The psychosis-proneness–persistence–impairment model of psychotic disorder incorporates notions of both phenomenological and temporal continuity (persistence) of psychotic experiences (PE), but not structural continuity. Specific testable propositions of phenomenological continuity and persistence are identified.

Propositions are tested by systematic reviews of the epidemiology of PE, persistence of PE and disorder outcomes, and meta-analyses (including Monte Carlo permutation sampling, MCPS) of reported rates and odds ratios (ORs).

Estimates of the incidence and prevalence of PE obtained from 61 cohorts revealed a median annual incidence of 2.5% and a prevalence of 7.2%. Meta-analysis of risk factors identified age, minority or migrant status, income, education, employment, marital status, alcohol use, cannabis use, stress, urbanicity and family history of mental illness as important predictors of PE. The mode of assessment accounted for significant variance in the observed rates. Across cohorts, the probability of persistence was very strongly related to the rate of PE at baseline. Of those who report PE, ∼20% go on to experience persistent PE whereas for ∼80%, PE remit over time. Of those with baseline PE, 7.4% develop a psychotic disorder outcome.

Compelling support is found for the phenomenological and temporal continuity between PE and psychotic disorder and for the fundamental proposition that this relationship is probabilistic. However, imprecision in epidemiological research design, measurement limitations and the epiphenomenological nature of PE invite further robust scrutiny of the continuity theory.

Hallucinations are a major aspect of psychosis and a diagnostic feature of both psychotic and mood disorders. However, the field lacks information regarding the long-term course of hallucinations in these disorders. Our goals were to determine the percentage of patients with hallucinations and the relationship between hallucinations and recovery, and work attainment.

The present study was a prospective evaluation of the 20-year trajectory of hallucinations in 150 young patients: 51 schizophrenia, 25 schizoaffective, 25 bipolar with psychosis, and 49 unipolar depression. The patients were studied at an index phase of hospitalization for hallucinations, and then reassessed longitudinally at six subsequent follow-ups over 20 years.

The longitudinal course of hallucinations clearly differentiated between schizophrenia and bipolar disorder with psychosis, and suggested some diagnostic similarities between schizophrenia and schizoaffective disorder, and between bipolar disorder and schizoaffective disorder and depression. Frequent or persistent hallucinatory activity over the 20-year period was a feature of 40–45% of schizophrenia patients. The early presence of hallucinations predicted the lack of future periods of recovery in all patients. Increased hallucinatory activity was associated with reduced work attainment in all patients.

This study provides data on the prospective longitudinal course of hallucinations, which were previously unavailable to the field, and are one of the key features of psychosis in major psychiatric disorders. This information on the clinical course of major psychiatric disorders can inform accurate classification and diagnosis.

Cognitive remediation (CR) is an effective treatment for several psychiatric disorders. To date, there have been no published studies examining solely first-episode psychiatric cohorts, despite the merits demonstrated by early intervention CR studies. The current study aimed to assess the effectiveness of CR in patients with a first-episode of either major depression or psychosis.

Fifty-five patients (mean age = 22.8 years, s.d. = 4.3) were randomly assigned to either CR (n = 28) or treatment as usual (TAU; n = 27). CR involved once-weekly 2-h sessions for a total of 10 weeks. Patients were comprehensively assessed before and after treatment. Thirty-six patients completed the study, and analyses were conducted using an intent-to-treat (ITT) approach with all available data.

In comparison to TAU, CR was associated with improved immediate learning and memory controlling for diagnosis and baseline differences. Similarly, CR patients demonstrated greater improvements than TAU patients in psychosocial functioning irrespective of diagnosis. Delayed learning and memory improvements mediated the effect of treatment on psychosocial functioning at a marginal level.

CR improves memory and psychosocial outcome in first-episode psychiatric out-patients for both depression and psychosis. Memory potentially mediated the functional gains observed. Future studies need to build on the current findings in larger samples using blinded allocation and should incorporate longitudinal follow-up and assessment of potential moderators (e.g. social cognition, self-efficacy) to examine sustainability and the precise mechanisms of CR effects respectively.

