thoughts in a mixed group of BD patients and healthy controls by using a bistable perception paradigm.

Eighty-three included participants formed three groups based on participants' levels of racing thoughts reported via the Racing and Crowded Thoughts Questionnaire. Participants reported reversals in their perception during viewing of the bistable Necker cube either spontaneously, while asked to focus on one interpretation of the cube, or while asked to accelerate perceptual reversals. The dynamics of perceptual alternations were studied both at a conscious level (with manual temporal windows reflecting perceptual reversals) and at a more automatic level (with ocular temporal windows derived from ocular fixations).

The rate of windows was less modulated by attentional conditions in participants with racing thoughts, and most clearly so for ocular windows. The rate of ocular windows was especially high when participants with racing thoughts were asked to focus on one interpretation of the Necker cube and when they received these instructions for the first time.

Our results indicate that in subjects with racing thoughts automatic perceptual processes escape cognitive control mechanisms. Racing thoughts may involve not only conscious thought mechanisms but also more automatic processes.

Low IQ is a risk factor for psychosis, but the effect of high IQ is more controversial. The aim was to explore the association of childhood school success with prodromal symptoms in adolescence and psychoses in adulthood.

In the general population-based Northern Finland Birth Cohort 1986 (n = 8 229), we studied the relationship between teacher-assessed learning deficits, special talents and general school success at age 8 years and both prodromal symptoms (PROD-screen) at age 15–16 years and the occurrence of psychoses by age 30 years.

More prodromal symptoms were experienced by those talented in oral presentation [boys: adjusted odds ratio (OR) 1.49; 95% confidence interval 1.14–1.96; girls: 1.23; 1.00–1.52] or drawing (boys: 1.44; 1.10–1.87). Conversely, being talented in athletics decreased the probability of psychotic-like symptoms (boys: OR 0.72; 0.58–0.90). School success below average predicted less prodromal symptoms with boys (OR 0.68; 0.48–0.97), whereas above-average success predicted more prodromal symptoms with girls (OR 1.22; 1.03–1.44). The occurrence of psychoses was not affected. Learning deficits did not associate with prodromal symptoms or psychoses.

Learning deficits in childhood did not increase the risk of prodromal symptoms in adolescence or later psychosis in this large birth cohort. Learning deficits are not always associated with increased risk of psychosis, which might be due to, e.g. special support given in schools. The higher prevalence of prodromal symptoms in talented children may reflect a different kind of relationship of school success with prodromal symptoms compared to full psychoses.

Depression is associated with broad deficits in cognitive control, including in visual selective attention tasks such as the flanker task. Previous computational modelling of depression and flanker task performance showed reduced pre-potent response bias and reduced executive control efficiency in depression. In the current study, we applied two computational models that account for the full dynamics of attentional selectivity.

Across three large-scale online experiments (one exploratory experiment followed by two confirmatory – and pre-registered – experiments; total N = 923), we measured attentional selectivity via the flanker task and obtained measures of depression symptomology as well as anhedonia. We then fit two computational models that account for the dynamics of attentional selectivity: The dual-stage two-phase model, and the shrinking spotlight (SSP) model.

No behavioural measures were related to depression symptomology or anhedonia. However, a parameter of the SSP model that indexes the strength of perceptual input was consistently negatively associated with the magnitude of depression symptomatology.

The findings provide evidence for deficits in perceptual representations in depression. We discuss the implications of this in relation to the hypothesis that perceptual deficits potentially exacerbate control deficits in depression.

Understanding risk factors related to suicidal ideation (SI) and suicidal behaviors (SB) in youth is important for informing prevention and intervention efforts. While it appears that psychotic-like experiences (PLEs) are strongly associated with both SI and SB at different points across the lifespan, the longitudinal nature of this relationship in middle childhood and early adolescence is understudied.

The study used the unique longitudinal Adolescent Brain Cognitive Development Study data. Mixed effects linear models examined associations between PLEs and SI and SB over time using three time points of data from ages 9–13.

