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BackgroundCognitive deficits may be characteristic for only a subgroup of first-episode psychosis (FEP) and the link with clinical and functional outcomes is less profound than previously thought. This study aimed to identify cognitive subgroups in a large sample of FEP using a clustering approach with healthy controls as a reference group, subsequently linking cognitive subgroups to clinical and functional outcomes.Methods204 FEP patients were included. Hierarchical cluster analysis was performed using baseline brief assessment of cognition in schizophrenia (BACS). Cognitive subgroups were compared to 40 controls and linked to longitudinal clinical and functional outcomes (PANSS, GAF, self-reported WHODAS 2.0) up to 12-month follow-up.ResultsThree distinct cognitive clusters emerged: relative to controls, we found one cluster with preserved cognition (n = 76), one moderately impaired cluster (n = 74) and one severely impaired cluster (n = 54). Patients with severely impaired cognition had more severe clinical symptoms at baseline, 6- and 12-month follow-up as compared to patients with preserved cognition. General functioning (GAF) in the severely impaired cluster was significantly lower than in those with preserved cognition at baseline and showed trend-level effects at 6- and 12-month follow-up. No significant differences in self-reported functional outcome (WHODAS 2.0) were present.ConclusionsCurrent results demonstrate the existence of three distinct cognitive subgroups, corresponding with clinical outcome at baseline, 6- and 12-month follow-up. Importantly, the cognitively preserved subgroup was larger than the severely impaired group. Early identification of discrete cognitive profiles can offer valuable information about the clinical outcome but may not be relevant in predicting self-reported functional outcomes.

Purpose The health correlates of polygenic risk (PRS-SCZ) and exposome (ES-SCZ) scores for schizophrenia may vary depending on age and sex. We aimed to examine age- and sex-specific associations of PRS-SCZ and ES-SCZ with self-reported health in the general population. Methods Participants were from the population-based Netherlands Mental Health Survey and Incidence Study–2 (NEMESIS-2). Mental and physical health were measured with the 36-item Short Form Survey 4 times between 2007 and 2018. The PRS-SCZ and ES-SCZ were respectively calculated from common genetic variants and exposures (cannabis use, winter birth, hearing impairment, and five childhood adversity categories). Moderation by age and sex was examined in linear mixed models. Results For PRS-SCZ and ES-SCZ analyses, we included 3099 and 6264 participants, respectively (age range 18–65 years; 55.7–56.1% female). Age and sex did not interact with PRS-SCZ. Age moderated the association between ES-SCZ and mental (interaction: p = 0.02) and physical health (p = 0.0007): at age 18, + 1.00 of ES-SCZ was associated with − 0.10 of mental health and − 0.08 of physical health, whereas at age 65, it was associated with − 0.21 and − 0.23, respectively (all units in standard deviations). Sex moderated the association between ES-SCZ and physical health (p Conclusion There were larger associations between higher ES-SCZ and poorer health among female and older individuals. Accounting for these interactions may increase ES-SCZ precision and help uncover populational determinants of environmental influences on health.

Aggression on psychiatric wards develops under influence of patient, staff and ward factors. Assessment of naturalistic derived staff and ward factors might increase better understanding of how aggressive incidents develop on psychiatric wards.ObjectiveStudying staff and ward factors including interactions between patients and nurses prior and after development of aggression, within a naturalistic closed ward setting.DesignA prospective naturalistic experience sampling method (ESM) study.Setting and participantsA high intensive care unit of a mental health institution in The Netherlands where 29 nurses answered beeps generated by an app during approximately 7 consecutive days with questions regarding their subjective feelings, ward atmosphere, location, interaction they had with patients and their colleagues and whether an incident took place.Main outcome measuresAssociations were established between different staff and ward factors and the occurrence of aggressive incidents on the ward.ResultsRisk for aggression was associated with the nurse being with a patient (OR=2.26, 95% CI 0.99 to 5.15, p=0.05). No significant association was found between discussing with the patient and setting a limit or physical absence of the nurse on the one hand and aggression on the other. More experienced nurses encountered more aggression (OR=3.5, 95% CI 1.32 to 8.26, p=0.01). Age and gender of the nurse were not associated with aggression development. Exceeding the maximum bed capacity was associated with a greater risk for aggression (OR=5.36, 95% CI 1.69 to 16.99, p=0.004). There was no significant association when analysing a more positive atmosphere on the ward or positive affect of the nurse, but negative affect of the nurses showed a trend for an association with less aggression.ConclusionAggression is a problem that should be managed from a multidimensional perspective. The quality of interaction between nurses and patients is crucial. Exceeding the maximum bed capacity is likely associated with more aggression.

