Mood Instability and Psychosis: Analyses of British National Survey Data

Background: We used British national survey data to test specific hypotheses that mood instability (1) is associated with psychosis and individual psychotic phenomena, (2) predicts the later emergence of auditory hallucinations and paranoid ideation, and (3) mediates the link between child sexual abuse and psychosis. Methods: We analyzed data from the 2000 and 2007 UK national surveys of psychiatric morbidity (N = 8580 and 7403, respectively). The 2000 survey included an 18-month follow-up of a subsample (N = 2406). Mood instability was assessed from the Structured Clinical Interview for DSM-IV Axis II (SCID-II) questionnaire. Our dependent variables comprised auditory hallucinations, paranoid ideation, the presence of psychosis overall, and a 15-item paranoia scale. Results: Mood instability was strongly associated in cross-sectional analyses with psychosis (2000: OR: 7.5; 95% CI: I 4.1–13.8; 2007: OR: 21.4; CI: 9.7–41.2), paranoid ideation (2000: OR: 4.7; CI: 4.1–5.4; 2007: OR: 5.7; CI: 4.9–6.7), auditory hallucinations (2000: OR: 3.4; CI: 2.6–4.4; 2007: OR 3.5; CI: 2.7–4.7), and paranoia total score (2000: Coefficient: 3.6; CI: 3.3–3.9), remaining so after adjustment for current mood state. Baseline mood instability significantly predicted 18-month inceptions of paranoid ideation (OR: 2.3; CI: 1.6–3.3) and of auditory hallucinations (OR: 2.6; CI: 1.5–4.4). Finally, it mediated a third of the total association of child sexual abuse with psychosis and persecutory ideation and a quarter of that with auditory hallucinations. Conclusions: Mood instability is a prominent feature of psychotic experience and may have a role in its genesis. Targeting mood instability could lead to innovative treatments for psychosis.Key words: epidemiology, psychopathology, paranoia, auditory hallucination, child sexual abuse     

Reliability and Comparability of Psychosis Patients’ Retrospective Reports of Childhood Abuse

An increasing number of studies are demonstrating an association between childhood abuse and psychosis. However, the majority of these rely on retrospective self-reports in adulthood that may be unduly influenced by current psychopathology. We therefore set out to explore the reliability and comparability of first-presentation psychosis patients’ reports of childhood abuse. Psychosis case subjects were drawn from the Aetiology and Ethnicity of Schizophrenia and Other Psychoses (ÆSOP) epidemiological study and completed the Childhood Experience of Care and Abuse Questionnaire to elicit abusive experiences that occurred prior to 16 years of age. High levels of concurrent validity were demonstrated with the Parental Bonding Instrument (antipathy: r_s = 0.350–0.737, P < .001; neglect: r_s = 0.688–0.715, P < .001), and good convergent validity was shown with clinical case notes (sexual abuse: κ = 0.526, P < .001; physical abuse: κ = 0.394, P < .001). Psychosis patients’ reports were also reasonably stable over a 7-year period (sexual abuse: κ = 0.590, P < .01; physical abuse: κ = 0.634, P < .001; antipathy: κ = 0.492, P < .01; neglect: κ = 0.432, P < .05). Additionally, their reports of childhood abuse were not associated with current severity of psychotic symptoms (sexual abuse: U = 1768.5, P = .998; physical abuse: U = 2167.5, P = .815; antipathy: U = 2216.5, P = .988; neglect: U = 1906.0, P = .835) or depressed mood (sexual abuse: χ² = 0.634, P = .277; physical abuse: χ² = 0.159, P = .419; antipathy: χ² = 0.868, P = .229; neglect: χ² = 0.639, P = .274). These findings provide justification for the use in future studies of retrospective reports of childhood abuse obtained from individuals with psychotic disorders.     