Brain activity is less organized in patients with schizophrenia than in healthy controls (HC). Noise power (scalp-recorded electroencephalographic activity unlocked to stimuli) may be of use for studying this disorganization.

Fifty-four patients with schizophrenia (29 minimally treated and 25 stable treated), 23 first-degree relatives and 27 HC underwent clinical and cognitive assessments and an electroencephalographic recording during an oddball P300 paradigm to calculate noise power magnitude in the gamma band. We used a principal component analysis (PCA) to determine the factor structure of gamma noise power values across electrodes and the clinical and cognitive correlates of the resulting factors.

The PCA revealed three noise power factors, roughly corresponding to the default mode network (DMN), frontal and occipital regions respectively. Patients showed higher gamma noise power loadings in the first factor when compared to HC and first-degree relatives. In the patients, frontal gamma noise factor scores related significantly and inversely to working memory and problem-solving performance. There were no associations with symptoms.

There is an elevated gamma activity unrelated to task processing over regions coherent with the DMN topography in patients with schizophrenia. The same type of gamma activity over frontal regions is inversely related to performance in tasks with high involvement in these frontal areas. The idea of gamma noise as a possible biological marker for schizophrenia seems promising. Gamma noise might be of use in the study of underlying neurophysiological mechanisms involved in this disease.

Previous cross-sectional studies report that cognitive impairment is associated with poor psychosocial functioning in euthymic bipolar patients. There is a lack of long-term studies to determine the course of cognitive impairment and its impact on functional outcome.

A total of 54 subjects were assessed at baseline and 6 years later; 28 had DSM-IV TR bipolar I or II disorder (recruited, at baseline, from a Lithium Clinic Program) and 26 were healthy matched controls. They were all assessed with a cognitive battery tapping into the main cognitive domains (executive function, attention, processing speed, verbal memory and visual memory) twice over a 6-year follow-up period. All patients were euthymic (Hamilton Rating Scale for Depression score lower than 8 and Young mania rating scale score lower than 6) for at least 3 months before both evaluations. At the end of follow-up, psychosocial functioning was also evaluated by means of the Functioning Assessment Short Test.

Repeated-measures multivariate analysis of covariance showed that there were main effects of group in the executive domain, in the inhibition domain, in the processing speed domain, and in the verbal memory domain (p<0.04). Among the clinical factors, only longer illness duration was significantly related to slow processing (p=0.01), whereas strong relationships were observed between impoverished cognition along time and poorer psychosocial functioning (p<0.05).

Executive functioning, inhibition, processing speed and verbal memory were impaired in euthymic bipolar out-patients. Although cognitive deficits remained stable on average throughout the follow-up, they had enduring negative effects on psychosocial adaptation of patients.

Clinical depression is associated with reductions in white-matter integrity in several long tracts of the brain. The extent to which these findings are localized or related to depressive symptoms or personality traits linked to disease risk remains unclear.

Members of the Lothian Birth Cohort 1936 (LBC936) were assessed in two waves at mean ages of 70 and 73 years. At wave 1, they underwent assessments of depressive symptoms and the personality traits of neuroticism and extraversion. Brain diffusion magnetic resonance imaging (MRI) data were obtained at the second wave and mood assessments were repeated. We tested whether depressive symptoms were related to reduced white-matter tract fractional anisotropy (FA), a measure of integrity, and then examined whether high neuroticism or low extraversion mediated this relationship.

Six hundred and sixty-eight participants provided useable data. Bilateral uncinate fasciculus FA was significantly negatively associated with depressive symptoms at both waves (standardized β=0.12–0.16). Higher neuroticism and lower extraversion were also significantly associated with lower uncinate FA bilaterally (standardized β=0.09–0.15) and significantly mediated the relationship between FA and depressive symptoms.

Trait liability to depression and depressive symptoms are associated with reduced structural connectivity in tracts connecting the prefrontal cortex with the amygdala and anterior temporal cortex. These effects suggest that frontotemporal disconnection is linked to the etiology of depression, in part through personality trait differences.