BACKGROUND: A set of enduring conditions have been reported in the literature involving persistent sexual dysfunction after discontinuation of serotonin reuptake inhibiting antidepressants, 5 alpha-reductase inhibitors and isotretinoin.OBJECTIVE: To develop diagnostic criteria for post-SSRI sexual dysfunction (PSSD), persistent genital arousal disorder (PGAD) following serotonin reuptake inhibitors, post-finasteride syndrome (PFS) and post-retinoid sexual dysfunction (PRSD).METHODS: The original draft was designed using data from two published case series (Hogan et al., 2014 and Healy et al., 2018), which represent the largest public collections of data on these enduring conditions. It was further developed with the involvement of a multidisciplinary panel of experts.RESULTS: A set of criteria were agreed upon for each of the above conditions. Features of PSSD, PFS and PRSD commonly include decreased genital and orgasmic sensation, decreased sexual desire and erectile dysfunction. Ancillary non-sexual symptoms vary depending on the specific condition but can include emotional blunting and cognitive impairment. PGAD presents with an almost mirror image of unwanted sensations of genital arousal or irritability in the absence of sexual desire. A new term, post-SSRI asexuality, is introduced to describe a dampening of sexual interest and pleasure resulting from a pre-natal or pre-teen exposure to a serotonin reuptake inhibitor.CONCLUSIONS: These criteria will help in both clinical and research settings. As with all criteria, they will likely need modification in the light of developments.

BackgroundA transdiagnostic and contextual framework of ‘clinical characterization’, combining clinical, psychopathological, sociodemographic, etiological, and other personal contextual data, may add clinical value over and above categorical algorithm-based diagnosis.MethodsPrediction of need for care and health care outcomes was examined prospectively as a function of the contextual clinical characterization diagnostic framework in a prospective general population cohort (n = 6646 at baseline), interviewed four times between 2007 and 2018 (NEMESIS-2). Measures of need, service use, and use of medication were predicted as a function of any of 13 DSM-IV diagnoses, both separately and in combination with clinical characterization across multiple domains: social circumstances/demographics, symptom dimensions, physical health, clinical/etiological factors, staging, and polygenic risk scores (PRS). Effect sizes were expressed as population attributable fractions.ResultsAny prediction of DSM-diagnosis in relation to need and outcome in separate models was entirely reducible to components of contextual clinical characterization in joint models, particularly the component of transdiagnostic symptom dimensions (a simple score of the number of anxiety, depression, mania, and psychosis symptoms) and staging (subthreshold, incidence, persistence), and to a lesser degree clinical factors (early adversity, family history, suicidality, slowness at interview, neuroticism, and extraversion), and sociodemographic factors. Clinical characterization components in combination predicted more than any component in isolation. PRS did not meaningfully contribute to any clinical characterization model.ConclusionA transdiagnostic framework of contextual clinical characterization is of more value to patients than a categorical system of algorithmic ordering of psychopathology.

Background Psychotic experiences (PEs) frequently occur and are associated with a range of negative health outcomes. Prospective studies on PEs are scarce, and to date no study investigated PE prevalence, incidence, persistence, their risk indicators, and psychiatric comorbidity, in one dataset. Furthermore, most studies are based on self-report, and it is unclear how this compares to clinical interviews. Methods Data are used from the Netherlands Mental Health Survey and Incidence Study-2 (NEMESIS-2), a psychiatric cohort study among a representative sample of adults (baseline characteristics: N = 6646; 49.6% female; 18–64 years). Results are presented for self-reported and clinically validated PEs. Associations are assessed for mental disorders, socio-demographic, vulnerability, physical health, and substance use factors. Results Based on self-report, at baseline 16.5% of respondents had at least one PE in their lifetime, of those, 30.1% also reported a PE at 3-year follow-up. 4.8% had a first PE at 3-year follow up. The 3-year prevalence of PE was associated with almost all studied risk indicators. Generally, the strongest associations were found for mental health disorders. Prevalence and incidence rates were two to three times higher in self-report than in clinical interview but results on associated factors were similar. Conclusions Validated prevalence and incidence estimates of PE are substantially lower than self-reported figures but results on associated factors were similar. Therefore, future studies on associations of PEs can rely on relatively inexpensive self-reports of PEs. The associations between PE and mental disorders underline the importance of assessment of PE in general practice.