Sexual Trauma Increases the Risk of Developing Psychosis in an Ultra High-Risk “Prodromal” Population

Studies indicate a high prevalence of childhood trauma in patient cohorts with established psychotic disorder and in those at risk of developing psychosis. A causal link between childhood trauma and development of psychosis has been proposed. We aimed to examine the association between experience of childhood trauma and the development of a psychotic disorder in a large “Ultra High Risk” (UHR) for psychosis cohort. The data were collected as part of a longitudinal cohort study of all UHR patients recruited to research studies at the Personal Assessment and Clinical Evaluation clinic between 1993 and 2006. Baseline data were collected at recruitment to these studies. The participants completed a comprehensive follow-up assessment battery (mean time to follow-up 7.5 years, range 2.4–14.9 years), which included the Childhood Trauma Questionnaire (CTQ), a self-report questionnaire that assesses experience of childhood trauma. The outcome of interest was transition to a psychotic disorder during the follow-up period. Data were available on 233 individuals. Total CTQ trauma score was not associated with transition to psychosis. Of the individual trauma types, only sexual abuse was associated with transition to psychosis (P = .02). The association remained when adjusting for potential confounding factors. Those with high sexual abuse scores were estimated to have a transition risk 2–4 times that of those with low scores. The findings suggest that sexual trauma may be an important contributing factor in development of psychosis for some individuals.Key words: trauma, psychosis, ultra high risk     

Childhood abuse as a risk factor for psychotic experiences

OBJECTIVE: To examine the hypothesis that individuals from the general population who report childhood abuse are at increased risk of developing positive psychotic symptoms. METHOD: Data were derived from a general population sample of 4045 subjects aged 18-64 years. First ever onset of positive psychotic symptoms at 2-year follow-up were assessed using the Composite International Diagnostic Interview and additional clinical interviews if necessary. Childhood abuse was assessed at baseline. RESULTS: Baseline reported childhood abuse predicted development of positive psychotic symptoms associated with need for care [odds ratio (OR) = 11.5, 95% CI 2.6-51.6]. This association remained after adjustment for demographic variables, reported risk factors and presence of any lifetime psychiatric diagnosis at baseline (OR = 7.3, 95% CI 1.1-49.0). CONCLUSION: The results suggest that early childhood trauma increases the risk for positive psychotic symptoms. This finding fits well with recent models that suggest that early adversities may lead to psychological and biological changes that increase psychosis vulnerability.     

Childhood adversities increase the risk of psychosis: a meta-analysis of patient-control, prospective- and cross-sectional cohort studies

Evidence suggests that adverse experiences in childhood are associated with psychosis. To examine the association between childhood adversity and trauma (sexual abuse, physical abuse, emotional/psychological abuse, neglect, parental death, and bullying) and psychosis outcome, MEDLINE, EMBASE, PsychINFO, and Web of Science were searched from January 1980 through November 2011. We included prospective cohort studies, large-scale cross-sectional studies investigating the association between childhood adversity and psychotic symptoms or illness, case-control studies comparing the prevalence of adverse events between psychotic patients and controls using dichotomous or continuous measures, and case-control studies comparing the prevalence of psychotic symptoms between exposed and nonexposed subjects using dichotomous or continuous measures of adversity and psychosis. The analysis included 18 case-control studies (n = 2048 psychotic patients and 1856 nonpsychiatric controls), 10 prospective and quasi-prospective studies (n = 41,803) and 8 population-based cross-sectional studies (n = 35,546). There were significant associations between adversity and psychosis across all research designs, with an overall effect of OR = 2.78 (95% CI = 2.34-3.31). The integration of the case-control studies indicated that patients with psychosis were 2.72 times more likely to have been exposed to childhood adversity than controls (95% CI = 1.90-3.88). The association between childhood adversity and psychosis was also significant in population-based cross-sectional studies (OR = 2.99 [95% CI = 2.12-4.20]) as well as in prospective and quasi-prospective studies (OR = 2.75 [95% CI = 2.17-3.47]). The estimated population attributable risk was 33% (16%-47%). These findings indicate that childhood adversity is strongly associated with increased risk for psychosis.     