Depression frequently co-occurs with somatization, and somatic complaints have been reported as a vulnerability marker for affective disorders observable before disease onset. Somatization is thought to result from an increased attention to somatic sensations, which should be reflected in long-latency somatosensory evoked electroencephalogram (EEG) potentials (SSEPs) at the physiological level. Previous studies revealed that SSEPs are altered in depressed patients and suggested late SSEP components as vulnerability markers for affective disorders. Neurotransmitters such as serotonin, γ-aminobutyric acid (GABA) and the neuropeptide substance P may play an important role for both affective disorders and somatosensory processing.

We investigated the associations between SSEPs and polymorphisms within candidate genes of the serotonergic, GABAergic as well as the substance P system in subjects at high risk for affective disorders. The sample was composed of high-risk families participating in the Munich Vulnerability Study and genetic association analyses were calculated using qfam (family-based association tests for quantitative traits) implemented in PLINK 1.05.

We observed significant associations (false discovery rate <0.05) withstanding correction for multiple testing between late SSEP components (response strength 170–370 ms after stimulation) and four single nucleotide polymorphisms within the GABA transaminase (ABAT) gene region coding for a protein responsible for GABA degradation. No effects were found with the classical disease trait approach, suggesting SSEP marker specificity of the observed associations.

Our findings point to a possible role of ABAT gene-regulated GABA catabolism for an altered processing of somatosensory stimuli as a potential vulnerability marker for affective disorders.

Recent models of major depressive disorder (MDD) have proposed the rostral anterior cingulate (rACC) and dorsomedial prefrontal cortex (dmPFC) as nexus sites in the dysfunctional regulation of cognitive-affective state. Limited evidence from remitted-state MDD supports these theories by suggesting that aberrant neural activity proximal to the rACC and the dmPFC may play a role in vulnerability to recurrence/relapse within this disorder. Here we present a targeted analysis assessing functional activity within these two regions of interest (ROIs) for groups with identified vulnerability to MDD: first, remitted, high predicted recurrence-risk patients; and second, patients suffering observed 1-year recurrence.

Baseline T2* images sensitive to blood oxygen level-dependent (BOLD) contrast were acquired from patients and controls during a Go/No-Go (GNG) task incorporating negative feedback, with 1-year patient follow-up to identify recurrence. BOLD contrast data for error commission (EC) and visual negative feedback (VNF) were used in an ROI analysis based on rACC and dmPFC coordinates from the literature, comparing patients versus controls and recurrence versus non-recurrence versus control groups.

Analysis of patients (n = 20) versus controls (n = 20) showed significant right dmPFC [Brodmann area (BA) 9] hypoactivity within the patient group, co-localized during EC and VNF, with additional significant rACC (BA 32) hypoactivity during EC. The results from the follow-up analysis were undermined by small groups and potential confounders but suggested persistent right dmPFC (BA 9) hypoactivity associated with 1-year recurrence.

Convergent hypoactive right dmPFC (BA 9) processing of VNF and EC, possibly impairing adaptive reappraisal of negative experience, was associated most clearly with clinically predicted vulnerability to MDD.

High occupational suicide rates are often linked to easy occupational access to a method of suicide. This study aimed to compare suicide rates across all occupations in Britain, how they have changed over the past 30 years, and how they may vary by occupational socio-economic group.

We used national occupational mortality statistics, census-based occupational populations and death inquiry files (for the years 1979–1980, 1982–1983 and 2001–2005). The main outcome measures were suicide rates per 100 000 population, percentage changes over time in suicide rates, standardized mortality ratios (SMRs) and proportional mortality ratios (PMRs).

Several occupations with the highest suicide rates (per 100 000 population) during 1979–1980 and 1982–1983, including veterinarians (ranked first), pharmacists (fourth), dentists (sixth), doctors (tenth) and farmers (thirteenth), have easy occupational access to a method of suicide (pharmaceuticals or guns). By 2001–2005, there had been large significant reductions in suicide rates for each of these occupations, so that none ranked in the top 30 occupations. Occupations with significant increases over time in suicide rates were all manual occupations whereas occupations with suicide rates that decreased were mainly professional or non-manual. Variation in suicide rates that was explained by socio-economic group almost doubled over time from 11.4% in 1979–1980 and 1982–1983 to 20.7% in 2001–2005.

