The base rate of transition from subthreshold psychotic experiences (the exposure) to clinical psychotic disorder (the outcome) in unselected, representative and non-help-seeking population-based samples is unknown.

A systematic review and meta-analysis was conducted of representative, longitudinal population-based cohorts with baseline assessment of subthreshold psychotic experiences and follow-up assessment of psychotic and non-psychotic clinical outcomes.

Six cohorts were identified with a 3–24-year follow-up of baseline subthreshold self-reported psychotic experiences. The yearly risk of conversion to a clinical psychotic outcome in exposed individuals (0.56%) was 3.5 times higher than for individuals without psychotic experiences (0.16%) and there was meta-analytic evidence of dose–response with severity/persistence of psychotic experiences. Individual studies also suggest a role for motivational impairment and social dysfunction. The evidence for conversion to non-psychotic outcome was weaker, although findings were similar in direction.

Subthreshold self-reported psychotic experiences in epidemiological non-help-seeking samples index psychometric risk for psychotic disorder, with strong modifier effects of severity/persistence. These data can serve as the population reference for selected and variable samples of help-seeking individuals at ultra-high risk, for whom much higher transition rates have been indicated.

Research mostly conducted in the UK and northern Europe has established that there are high rates of first-episode psychosis (FEP) in large cities and immigrant populations; moreover, psychosis has been found to be associated with cannabis use and early trauma. The present study aimed to evaluate the incidence rate of FEP and the distribution of several risk factors (e.g. age, ethnicity, substance abuse) in Bologna, Italy.

The Bologna FEP (BoFEP) study is an 8-year prospective study. All FEP patients, 18–64 years old, consecutively referred to the West Bologna Community Mental Health Centre (CMHC) from 2002 to 2009 were evaluated. Sociodemographic information, migration history and clinical data were collected through an ad-hoc schedule. Psychiatric diagnoses were recorded using the Schedule for Clinical Assessment of Neuropsychiatry (SCAN).

The overall incidence rate (IR) in the BoFEP study was 16.4 per 100 000 person-years [95% confidence interval (CI) 13.9–18.9]. The incidence was higher in young people, men and migrants (MI).

The IR of FEP found by the Bologna study is lower than that found by other European studies. However, as in other studies, the incidence was higher in certain groups. This heterogeneity has implications for policy and mental health service development, and for understanding the aetiology of psychosis.

After de-escalation techniques have failed, restraints, seclusion and/or rapid tranquillization may be used for people whose aggression is due to psychosis. Most coercive acts of health care have not been evaluated in trials.

People admitted to the emergency room of Instituto Philippe Pinel, Rio de Janeiro, Brazil, whose aggression/agitation was thought due to psychosis and for whom staff were unsure if best to restrict using physical restraints or a seclusion room, were randomly allocated to one or the other and followed up to 14 days. The primary outcomes were ‘no need to change intervention early – within 1 h’ and ‘not restricted by 4 h’.

A total of 105 people were randomized. Two-thirds of the people secluded were able to be fully managed in this way. Even taking into account the move out of seclusion into restraints, this study provides evidence that embarking on the less restrictive care pathway (seclusion) does not increase overall time in restriction of some sort [not restricted by 4 h: relative risk 1.09, 95% confidence interval 0.75–1.58; mean time to release: restraints 337.6 (s.d.=298.2) min, seclusion room 316.3 (s.d.=264.5) min, p=0.48]. Participants tended to be more satisfied with their care in the seclusion group (17.0% v. 11.1%) but this did not reach conventional levels of statistical significance (p=0.42).

This study should be replicated, but suggests that opting for the least restrictive option in circumstances where there is clinical doubt does not harm or prolong coercion.

Patients with schizophrenia have excess cardiovascular morbidity and mortality. Previous studies suggest that this may be partly due to inadequate somatic treatment and care, such as non-optimal use of lipid-lowering and antihypertensive pharmacotherapy, but longitudinal studies on such aetiological pathways are scarce.