Is Arson the Crime Most Strongly Associated With Psychosis?—A National Case-Control Study of Arson Risk in Schizophrenia and Other Psychoses

Background: The association of psychosis with certain serious crimes, such as homicide, has been clearly demonstrated, but it is uncertain to what extent psychotic disorders are associated with arson. Methods: We used a case-control design to investigate the association of being diagnosed with schizophrenia and other psychoses and committing arson. Data were obtained from Swedish national registers for criminal convictions, hospital discharge diagnoses (International Classification of Diseases, Ninth Revision [ICD-9], and International Classification of Diseases, Tenth Revision [ICD-10]), and sociodemographic factors for 1988–2000. We included all convicted arson offenders of both sexes in Sweden (N = 1689) and compared them with a random sample of general population control subjects (N = 40 560). Results: After adjustment for sociodemographic confounders, arson offenders were more likely to be diagnosed with schizophrenia (in men, adjusted odds ratio [OR] = 22.6, 95% confidence interval [CI] = 14.8–34.4; in women, adjusted OR = 38.7, 95% CI = 20.4–73.5) or other psychoses (in men, adjusted OR = 17.4, 95% CI = 11.1–27.5; in women, adjusted OR = 30.8, 95% CI = 18.8–50.6). Conclusions: Individuals with schizophrenia and other psychoses have significantly increased risks of an arson conviction. These risk estimates are higher than those reported for other violent crimes and place arson in the same category as homicide as crimes that are most strongly associated with psychotic disorders.     

Development and Validation of a Computerized Adaptive Assessment Tool for Discrimination and Measurement of Psychotic Symptoms

ObjectiveTime constraints limit the use of measurement-based approaches in research and routine clinical management of psychosis. Computerized adaptive testing (CAT) can reduce administration time, thus increasing measurement efficiency. This study aimed to develop and test the capacity of the CAT-Psychosis battery, both self-administered and rater-administered, to measure the severity of psychotic symptoms and discriminate psychosis from healthy controls.MethodsAn item bank was developed and calibrated. Two raters administered CAT-Psychosis for inter-rater reliability (IRR). Subjects rated themselves and were retested within 7 days for test-retest reliability. The Brief Psychiatric Rating Scale (BPRS) was administered for convergent validity and chart diagnosis, and the Structured Clinical Interview (SCID) was used to test psychosis discriminant validity.ResultsDevelopment and calibration study included 649 psychotic patients. Simulations revealed a correlation of r = .92 with the total 73-item bank score, using an average of 12 items. Validation study included 160 additional patients and 40 healthy controls. CAT-Psychosis showed convergent validity (clinician: r = 0.690; 95% confidence interval [95% CI]: 0.610–0.757; self-report: r = .690; 95% CI: 0.609–0.756), IRR (intraclass correlation coefficient [ICC] = 0.733; 95% CI: 0.611–0.828), and test-retest reliability (clinician ICC = 0.862; 95% CI: 0.767–0.922; self-report ICC = 0.815; 95%CI: 0.741–0.871). CAT-Psychosis could discriminate psychosis from healthy controls (clinician: area under the receiver operating characteristic curve [AUC] = 0.965, 95% CI: 0.945–0.984; self-report AUC = 0.850, 95% CI: 0.807–0.894). The median length of the clinician-administered assessment was 5 minutes (interquartile range [IQR]: 3:23–8:29 min) and 1 minute, 20 seconds (IQR: 0:57–2:09 min) for the self-report.ConclusionCAT-Psychosis can quickly and reliably assess the severity of psychosis and discriminate psychotic patients from healthy controls, creating an opportunity for frequent remote assessment and patient/population-level follow-up.     

Childhood trauma and increased stress sensitivity in psychosis

Lardinois M, Lataster T, Mengelers R, van Os J, Myin‐Germeys I. Childhood trauma and increased stress sensitivity in psychosis. Objective: The notion that traumatic experiences in childhood may predict later psychotic outcomes would be strengthened if a plausible mechanism could be demonstrated. Because increased stress sensitivity is part of the behavioural expression of psychosis liability, the possible mediating role of childhood trauma was investigated. Method: Fifty patients with psychosis were studied with the experience sampling method to assess stress reactivity in daily life, defined as emotional and psychotic reactivity to stress. Traumatic experiences in childhood were assessed with the Childhood Trauma Questionnaire. Results: A significant interaction was found between stress and CT on both negative affect (event stress: β = 0.04, P < 0.04; activity stress: β = 0.12, P < 0.001) and psychotic intensity (event stress: β = 0.06, P < 0.001; activity stress: β = 0.11, P < 0.001), showing that a history of CT is associated with increased sensitivity to stress. Conclusion: A history of childhood trauma in patients with psychosis is associated with increased stress reactivity later in life, suggestive for an underlying process of behavioural sensitization.     