Background Empirical evidence suggests that people use cannabis to ameliorate anxiety and depressive symptoms, yet cannabis also acutely worsens psychosis and affective symptoms. However, the temporal relationship between cannabis use, anxiety and depressive symptoms and psychotic experiences (PE) in longitudinal studies is unclear. This may be informed by examination of mutually mediating roles of cannabis, anxiety and depressive symptoms in the emergence of PE. Methods Data were derived from the second longitudinal Netherlands Mental Health Survey and Incidence Study. Mediation analysis was performed to examine the relationship between cannabis use, anxiety/depressive symptoms and PE, using KHB logit in STATA while adjusting for age, sex and education status. Results Cannabis use was found to mediate the relationship between preceding anxiety, depressive symptoms and later PE incidence, but the indirect contribution of cannabis use was small (for anxiety: % of total effect attributable to cannabis use = 1.00%; for depression: % of total effect attributable to cannabis use = 1.4%). Interestingly, anxiety and depressive symptoms were found to mediate the relationship between preceding cannabis use and later PE incidence to a greater degree (% of total effect attributable to anxiety = 17%; % of total effect attributable to depression = 37%). Conclusion This first longitudinal cohort study examining the mediational relationship between cannabis use, anxiety/depressive symptoms and PE, shows that there is a bidirectional relationship between cannabis use, anxiety/depressive symptoms and PE. However, the contribution of anxiety/depressive symptoms as a mediator was greater than that of cannabis.

Previously, we established an estimated exposome score for schizophrenia (ES-SCZ) as a cumulative measure of environmental liability for schizophrenia to use in gene–environment interaction studies and for risk stratification in population cohorts. Hereby, we examined the discriminative function of ES-SCZ for identifying individuals diagnosed with schizophrenia spectrum disorder in the general population by measuring the area under the receiver operating characteristic curve (AUC). Furthermore, we compared this ES-SCZ method to an environmental sum score (Esum-SCZ) and an aggregate environmental score weighted by the meta-analytical estimates (Emet-SCZ). We also estimated ORs and Nagelkerke’s R2 for ES-SCZ in association with psychiatric diagnoses and other medical outcomes. ES-SCZ showed a good discriminative function (AUC = 0.84) and statistically significantly performed better than both Esum-SCZ (AUC = 0.80) and Emet-SCZ (AUC = 0.80). At optimal cut point, ES-SCZ showed similar performance in ruling out (LR− = 0.20) and ruling in (LR+ = 3.86) schizophrenia. ES-SCZ at optimal cut point showed also a progressively greater magnitude of association with increasing psychosis risk strata. Among all clinical outcomes, ES-SCZ was associated with schizophrenia diagnosis with the highest OR (2.76, P < .001) and greatest explained variance (R2 = 14.03%), followed by bipolar disorder (OR = 2.61, P < .001, R2 = 13.01%) and suicide plan (OR = 2.44, P < .001, R2 = 12.44%). Our findings from an epidemiologically representative general population cohort demonstrate that an aggregate environmental exposure score for schizophrenia constructed using a predictive modeling approach—ES-SCZ—has the potential to improve risk prediction and stratification for research purposes and may help gain insight into the multicausal etiology of psychopathology.

This cohort study assesses whether recent stressful life events interact with genetic and environmental liability for schizophrenia in models of mental and physical health in the Dutch adult population.Key PointsQuestionIs the association of adulthood life stress with mental and physical health moderated by polygenic risk and exposome scores for schizophrenia? FindingsThis population-based cohort study of 6646 participants provides novel evidence of the associations of genetic and environmental liability for schizophrenia with mental health in the general population. Both genetic and environmental liability were associated with poor outcomes, particularly mental health, and the association between stressful life events and health outcomes was moderated by exposome score but not polygenic risk score for schizophrenia. MeaningThese findings showing an interaction between adulthood stressful life events and lifetime exposomic liability lend further support to the diathesis-stress model.ImportanceBoth adulthood stressful life events (SLEs) and liability for schizophrenia have been associated with poor mental and physical health in the general population, but their interaction remains to be elucidated to improve population-based health outcomes. ObjectiveTo test whether recent SLEs interact with genetic and environmental liability for schizophrenia in models of mental and physical health. Design, Setting, and ParticipantsThe Netherlands Mental Health Survey and Incidence Study-2 is a population-based prospective cohort study designed to investigate the prevalence, incidence, course, and consequences of mental disorders in the Dutch general population. Participants were enrolled from November 5, 2007, to July 31, 2009, and followed up with 3 assessments during 9 years. Follow-up was completed on June 19, 2018, and data were analyzed from September 1 to November 1, 2019. ExposuresRecent SLEs assessed at each wave and aggregate scores of genetic and environmental liability for schizophrenia: polygenic risk score for schizophrenia (PRS-SCZ) trained using the Psychiatric Genomics Consortium analysis results and exposome score for schizophrenia (ES-SCZ) trained using an independent data set. Main Outcomes and MeasuresIndependent and interacting associations of SLEs with ES-SCZ and PRS-SCZ on mental and physical health assessed at each wave using regression coefficients. ResultsOf the 6646 participants included at baseline, the mean (SD) age was 44.26 (12.54) years, and 3672 (55.25%) were female. The SLEs were associated with poorer physical health (B=-3.22 [95% CI, -3.66 to -2.79]) and mental health (B=-3.68 [95% CI, -4.05 to -3.32]). Genetic and environmental liability for schizophrenia was associated with poorer mental health (ES-SCZ: B=-3.07 [95% CI, -3.35 to -2.79]; PRS-SCZ: B=-0.93 [95% CI, -1.31 to -0.54]). Environmental liability was also associated with poorer physical health (B=-3.19 [95% CI, -3.56 to -2.82]). The interaction model showed that ES-SCZ moderated the association of SLEs with mental (B=-1.08 [95% CI, -1.47 to -0.69]) and physical health (B=-0.64 [95% CI, -1.11 to -0.17]), whereas PRS-SCZ did not. Several sensitivity analyses confirmed these results. Conclusions and RelevanceIn this study, schizophrenia liability was associated with broad mental health outcomes at the population level. Consistent with the diathesis-stress model, exposure to SLEs, particularly in individuals with high environmental liability for schizophrenia, was associated with poorer health. These findings underline the importance of modifiable environmental factors during the life span for population-based mental health outcomes.