We investigated the use of lipid-lowering and antihypertensive pharmacotherapy, and the risk of hospitalization for and death from coronary heart disease and stroke among patients with schizophrenia in a birth cohort of 12 939 subjects (Helsinki Birth Cohort Study). This cohort was followed for over 30 adult years by using national databases on cardio- and cerebrovascular hospitalizations and mortality and on reimbursement entitlements and use of drugs for treatment of hypertension, dyslipidaemia, coronary heart disease and diabetes.

Individuals with schizophrenia had a higher risk of hospitalization for coronary heart disease [hazard ratio (HR) 1.65, 95% confidence interval (CI) 1.03–2.57], and mortality from this disease was markedly higher (HR 2.92, 95% CI 1.70–5.00), particularly among women (p=0.001 for women, p=0.008 for men). Women with schizophrenia had also marginally increased stroke mortality (p=0.06). However, patients with schizophrenia used less lipid-lowering (odds ratio 0.47, 95% CI 0.27–0.80) and antihypertensive drug treatment (HR 0.37, 95% CI 0.22–0.61).

In this longitudinal study, coronary heart disease morbidity was increased and coronary heart disease mortality markedly increased in patients, especially in women with schizophrenia. These patients nevertheless received less antihypertensive and lipid-lowering treatment.

Social cognition has been identified as a significant construct for schizophrenia research with relevance to diagnosis, assessment, treatment and functional outcome. However, social cognition has not been clearly understood in terms of its relationships with neurocognition and functional outcomes. The present study sought to examine the empirical independence of social cognition and neurocognition; to investigate the possible causal structure among social cognition, neurocognition and psychosocial functioning.

The sample consists of 130 individuals diagnosed with schizophrenia. All participants were recruited as they were admitted to four community-based psychosocial rehabilitation programs. Social cognition, neurocognition and psychosocial functioning were measured at baseline and 12 months. The empirical independence of social cognition and neurocognition was tested using confirmatory factor analysis (CFA) and the possible causal structure among social cognition, neurocognition and psychosocial functioning was investigated using latent difference score (LDS) analysis.

A two-factor model of social cognition and neurocognition fit the data very well, indicating the empirical independence of social cognition, whereas the longitudinal CFA results show that the empirical independence of neurocognition and social cognition is maintained over time. The results of the LDS analysis support a causal model that indicates that neurocognition underlies and is causally primary to social cognition, and that neurocognition and social cognition are causally primary to functional outcome.

Social cognition and neurocognition could have independent and distinct upward causal effects on functional outcome. It is also suggested that the approaches for remediation of neurocognition and social cognition might need to be distinct.

Belief inflexibility is a thinking style observed in patients with schizophrenia, in which patients tend to refute evidence that runs counter to their prior beliefs. This bias has been related to a dominance of prior expectations (prior beliefs) over incoming sensory evidence. In this study we investigated the reliance on prior expectations for the processing of emotional faces in schizophrenia.

Eighteen patients with schizophrenia and 18 healthy controls were presented with sequences of emotional (happy, fearful, angry or neutral) faces. Perceptual decisions were biased towards a particular expression by a specific instruction at the start of each sequence, referred to as the context in which stimuli occurred. Participants were required to judge the emotion on each face and the effect of the context on emotion discrimination was investigated.

For threatening emotions (anger and fear), there was a performance cost for facial expressions that were incongruent with, and perceptually close to, the expression named in the instruction. For example, for angry faces, participants in both groups made more errors and reaction times (RTs) were longer when they were asked to look out for fearful faces compared with the other contexts. This bias against sensory evidence that runs counter to prior information was stronger in the patients, evidenced by a group by context interaction in accuracy and RTs for anger and fear respectively.

Overall, the present data suggest an overdependence on prior expectations for threatening stimuli, reflecting belief inflexibility, in schizophrenia.

Intrusions are common symptoms of both post-traumatic stress disorder (PTSD) and schizophrenia. It has been suggested that an information processing style characterized by weak trait contextual integration renders psychotic individuals vulnerable to intrusive experiences. This ‘contextual integration hypothesis’ was tested in individuals reporting anomalous experiences in the absence of a need for care.