Hospital Admission With Infection During Childhood and Risk for Psychotic Illness—A Population-based Cohort Study

A growing body of literature suggests that exposure to infections, particularly maternal infections, during pregnancy confers risk for later development of psychotic disorder. Though brain development proceeds throughout childhood and adolescence, the influence of infections during these ages on subsequent psychosis risk is insufficiently examined. The aim of this study was to investigate the potential association between infections during childhood and nonaffective psychoses in a large population-based birth cohort with follow up long enough to include peak incidence of nonaffective psychosis. We included all individuals born in Sweden between 1973 and 1985, (N = 1172879), with follow up on first time inpatient care with nonaffective psychosis from age 14 years until 2006, (N = 4638). Following adjustment for differences in sex, socioeconomic status, family history of psychosis, and hospital admissions involving noninfectious, nonpsychiatric care, we observed a small but statistically significant association between hospital admissions for infections, in general, throughout childhood (0–13 years) and a later diagnosis of nonaffective psychosis, hazard ratio (HR) = 1.10 (95% CI 1.03–1.18), and this association seemed to be driven by bacterial infection, HR = 1.23 (95% CI 1.08–1.40). Bacterial infections and central nervous system infections during preadolescence (10–13 years) conferred the strongest risk, HR 1.57 (95% CI 1.21–2.05) and HR 1.96 (95% CI 1.05–3.62), respectively. Although preadolescence appeared to be a vulnerable age period, and bacterial infection the most severe in relation to psychosis development, the present findings can also indicate an increased susceptibility to hospital admission for infections among children who will later develop nonaffective psychosis due to social or familial/genetic factors.Key words: psychosis, prenatal, schizophrenia, epidemiology, cohort study     

Preventing the Second Episode: A Systematic Review and Meta-analysis of Psychosocial and Pharmacological Trials in First-Episode psychosis

Objective: The majority of first-episode psychosis (FEP) patients reach clinical remission; however, rates of relapse are high. This study sought to undertake a systematic review and meta-analysis of randomized controlled trials (RCTs) to determine the effectiveness of pharmacological and non-pharmacological interventions to prevent relapse in FEP patients. Methods: Systematic review and meta-analysis of RCTs. Results: Of 66 studies retrieved, 18 were eligible for inclusion. Nine studies investigated psychosocial interventions and 9 pharmacological treatments. The analysis of 3 RCTs of psychosocial interventions comparing specialist FEP programs vs treatment as usual involving 679 patients demonstrated the former to be more effective in preventing relapse (odds ratio [OR] = 1.80, 95% confidence interval [CI] = 1.31–2.48; P < .001; number needed to treat [NNT] = 10). While the analysis of 3 different cognitive-behavioral studies not specifically intended at preventing relapse showed no further benefits compared with specialist FEP programs (OR = 1.95, 95% CI = 0.76–5.00; P = .17), the combination of specific individual and family intervention targeted at relapse prevention may further improve upon these outcomes (OR = 4.88, 95% CI = 0.97–24.60; P = .06). Only 3 small studies compared first-generation antipsychotics (FGAs) with placebo with no significant differences regarding relapse prevention although all individual estimates favored FGAs (OR = 2.82, 95% CI = 0.54–14.75; P = .22). Exploratory analysis involving 1055 FEP patients revealed that relapse rates were significantly lower with second-generation antipsychotics (SGAs) compared with FGAs (OR = 1.47, 95% CI = 1.07–2.01; P < .02; NNT = 10). Conclusions: Specialist FEP programs are effective in preventing relapse. Cognitive-based individual and family interventions may need to specifically target relapse to obtain relapse prevention benefits that extend beyond those provided by specialist FEP programs. Overall, the available data suggest that FGAs and SGAs have the potential to reduce relapse rates. Future trials should examine the effectiveness of placebo vs antipsychotics in combination with intensive psychosocial interventions in preventing relapse in the early course of psychosis. Further studies should identify those patients who may not need antipsychotic medication to be able to recover from psychosis.     