Socio-economic forces now seem to be a major determinant of high occupational suicide rates in Britain. As the increases in suicide rates among manual occupations occurred during a period of economic prosperity, carefully targeted suicide prevention initiatives could be beneficial.

Much is still unclear about the role of personality in the structure of common psychiatric disorders such as depressive/anxiety disorders and alcohol dependence. This study will therefore examine whether various traits of negative emotionality and impulsivity showed shared or specific associations with these disorders.

Cross-sectional data were used from the Netherlands Study of Depression and Anxiety (NESDA), including individuals with no DSM-IV psychiatric disorder (n = 460), depressive/anxiety disorder only (i.e. depressive and/or anxiety disorder; n = 1398), alcohol dependence only (n = 32) and co-morbid depressive/anxiety disorder plus alcohol dependence (n = 358). Aspects of negative emotionality were neuroticism, hopelessness, rumination, worry and anxiety sensitivity, whereas aspects of impulsivity included disinhibition, thrill/adventure seeking, experience seeking and boredom susceptibility.

Aspects of negative emotionality formed a homogeneous dimension, which was unrelated to the more heterogeneous construct of impulsivity. Although all aspects of negative emotionality were associated with alcohol dependence only, associations were much stronger for depressive/anxiety disorder only and co-morbid depressive/anxiety disorder with alcohol dependence. The results for impulsivity traits were less profound and more variable, with disinhibition and boredom susceptibility showing modest associations with both depressive/anxiety disorder and alcohol dependence, whereas low thrill/adventure seeking and high disinhibition were more strongly related with the first and the latter, respectively.

Our results suggest that depressive/anxiety disorder and alcohol dependence result from shared as well as specific aetiological pathways as they showed the same associations with all aspects of negative emotionality, disinhibition and boredom susceptibility as well as specific associations with thrill/adventure seeking and disinhibition.

Cannabis can induce transient psychotic symptoms, but not all users experience these adverse effects. We compared the neural response to Δ9-tetrahydrocannabinol (THC) in healthy volunteers in whom the drug did or did not induce acute psychotic symptoms.

In a double-blind, placebo-controlled, pseudorandomized design, 21 healthy men with minimal experience of cannabis were given either 10 mg THC or placebo, orally. Behavioural and functional magnetic resonance imaging measures were then recorded whilst they performed a go/no-go task.

The sample was subdivided on the basis of the Positive and Negative Syndrome Scale positive score following administration of THC into transiently psychotic (TP; n = 11) and non-psychotic (NP; n = 10) groups. During the THC condition, TP subjects made more frequent inhibition errors than the NP group and showed differential activation relative to the NP group in the left parahippocampal gyrus, the left and right middle temporal gyri and in the right cerebellum. In these regions, THC had opposite effects on activation relative to placebo in the two groups. The TP group also showed less activation than the NP group in the right middle temporal gyrus and cerebellum, independent of the effects of THC.

In this first demonstration of inter-subject variability in sensitivity to the psychotogenic effects of THC, we found that the presence of acute psychotic symptoms was associated with a differential effect of THC on activation in the ventral and medial temporal cortex and cerebellum, suggesting that these regions mediate the effects of the drug on psychotic symptoms.

Prior research has indicated that affiliation with delinquent peers activates genetic influences on delinquency during adolescence. However, because other studies have indicated that the socializing effects of delinquent peers vary dramatically across childhood and adolescence, it is unclear whether delinquent peer affiliation (DPA) also moderates genetic influences on delinquency during childhood.

The current study sought to evaluate whether and how DPA moderated the etiology of delinquency in a sample of 726 child twins from the Michigan State University Twin Registry (MSUTR).

The results robustly supported etiological moderation of childhood delinquency by DPA. However, this effect was observed for shared environmental, rather than genetic, influences. Shared environmental influences on delinquency were found to be several-fold larger in those with higher levels of DPA as compared to those with lower levels. This pattern of results persisted even when controlling for the overlap between delinquency and DPA.

Our findings bolster prior work in suggesting that, during childhood, the association between DPA and delinquency is largely (although not solely) attributable to the effects of socialization as compared to selection. They also suggest that the process of etiological moderation is not specific to genetic influences. Latent environmental influences are also amenable to moderation by measured environmental factors.