Twenty-six low schizotypes and 23 individuals reporting anomalous experiences were shown a traumatic film with and without a concurrent visuospatial task (VST). Participants rated post-traumatic intrusions for frequency and form, and completed self-report measures of information processing style. It was predicted that, because of their weaker trait contextual integration, the anomalous experiences (AE) group would (1) exhibit more intrusions following exposure to the trauma film, (2) display intrusions characterized by more PTSD qualities and (3) show a greater reduction of intrusions with the concurrent VST.

As predicted, the AE group reported a lower level of trait contextual integration and more intrusions than the low schizotypes, both immediately after watching the film and during the following 7 days. Their post-traumatic intrusive memories were more PTSD-like (more intrusive, vivid and associated with emotion). The VST had no effect on the number of intrusions in either group.

These findings provide some support for the proposal that weak trait contextual integration underlies the development of intrusions within both PTSD and psychosis.

Enhanced acquisition and delayed extinction of fear conditioning are viewed as major determinants of anxiety disorders, which are often characterized by a dysfunctional hypothalamic–pituitary–adrenal (HPA) axis.

In this study we employed cued fear conditioning in two independent samples of healthy subjects (sample 1: n=60, sample 2: n=52). Two graphical shapes served as conditioned stimuli and painful electrical stimulation as the unconditioned stimulus. In addition, guided by findings from published animal studies on HPA axis-related genes in fear conditioning, we examined variants of the glucocorticoid receptor and corticotropin-releasing hormone receptor 1 genes.

Variation in these genes showed enhanced amygdala activation during the acquisition and reduced prefrontal activation during the extinction of fear as well as altered amygdala–prefrontal connectivity.

This is the first demonstration of the involvement of genes related to the HPA axis in human fear conditioning.

Functional neuroimaging studies have shown increased Stroop interference coupled with altered anterior cingulate cortex (ACC) and insula activation in post-traumatic stress disorder (PTSD). These brain areas are associated with error detection and emotional arousal. There is some evidence that treatment can normalize these activation patterns.

At baseline, we compared classic and emotional Stroop performance and blood oxygenation level-dependent responses (functional magnetic resonance imaging) of 29 child abuse-related complex PTSD patients with 22 non-trauma-exposed healthy controls. In 16 of these patients, we studied treatment effects of psycho-educational and cognitive behavioural stabilizing group treatment (experimental treatment; EXP) added to treatment as usual (TAU) versus TAU only, and correlations with clinical improvement.

At baseline, complex PTSD patients showed a trend for increased left anterior insula and dorsal ACC activation in the classic Stroop task. Only EXP patients showed decreased dorsal ACC and left anterior insula activation after treatment. In the emotional Stroop contrasts, clinical improvement was associated with decreased dorsal ACC activation and decreased left anterior insula activation.

We found further evidence that successful treatment in child abuse-related complex PTSD is associated with functional changes in the ACC and insula, which may be due to improved selective attention and lower emotional arousal, indicating greater cognitive control over PTSD symptoms.

Many studies have linked depression and obesity; few have more than two assessments of depressive symptoms and adiposity to address the potential bidirectional relationship between adiposity and depressive symptoms from young adulthood through old age. We tested whether baseline depressive symptoms are associated with changes in weight, whether baseline adiposity is associated with changes in depressive symptoms, and whether these associations vary by sex.

Participants (n=2251; 47% female) were from the Baltimore Longitudinal Study of Aging (BLSA). Using hierarchical linear modeling (HLM) on 30 years of data, the trajectory of adiposity and depressive symptoms over adulthood was estimated from >10 000 observations (mean=4.5 assessments per participant) of body mass index (BMI; kg/m2), waist circumference and hip circumference and >10 000 observations (mean=4.5 assessments per participant) of the Center for Epidemiological Studies Depression Scale (CES-D). Baseline depressive symptoms and adiposity were then tested as predictors of the trajectory of adiposity and depressive symptoms respectively. Additional analyses tested for sex-specific associations.