Daily Use,Especially of High-Potency Cannabis,Drives the Earlier Onset of Psychosis in Cannabis Users

Cannabis use is associated with an earlier age of onset of psychosis (AOP). However, the reasons for this remain debated. Methods: We applied a Cox proportional hazards model to 410 first-episode psychosis patients to investigate the association between gender, patterns of cannabis use, and AOP. Results: Patients with a history of cannabis use presented with their first episode of psychosis at a younger age (mean years = 28.2, SD = 8.0; median years = 27.1) than those who never used cannabis (mean years = 31.4, SD = 9.9; median years = 30.0; hazard ratio [HR] = 1.42; 95% CI: 1.16–1.74; P < .001). This association remained significant after controlling for gender (HR = 1.39; 95% CI: 1.11–1.68; P < .001). Those who had started cannabis at age 15 or younger had an earlier onset of psychosis (mean years = 27.0, SD = 6.2; median years = 26.9) than those who had started after 15 years (mean years = 29.1, SD = 8.5; median years = 27.8; HR = 1.40; 95% CI: 1.06–1.84; P = .050). Importantly, subjects who had been using high-potency cannabis (skunk-type) every day had the earliest onset (mean years = 25.2, SD = 6.3; median years = 24.6) compared to never users among all the groups tested (HR = 1.99; 95% CI: 1.50- 2.65; P < .0001); these daily users of high-potency cannabis had an onset an average of 6 years earlier than that of non-cannabis users. Conclusions: Daily use, especially of high-potency cannabis, drives the earlier onset of psychosis in cannabis users.Key words: psychotic disorders, age of onset, gender, cannabis, survival plots, drug use, high-potency cannabis     

Schizophrenia Polygenic Risk and Experiences of Childhood Adversity: A Systematic Review and Meta-analysis

Background and HypothesisSchizophrenia has been robustly associated with multiple genetic and environmental risk factors. Childhood adversity is one of the most widely replicated environmental risk factors for schizophrenia, but it is unclear if schizophrenia genetic risk alleles contribute to this association.Study DesignIn this systematic review and meta-analysis, we assessed the evidence for gene-environment correlation (genes influence likelihood of environmental exposure) between schizophrenia polygenic risk score (PRS) and reported childhood adversity. We also assessed the evidence for a gene-environment interaction (genes influence sensitivity to environmental exposure) in relation to the outcome of schizophrenia and/or psychosis. This study was registered on PROSPERO (CRD42020182812). Following PRISMA guidelines, a search for relevant literature was conducted using Cochrane, MEDLINE, PsycINFO, Web of Science, and Scopus databases until February 2022. All studies that examined the association between schizophrenia PRS and childhood adversity were included.Study ResultsSeventeen of 650 identified studies met the inclusion criteria and were assessed against the Newcastle-Ottawa Scale for quality. The meta-analysis found evidence for gene-environment correlation between schizophrenia PRS and childhood adversity (r = .02; 95% CI = 0.01, 0.03; P = .001), but the effect was small and therefore likely to explain only a small proportion of the association between childhood adversity and psychosis. The 4 studies that investigated a gene-environment interaction between schizophrenia PRS and childhood adversity in increasing risk of psychosis reported inconsistent results.ConclusionsThese findings suggest that a gene-environment correlation could explain a small proportion of the relationship between reported childhood adversity and psychosis.     