Patients with borderline personality disorder (BPD) show a high prevalence of early adversity, such as childhood trauma. It has also been reported that prenatal adverse conditions, such as prenatal maternal stress, drug taking, tobacco smoking or medical complications, may be associated with an increased risk of mental disorders in the offspring. Prenatal adversity is investigated here for the first time as a potential risk factor in the diagnosis of BPD.

A total of 100 patients with a DSM-IV diagnosis of BPD and 100 matched healthy controls underwent semi-structured interviews about the course of pregnancy, maternal stressors, birth complications and childhood trauma. Further information was obtained from the participants' mothers and from prenatal medical records.

Borderline patients were significantly more often exposed to adverse intrauterine conditions, such as prenatal tobacco exposure (p=0.004), medical complications (p=0.008), prenatal maternal traumatic stress (p=0.015), familial conflicts (p=0.004), low social support (p=0.004) and partnership problems during pregnancy (p=0.014). Logistic regression analyses revealed that the reported prenatal risk factors accounted for 25.7% of the variance in BPD. Prenatal tobacco exposure [odds ratio (OR) 3.37, 95% confidence interval (CI) 1.49–7.65, p=0.004] and medical complications (OR 2.87, 95% CI 1.29–6.38, p=0.010) emerged as important predictors. After controlling for childhood adversity and parental socio-economic status (SES), prenatal risk factors predicted relevant borderline subdomains, such as impulsivity, affective instability, identity disturbance, dissociation and severity of borderline symptoms.

This study provides evidence of an association between prenatal adversity and the diagnosis of BPD. Our findings suggest that prenatal adversity may constitute a potential risk factor in the pathogenesis of BPD.

Studies investigating early developmental factors in relation to psychopathology have mainly focused on schizophrenia. The personality dimension of neuroticism seems to be a general risk factor for psychopathology, but evidence on associations between early developmental precursors and personality traits is almost non-existent. This study is therefore the first to investigate associations between early motor developmental milestones and neuroticism in adulthood.

Mothers of 9125 children of the Copenhagen Perinatal Cohort recorded 12 developmental milestones during the child's first year of life. A subsample of the cohort comprising 1182 individuals participated in a follow-up when they were aged 20–34 years and were administered the Eysenck Personality Questionnaire (EPQ). Associations between motor developmental milestones and level of neuroticism, extraversion and psychoticism were analysed by multiple linear regression adjusting for for sex, single-mother status, parity, mother's age, father's age, parental social status and birth weight.

Among the 1182 participants with information on the EPQ, information on milestones was available for 968 participants. Infants who developed high levels of neuroticism as adults tended to sit without support, crawl, and walk with and without support significantly later than individuals with low levels of neuroticism (p values <0.05). These results remained significant after adjustment for the included covariates and for adult intelligence.

The findings are the first of their kind and suggest that delays in early motor development may not only characterize psychopathological disorders such as schizophrenia, but may also be associated with the personality dimension of neuroticism in adulthood.

Happiness and higher intelligent quotient (IQ) are independently related to positive health outcomes. However, there are inconsistent reports about the relationship between IQ and happiness. The aim was to examine the association between IQ and happiness and whether it is mediated by social and clinical factors.

The authors analysed data from the 2007 Adult Psychiatric Morbidity Survey in England. The participants were adults aged 16 years or over, living in private households in 2007. Data from 6870 participants were included in the study. Happiness was measured using a validated question on a three-point scale. Verbal IQ was estimated using the National Adult Reading Test and both categorical and continuous IQ was analysed.

Happiness is significantly associated with IQ. Those in the lowest IQ range (70–99) reported the lowest levels of happiness compared with the highest IQ group (120–129). Mediation analysis using the continuous IQ variable found dependency in activities of daily living, income, health and neurotic symptoms were strong mediators of the relationship, as they reduced the association between happiness and IQ by 50%.

Those with lower IQ are less happy than those with higher IQ. Interventions that target modifiable variables such as income (e.g. through enhancing education and employment opportunities) and neurotic symptoms (e.g. through better detection of mental health problems) may improve levels of happiness in the lower IQ groups.