Sex moderated the association between depressive symptoms and weight gain such that women who experienced depressed affect had greater increases in BMI (binteraction=0.12, s.e.=0.04), waist (binteraction=0.22, s.e.=0.10) and hip circumference (binteraction=0.20, s.e.=0.07) across the adult lifespan, controlling for relevant demographic and behavioral covariates. Baseline adiposity was unrelated to the trajectory of depressive symptoms (median b=0.00) for both sexes.

Women who experience symptoms of depression tend to gain more weight across adulthood than men who experience such symptoms. Whether an individual was normal weight or overweight was unrelated to changes in depressive symptoms across adulthood.

Depression in fathers in the postnatal period is associated with an increased risk of child behaviour problems. A key potential pathway of risk transmission is exposure of the child to negative cognitions and affect in the context of early parenting. This study examines paternal speech during face-to-face father–infant interactions at 3 months.

Currently depressed (n=19) and non-depressed (n=19) fathers were individually matched on age and education. Speech was coded for cognitive biases and mentalizing statements using a modified version of previous measures of maternal speech. Paternal depression was diagnosed using a structured psychiatric interview.

Depression in fathers was associated with more speech focused on the paternal experience and less on the infants' experience. Depressed fathers' speech comprised more negative and critical utterances, compared with non-depressed fathers.

Important differences emerge in the speech of fathers who experience depression. Examining negative cognitions in the speech of these fathers as early as 3 months may help in understanding children's risk in relation to paternal psychopathology.

Suicidal behavior is frequently associated with a history of childhood abuse yet it remains unclear precisely how early life adversity may increase suicide risk later in life. As such, our aim was to examine whether lifetime trajectories of disruptiveness and anxiousness trait dysregulation explain the association between childhood adversity and suicidal behavior; and moreover, to test the potential modifying effects of mental disorders on these associations.

A sample of 1776 individuals from a prospective school-based cohort followed longitudinally for over 22 years was investigated. We tested the influence of disruptiveness and anxiousness trajectories from age 6 to 12 years on the association between childhood adversity (i.e. sexual and physical abuse) and history of suicide attempts (SA) using logistic regression models. Both adolescent externalizing and internalizing Axis I disorders and gender were tested as potential modifiers of these associations.

Four distinct longitudinal trajectories were identified for both disruptiveness and anxiousness. The high disruptiveness trajectory accounted for the association between childhood adversity and SA, but only for females. The high anxiousness trajectory also explained the association between adversity and SA; however, in this case it was not sex but mental disorders that influenced the potency of the mediating effect. More specifically, anxiousness fully explained the effect of adversity on SA in the presence of externalizing disorders, whereas in the absence of these disorders, this effect was significantly attenuated.

This study provides evidence that both disruptiveness and anxiousness play an important role in explaining the relationship between childhood adversity and SA.

Self-harm is a common reason for Emergency Department (ED) attendance. We aimed to develop a clinical tool to help identify patients at higher risk of repeat self-harm, or suicide, within 6 months of an ED self-harm presentation.

The tool, the ReACT Self-Harm Rule, was derived using multicentre data from a prospective cohort study. Binary recursive partitioning was applied to data from two centres, and data from a separate centre were used to test the tool. There were 29 571 self-harm presentations to five hospital EDs between January 2003 and June 2007, involving 18 680 adults aged ⩾16 years. We estimated sensitivity, specificity and positive and negative predictive values to measure the performance of the tool.

A self-harm presentation was classified as higher risk if at least one of the following factors was present: recent self-harm (in the past year), living alone or homelessness, cutting as a method of harm and treatment for a current psychiatric disorder. The rule performed with 95% sensitivity [95% confidence interval (CI) 94–95] and 21% specificity (95% CI 21–22), and had a positive predictive value of 30% (95% CI 30–31) and a negative predictive value of 91% (95% CI 90–92) in the derivation centres; it identified 83/92 of all subsequent suicides.

The ReACT Self-Harm Rule might be used as a screening tool to inform the process of assessing self-harm presentations to ED. The four risk factors could also be used as an adjunct to in-depth psychosocial assessment to help guide risk formulation. The use of multicentre data helped to maximize the generalizability of the tool, but we need to further verify its external validity in other localities.