Testing the Independent and Joint Contribution of Exposure to Neurodevelopmental Adversity and Childhood Trauma to Risk of Psychotic Experiences in Adulthood

Exposure to neurodevelopmental adversity and childhood trauma are both independently associated with psychosis. However, there is little research on the mechanism underlying their relationship with each other. The current study investigated both the independent and joint effects of neurodevelopmental adversity and childhood trauma to better understand the etiology of psychosis. A large population-based cohort (N = 3514) followed from birth was assessed on psychotic experiences (PE) at 24 years. Neurodevelopmental adversity included obstetric complications (birth weight, gestational age, in-utero influenza exposure, resuscitation) and developmental impairment (cognitive and motor impairments). Trauma exposure included caregiver and peer inflicted trauma up to 17 years. Multiple regression models tested their independent and interactive effect on PE, and path analysis estimated the indirect effect of neurodevelopmental adversity on PE via trauma. Neurodevelopmental adversity (OR = 1.32, 95%CI: 1.08–1.62) and trauma (OR = 1.97, 95%CI: 1.65–2.36) independently increased the odds of PE. There was also an indirect relationship between neurodevelopmental adversity and PE via increased exposure to childhood trauma (β = 0.01, 95%CI: 0.004–0.024). In particular, peer bullying mediated the association between developmental impairment to PE (β = 0.02, 95%CI: 0.01–0.03). In conclusion, children with neurodevelopmental adversity, in particular those with developmental impairment, are more likely to be exposed to trauma. This new etiological understanding of psychosis suggests that PE may be partially modifiable through reducing exposure to peer bullying, especially in children with developmental impairment.     

Delusions,Anger, and Serious Violence: New Findings From the MacArthur Violence Risk Assessment Study

Introduction:

Recent research on the association between delusions and violence has suggested complex and differing pathways. Furthermore, it has been emphasized that temporal proximity is fundamental when investigating these relationships. We reanalyzed data from the MacArthur Violence Risk Assessment Study utilizing a different methodological approach to investigate associations between specific delusions and violence.

Methods:

Longitudinal study of 1136 male and female civil psychiatric inpatients after discharge. Delusions, affect due to delusions, and violence were measured at baseline and in 5 follow-up assessments. Serious violence was established using the MacArthur Community Violence Interview. Logistic mixed-effect models for repeated measures were performed.

Results:

A “prospective” model confirmed previous findings that delusions do not predict later violence. However, reanalysis, considering temporal proximity, indicated a relationship between specific delusions and outcome including: being spied upon (adjusted OR [AOR] = 1.62, 95% CI = 1.06–2.47, P = .027), being followed (AOR = 1.90, 95% CI = 1.29–2.80, P = .001), being plotted against (AOR = 1.70, 95% CI = 1.14–2.52, P = .009), being under control of person/force (AOR = 1.92, 95% CI = 1.24–2.97, P = .003), thought insertion (AOR = 1.63, 95% CI = 1.00–2.66, P = .048), and having special gifts/powers (AOR = 1.95, 95% CI = 1.31–2.92, P = .001). All these delusions were associated with angry affect (P < .05). Inclusion of anger in the model significantly attenuated the main effects (except grandiose delusions), indicating an indirect pathway.

Conclusions:

Temporal proximity is crucial when investigating relationships between delusions and violence. Anger due to delusions is the key factor in this pathway. Our findings have important implications for identification of psychotic patients at risk for violent behavior and, most importantly, management of their risk.Key words: psychosis, anger, delusions implying threat, indirect pathway, management of risk for violence     

The CCC2000 Birth Cohort Study of Register-Based Family History of Mental Disorders and Psychotic Experiences in Offspring