First, analyses indicated that endorsement of SI and SB increased as youth grew older for those with increased distressing PLEs. Analyses found evidence of bidirectional relationships between PLEs with SI and SB, with evidence that PLEs at baseline were associated with worsening SI and SB over time, including a transition from SI to SB (β = 0.032, FDRp = 0.002). Exploratory analyses showed consistent evidence for strengthened associations over time for higher delusional ideation with both SI and SB (βs > 0.04, FDRps < 0.001), and for perceptual distortions with SB (βs = 0.046, FDRp < 0.001). When accounting for general psychopathology, for SB, the strengthened associations over time was significantly stronger for PLEs (β = 0.053, FDRp < 0.001) compared to general psychopathology (β = 0.022, FDRp = 0.01).

The present study indicates both SI and SB show strengthened associations with PLEs over time, and that baseline PLEs may predict worsening of suicidality over time. The findings are important clarifications about the nature of the associations between youth-reported PLEs and suicidality over time.

Psychosocial factors may influence mortality and morbidity after coronary bypass surgery (CABG), but it is unclear when, post-surgery, they best predict the outcome, if they interact, or whether results differ for men and women.

This prospective, observational study assessed depression symptoms, social support, marital status, household responsibility, functional impairment, mortality and need for further coronary procedures over 14 years of follow-up. Data were collected in-hospital post-CABG and at home 1-year later. Mortality and subsequent cardiac procedure data were extracted from a Cardiac Registry.

Of 296 baseline participants, 78% (43% were women) completed data at 1-year post-CABG. Long-term survival was shorter with 1-year depression and lower household responsibility but that was not true for the measures taken at baseline [HR for depression = 1.27; 95% CI 1.02–1.59 v. 0.99 (0.78–1.25), and HR = 0.71; 95% CI 0.52–0.97 v. 0.97 (0.80–1.16)] for household responsibility. An interaction between depression symptoms and social support at year 1 [χ2 (11) = 111.05, p < 0.001] revealed a greater hazard of mortality d with increased depression only at mean (HR = 1.67; 95% CI 1.21–2.26) and high social support (HR = 2.23; 95% CI 1.46–3.40). Depression also accounted for increased event recurrence. There were no significant interactions of sex with medical long-term outcomes.

In a sex-balanced sample, depression and household responsibility measured at 1-year post-CABG were associated with significant variance in unadjusted and adjusted predictor models of long-term mortality whereas the same indices determined right after the procedure were not significant predictors.

Clinical intervention in early stages of psychotic disorders is crucial for the prevention of severe symptomatology trajectories and poor outcomes. Genetic variability is studied as a promising modulator of prognosis, thus novel approaches considering the polygenic nature of these complex phenotypes are required to unravel the mechanisms underlying the early progression of the disorder.

The sample comprised of 233 first-episode psychosis (FEP) subjects with clinical and cognitive data assessed periodically for a 2-year period and 150 matched controls. Polygenic risk scores (PRSs) for schizophrenia, bipolar disorder, depression, education attainment and cognitive performance were used to assess the genetic risk of FEP and to characterize their association with premorbid, baseline and progression of clinical and cognitive status.

Schizophrenia, bipolar disorder and cognitive performance PRSs were associated with an increased risk of FEP [false discovery rate (FDR) ⩽ 0.027]. In FEP patients, increased cognitive PRSs were found for FEP patients with more cognitive reserve (FDR ⩽ 0.037). PRSs reflecting a genetic liability for improved cognition were associated with a better course of symptoms, functionality and working memory (FDR ⩽ 0.039). Moreover, the PRS of depression was associated with a worse trajectory of the executive function and the general cognitive status (FDR ⩽ 0.001).

Our study provides novel evidence of the polygenic bases of psychosis and its clinical manifestation in its first stage. The consistent effect of cognitive PRSs on the early clinical progression suggests that the mechanisms underlying the psychotic episode and its severity could be partially independent.