It is clinically important to understand the factors that increase the likelihood of the frequent and recurrent suicide attempts seen in those with borderline personality disorder (BPD). Although several studies have examined this subject in a cross-sectional manner, the aim of this study was to determine the most clinically relevant baseline and time-varying predictors of suicide attempts over 16 years of prospective follow-up among patients with BPD.

Two-hundred and ninety in-patients meeting Revised Diagnostic Interview for Borderlines (DIB-R) and DSM-III-R criteria for BPD were assessed during their index admission using a series of semistructured interviews and self-report measures. These subjects were then reassessed using the same instruments every 2 years. The generalized estimating equations (GEE) approach was used to model the odds of suicide attempts in longitudinal analyses, controlling for assessment period, yielding an odds ratio (OR) and 95% confidence interval (CI) for each predictor.

Nineteen variables were found to be significant bivariate predictors of suicide attempts. Eight of these, seven of which were time-varying, remained significant in multivariate analyses: diagnosis of major depressive disorder (MDD), substance use disorder (SUD), post-traumatic stress disorder (PTSD), presence of self-harm, adult sexual assault, having a caretaker who has completed suicide, affective instability, and more severe dissociation.

The results of this study suggest that prediction of suicide attempts among borderline patients is complex, involving co-occurring disorders, co-occurring symptoms of BPD (self-harm, affective reactivity and dissociation), adult adversity, and a family history of completed suicide.

Retrospective studies have consistently indicated an association between maladaptive parenting and borderline personality disorder (BPD). This requires corroboration with prospective, longitudinal designs. We investigated the association between suboptimal parenting and parent conflict in childhood and BPD symptoms in late childhood using a prospective sample.

A community sample of 6050 mothers and their children (born between April 1991 and December 1992) were assessed. Mothers' family adversity was assessed during pregnancy and parenting behaviours such as hitting, shouting, hostility and parent conflict across childhood. Intelligence quotient (IQ) and DSM-IV Axis I diagnoses were assessed at 7–8 years. Trained psychologists interviewed children at 11 years (mean age 11.74 years) to ascertain BPD symptoms.

After adjustment for confounders, family adversity in pregnancy predicted BPD probable 1 to 2 adversities: odds ratio (OR)=1.34 [95% confidence interval (CI) 1.01–1.77]; >2 adversities: OR 1.99 (95% CI 1.34–2.94) and definite 1 to 2 adversities: OR 2.48 (95% CI 1.01–6.08) symptoms. Each point increase in the suboptimal parenting index predicted BPD probable: OR 1.13 (95% CI 1.05–1.23) and definite: OR 1.28 (95% CI 1.03–1.60) symptoms. Parent conflict predicted BPD probable: OR 1.19 (95% CI 1.06–1.34) and definite: OR 1.42 (95% CI 1.06–1.91) symptoms. Within the path analysis, the association between suboptimal parenting and BPD outcome was partially mediated by DSM-IV diagnoses and IQ at 7–8 years.

Children from adverse family backgrounds, who experience suboptimal parenting and more conflict between parents, have poor cognitive abilities and a DSM-IV diagnosis, are at increased risk of BPD symptoms at 11 years.

Familial influences on remission from alcohol use disorder (AUD) have been studied using family history of AUD rather than family history of remission. The current study used a remission phenotype in a twin sample to examine the relative contributions of genetic and environmental influences to remission.

The sample comprised 6183 twins with an average age of 30 years from the Australian Twin Registry. Lifetime history of alcohol abuse and dependence symptoms and symptom recency were assessed with a structured telephone interview. AUD was defined broadly and narrowly as history of two or more or three or more abuse or dependence symptoms. Remission was defined as absence of symptoms at time of interview among individuals with lifetime AUD. Standard bivariate genetic analyses were conducted to derive estimates of genetic and environmental influences on AUD and remission.