Psychotic experiences (PE) in individuals of the general population are hypothesized to mark the early expression of the pathology underlying psychosis. This notion of PE as an intermediate phenotype is based on the premise that PE share genetic liability with psychosis. We examined whether PE in childhood was predicted by a family history of mental disorder with psychosis rather than a family history of nonpsychotic mental disorder and whether this association differed by severity of PE. The study examined data on 1632 children from a general population birth cohort assessed at age 11–12 years by use of a semistructured interview covering 22 psychotic symptoms. The Danish national registers were linked to describe the complete family history of hospital-based psychiatric diagnoses. Uni- and multivariable logistic regressions were used to test whether a family history of any mental disorder with psychosis, or of nonpsychotic mental disorder, vs no diagnoses was associated with increased risk of PE in offspring (hierarchical exposure variable). The occurrence of PE in offspring was significantly associated with a history of psychosis among the first-degree relatives (adjusted relative risk [RR] = 3.29, 95% CI: 1.82–5.93). The risk increased for combined hallucinations and delusions (adjusted RR = 5.90, 95% CI: 2.64–13.16). A history of nonpsychotic mental disorders in first-degree relatives did not contribute to the risk of PE in offspring nor did any mental disorder among second-degree relatives. Our findings support the notion of PE as a vulnerability marker of transdiagnostic psychosis. The effect of psychosis in first-degree relatives may operate through shared genetic and environmental factors.Key words: psychosis, schizophrenia, epidemiology, family liability, general population, psychiatric family history     

Psychotic Disorders and Repeat Offending: Systematic Review and Meta-analysis

Objective: To undertake a systematic review and meta-analysis on the risk of repeat offending in individuals with psychosis and to assess the effect of potential moderating characteristics on risk estimates. Methods: A systematic search was conducted in 6 bibliographic databases from January 1966 to January 2009, supplemented with correspondence with authors. Studies that reported risks of repeat offending in individuals with psychotic disorders (n = 3511) compared with individuals with other psychiatric disorders (n = 5446) and healthy individuals (n = 71 552) were included. Risks of repeat offending were calculated using fixed- and random-effects models to calculate pooled odds ratios (ORs). Subgroup and meta-regression analyses were conducted to examine how risk estimates were affected by various study characteristics including mean sample age, study location, sample size, study period, outcome measure, duration of follow-up, and diagnostic criteria. Results: Twenty-seven studies, which included 3511 individuals with psychosis, were identified. Compared with individuals without any psychiatric disorders, there was a significantly increased risk of repeat offending in individuals with psychosis (pooled OR = 1.6, 95% confidence interval [CI] = 1.4–1.8), although this was only based on 4 studies. In contrast, there was no association when individuals with other psychiatric disorders were used as the comparison group (pooled OR = 1.0, 95% CI = 0.7–1.3), although there was substantial heterogeneity. Higher risk estimates were found in female-only samples with psychosis and in studies conducted in the United States. Conclusions: The association between psychosis and repeat offending differed depending on the comparison group. Despite this, we found no support for the findings of previous reviews that psychosis is associated with a lower risk of repeat offending.     

Association Between Childhood Green Space,Genetic Liability,and the Incidence of Schizophrenia

Childhood exposure to green space has previously been associated with lower risk of developing schizophrenia later in life. It is unclear whether this association is mediated by genetic liability or whether the 2 risk factors work additively. Here, we investigate possible gene–environment associations with the hazard ratio (HR) of schizophrenia by combining (1) an estimate of childhood exposure to residential-level green space based on the normalized difference vegetation index (NDVI) from Landsat satellite images, with (2) genetic liability estimates based on polygenic risk scores for 19 746 genotyped individuals from the Danish iPSYCH sample. We used information from the Danish registers of health, residential address, and socioeconomic status to adjust HR estimates for established confounders, ie, parents’ socioeconomic status, and family history of mental illness. The adjusted HRs show that growing up surrounded by the highest compared to the lowest decile of NDVI was associated with a 0.52-fold (95% confidence interval [CI]: 0.40 to 0.66) lower schizophrenia risk, and children with the highest polygenic risk score had a 1.24-fold (95% CI: 1.18 to 1.30) higher schizophrenia risk. We found that NDVI explained 1.45% (95% CI: 1.07 to 1.90) of the variance on the liability scale, while polygenic risk score for schizophrenia explained 1.01% (95% CI: 0.77 to 1.46). Together they explained 2.40% (95% CI: 1.99 to 3.07) with no indication of a gene–environment interaction (P = .29). Our results suggest that risk of schizophrenia is associated additively with green space exposure and genetic liability, and provide no support for an environment-gene interaction between NDVI and schizophrenia.     