The goal of the current study was to investigate asthma and mental health among youth in the community, and to consider the role of asthma severity and persistence in this link.

Data were drawn from the Raine Study, a population-based birth cohort study in Western Australia. Logistic regression models and generalized estimating equations were used to examine the relationship between asthma at age 5 years and the range of internalizing and externalizing mental health problems at ages 5–17 years. Analyses were stratified by asthma severity and persistence, and adjusted for a range of potential confounders.

More severe and persistent asthma at age 5 was associated with significantly increased odds of affective, anxiety, somatic, oppositional defiant and conduct problems at ages 5–17. Mild asthma and remitted asthma were not associated with heightened vulnerability to mental disorders.

Our results suggest that youth with symptomatic asthma are more likely to suffer from a wide range of mental health problems, and that the likelihood of mental health problems appears to increase as a function of asthma severity. Youth with poorly controlled and/or more severe and persistent asthma may be considered a vulnerable group who might benefit from mental health screening in clinical, school and community settings.

Increased reaction time variability (RTV) on cognitive tasks requiring a speeded response is characteristic of several psychiatric disorders. In attention deficit hyperactivity disorder (ADHD), the association with RTV is strong phenotypically and genetically, yet high RTV is not a stable impairment but shows ADHD-sensitive improvement under certain conditions, such as those with rewards. The state regulation theory proposed that the RTV difference score, which captures change from baseline to a rewarded or fast condition, specifically measures ‘state regulation’. By contrast, the interpretation of RTV baseline (slow, unrewarded) scores is debated. We aimed to investigate directly the degree of phenotypic and etiological overlap between RTV baseline and RTV difference scores.

We conducted genetic model fitting analyses on go/no-go and fast task RTV data, across task conditions manipulating rewards and event rate, from a population-based twin sample (n=1314) and an ADHD and control sibling-pair sample (n=1265).

Phenotypic and genetic/familial correlations were consistently high (0.72–0.98) between RTV baseline and difference scores, across tasks, manipulations and samples. By contrast, correlations were low between RTV in the manipulated condition and difference scores. A comparison across two different go/no-go task RTV difference scores (slow-fast/slow-incentive) showed high phenotypic and genetic/familial overlap (r = 0.75–0.83).

Our finding that RTV difference scores measure largely the same etiological process as RTV under baseline condition supports theories emphasizing the malleability of the observed high RTV. Given the statistical shortcomings of difference scores, we recommend the use of RTV baseline scores for most analyses, including genetic analyses.

Undue influence of body shape or weight on self-evaluation – referred to as overvaluation – is considered a core feature across eating disorders, but is not a diagnostic requirement for binge eating disorder (BED). This study examined the concurrent and predictive significance of overvaluation of shape/weight in obese patients with BED participating in a randomized clinical trial testing cognitive behavioral therapy (CBT) and behavioral weight loss (BWL).

A total of 90 participants were randomly assigned to 6-month group treatments of CBT or BWL. Assessments were performed at baseline, throughout- and post-treatment, and at 6- and 12-month follow-ups after completing treatments with reliably administered semi-structured interviews and established measures.

Participants categorized with overvaluation (n = 52, 58%) versus without overvaluation (n = 38, 42%) did not differ significantly in demographic features (age, gender and ethnicity), psychiatric co-morbidity, body mass index or binge eating frequency. The overvaluation group had significantly greater levels of eating disorder psychopathology and poorer psychological functioning (higher depression and lower self-esteem) than the non-overvaluation group. Overvaluation of shape/weight significantly predicted non-remission from binge eating and higher frequency of binge eating at the 12-month follow-up, even after adjusting for group differences in depression and self-esteem levels.

Our findings suggest that overvaluation does not simply reflect concern commensurate with being obese or more frequent binge eating, but also is strongly associated with heightened eating-related psychopathology and psychological distress, and has negative prognostic significance for longer-term treatment outcomes. Overvaluation of shape/weight warrants consideration as a diagnostic specifier for BED as it provides important information about severity and treatment outcome.