Environmental influences alone accounted for remission in males and for 89% of influences on remission in females, with 11% due to genetic influences shared with AUD, which decreased the likelihood of remission. For women, more than 80% of influences on remission were distinct from influences on AUD, and environmental influences were from individual experiences only. For men, just over 50% of influences on remission were distinct from those on AUD, and the influence of environments shared with the co-twin were substantial. The results for the broad and narrow phenotypes were similar.

The current study establishes young adult remission as a phenotype distinct from AUD and highlights the importance of environmental influences on remission.

When gambling opportunities are made available to the public in a given jurisdiction, some individuals participate occasionally and others more frequently. Among frequent gamblers, some individuals develop problematic involvement and some do not. This study addresses the association among demographic and social risk factors, frequency of gambling and gambling disorders.

Data from an adult community sample (n=1372) were used to identify risk factors for higher-frequency gambling and disordered gambling involvement.

Individuals with higher intelligence, older individuals and more religious individuals were less frequent gamblers. Males, single individuals and those exposed to gambling environments (friends and family who gamble) and those who started to gamble at a younger age were more frequent gamblers. Excitement-seeking personality traits were also higher among more frequent gamblers. A different set of risk factors was associated with the likelihood of gambling disorder among these higher-frequency gamblers. These variables included mental health indicators, childhood maltreatment and parental gambling involvement. Among higher-frequency gamblers, individuals who smoke cigarettes, those with a diagnosis of alcohol or drug dependence or obsessive–compulsive disorder, those with higher anxiety or depression and those with higher impulsivity and antisocial personality traits were more likely to report gambling-related problems. These individuals were also more likely to report gambling on electronic gambling machines (e.g. slot machines).

These data suggest a model in which higher-frequency gambling, particularly with electronic gambling machines, when combined with any type of emotional vulnerability increased the likelihood of gambling disorder.

We recently demonstrated that decline in fluid intelligence is a substantial contributor to frontal deficits. For some classical ‘executive’ tasks, such as the Wisconsin Card Sorting Test (WCST) and Verbal Fluency, frontal deficits were entirely explained by fluid intelligence. However, on a second set of frontal tasks, deficits remained even after statistically controlling for this factor. These tasks included tests of theory of mind and multitasking. As frontal dysfunction is the most frequent cognitive deficit observed in early Parkinson's disease (PD), the present study aimed to determine the role of fluid intelligence in such deficits.

We assessed patients with PD (n=32) and control subjects (n=22) with the aforementioned frontal tests and with a test of fluid intelligence. Group performance was compared and fluid intelligence was introduced as a covariate to determine its role in frontal deficits shown by PD patients.

In line with our previous results, scores on the WCST and Verbal Fluency were closely linked to fluid intelligence. Significant patient–control differences were eliminated or at least substantially reduced once fluid intelligence was introduced as a covariate. However, for tasks of theory of mind and multitasking, deficits remained even after fluid intelligence was statistically controlled.

The present results suggest that clinical assessment of neuropsychological deficits in PD should include tests of fluid intelligence, together with one or more specific tasks that allow for the assessment of residual frontal deficits associated with theory of mind and multitasking.

The results from recent studies suggest that alexithymia, a disorder characterized by impairments in understanding personal experiences of emotion, is frequently co-morbid with autism spectrum disorder (ASD). However, the extent that alexithymia is associated with primary deficits in recognizing external emotional cues, characteristic in ASD, has yet to be determined.

Twenty high-functioning adults with ASD and 20 age- and intelligence-matched typical controls categorized vocal and verbal expressions of emotion and completed an alexithymia assessment.

Emotion recognition scores in the ASD group were significantly poorer than in the control group and performance was influenced by the severity of alexithymia and the psycho-acoustic complexity of the presented stimuli. For controls, the effect of complexity was significantly smaller than for the ASD group, although the association between total emotion recognition scores and alexithymia was still strong.

Higher levels of alexithymia in the ASD group accounted for some, but not all, of the group difference in emotion recognition ability. However, alexithymia was insufficient to explain the different sensitivities of the two groups to the effects of psycho-acoustic complexity on performance. The results showing strong associations between emotion recognition and alexithymia scores in controls suggest a potential explanation for variability in emotion recognition in non-clinical populations.