Do urbanicity and familial liability coparticipate in causing psychosis?

OBJECTIVE: The urban environment and familial liability are risk factors for psychotic illness, but it is not known whether a biological synergism exists between these two proxy causes. METHOD: The amount of biological synergism between familial liability (defined as a family history of delusions and/or hallucinations necessitating psychiatric treatment) and a five-level rating of population density of place of residence was estimated from the additive statistical interaction in a general population risk set of 5,550 individuals. RESULTS: Both the level of urbanicity (adjusted summary odds ratio=1.57, 95% CI=1.30-1.89) and familial liability (adjusted odds ratio=4.59, 95% CI=2.41-8.74) increased the risk for psychotic disorder, independently of each other. However, the effect of urbanicity on the additive scale was much larger for individuals with evidence of familial liability (risk difference=2.58%) than in those without familial liability (risk difference=0.40%). An estimated 60%-70% of the individuals exposed to both urbanicity and familial liability had developed psychotic disorder because of the synergistic action of the two proxy causes. CONCLUSIONS: Given that familial clustering of psychosis is thought to reflect the effect of shared genes, the findings support a mechanism of gene-environment interaction in the causation of psychosis.     

Cognitive Behavioral Therapy for Subjects at Ultrahigh Risk for Developing Psychosis: A Randomized Controlled Clinical Trial

Background

: Evidence for the effectiveness of treatments for subjects at ultrahigh risk (UHR) for developing psychosis remains inconclusive. Objective : A new cognitive behavioral intervention specifically targeted at cognitive biases (ie, Cognitive Behavioral Therapy [CBT] for UHR patients plus treatment as usual [TAU] called CBTuhr) is compared with TAU in a group of young help-seeking UHR subjects. Methods : A total of 201 patients were recruited at 4 sites and randomized. In most cases, CBTuhr was an add-on therapy because most people were seeking help for a comorbid disorder. The CBT was provided for 6 months, and the follow-up period was 18 months. Results : In the CBTuhr condition, 10 patients transitioned to psychosis compared with 22 in the TAU condition (χ ² (1) = 5.575, P = .03). The number needed to treat (NNT) was 9 (95% confidence interval [CI]: 4.7–89.9). At 18-month follow-up the CBTuhr group was significantly more often remitted from an at-risk mental state, with a NNT of 7 (95% CI: 3.7–71.2). Intention-to-treat analysis, including 5 violations against exclusion criteria, showed a statistical tendency (χ ² (1) = 3.338, P = .06). Conclusions : Compared with TAU, this new CBT (focusing on normalization and awareness of cognitive biases) showed a favorable effect on the transition to psychosis and reduction of subclinical psychotic symptoms in subjects at UHR to develop psychosis. Key words: cognitive behavioral therapy, ultrahigh risk, cognitive biases, prevention, psychosis, schizophrenia     

Childhood trauma and dissociation in first-episode psychosis,chronic schizophrenia and community controls

Increasing evidence supports the role of childhood trauma in the etiology of psychosis but underlying mechanisms are poorly understood. Early maltreatment has been linked to dissociative symptoms in psychosis patients. We explored associations between childhood trauma (Childhood Trauma Questionnaire) and dissociation (Dissociative Experiences Scale) in first-episode psychotic patients (n=62), chronic psychotic patients (n=43), and non-psychotic community controls (n=66). Multivariate analyses of covariance were used to test associations between childhood trauma and dissociation by group while controlling for sex. Chronic patients reported the highest level of dissociation. More severe childhood trauma was associated with greater dissociative symptoms in all groups although most strongly in chronic patients. Emotional abuse showed the strongest associations with dissociation, with these being strongest for chronic patients, followed by first-episode patients — and least for controls. Men showed a stronger association between physical neglect and dissociation than women, irrespective of group. There were no significant group by sex interactions. Our findings replicate the strong association between childhood trauma and dissociative symptoms in chronic and first-episode psychotic patients relative to non-psychotic control subjects. We also demonstrate the salience of emotional abuse in explaining variance in dissociation, especially in chronic patients.