BackgroundThere is evidence that environmental and genetic risk factors for schizophrenia spectrum disorders are transdiagnostic and mediated in part through a generic pathway of affective dysregulation.MethodsWe analysed to what degree the impact of schizophrenia polygenic risk (PRS-SZ) and childhood adversity (CA) on psychosis outcomes was contingent on co-presence of affective dysregulation, defined as significant depressive symptoms, in (i) NEMESIS-2 (n = 6646), a representative general population sample, interviewed four times over nine years and (ii) EUGEI (n = 4068) a sample of patients with schizophrenia spectrum disorder, the siblings of these patients and controls.ResultsThe impact of PRS-SZ on psychosis showed significant dependence on co-presence of affective dysregulation in NEMESIS-2 [relative excess risk due to interaction (RERI): 1.01, p = 0.037] and in EUGEI (RERI = 3.39, p = 0.048). This was particularly evident for delusional ideation (NEMESIS-2: RERI = 1.74, p = 0.003; EUGEI: RERI = 4.16, p = 0.019) and not for hallucinatory experiences (NEMESIS-2: RERI = 0.65, p = 0.284; EUGEI: −0.37, p = 0.547). A similar and stronger pattern of results was evident for CA (RERI delusions and hallucinations: NEMESIS-2: 3.02, p < 0.001; EUGEI: 6.44, p < 0.001; RERI delusional ideation: NEMESIS-2: 3.79, p < 0.001; EUGEI: 5.43, p = 0.001; RERI hallucinatory experiences: NEMESIS-2: 2.46, p < 0.001; EUGEI: 0.54, p = 0.465).ConclusionsThe results, and internal replication, suggest that the effects of known genetic and non-genetic risk factors for psychosis are mediated in part through an affective pathway, from which early states of delusional meaning may arise.

The polygenic risk score (PRS) allows for quantification of the relative contributions of genes and environment in population-based studies of mental health. We analyzed the impact of transdiagnostic schizophrenia PRS and measures of familial and environmental risk on the level of and change in general mental health (Short-Form-36 mental health) in the Netherlands Mental Health Survey and Incidence Study-2 general population sample, interviewed 4 times over a period of 9 years, yielding 8901 observations in 2380 individuals. Schizophrenia PRS, family history, somatic pain, and a range of environmental risks and social circumstances were included in the regression model of level of and change in mental health. We calculated the relative contribution of each (group of) risk factor(s) to the variance in (change in) mental health. In the combined model, familial and environmental factors explained around 17% of the variance in mental health, of which around 5% was explained by age and sex, 30% by social circumstances, 16% by pain, 22% by environmental risk factors, 24% by family history, and 3% by PRS for schizophrenia (PRS-SZ). Results were similar, but attenuated, for the model of mental health change over time. Childhood trauma and gap between actual and desired social status explained most of the variance. PRS for bipolar disorder, cross-disorder, and depression explained less variance in mental health than PRS-SZ. Polygenic risk for mental suffering, derived from significance-testing in massive samples, lacks impact in analyses focusing on prediction in a general population epidemiological setting. Social-environmental circumstances, particularly childhood trauma and perceived status gap, drive most of the attributable variation in population mental health.

Introduction On psychiatric wards, aggressive behaviour displayed by patients is common and problematic. Understanding factors associated with the development of aggression offers possibilities for prevention and targeted interventions. This review discusses factors that contribute to the development of aggression on psychiatric wards. Method In Pubmed and Embase, a search was performed aimed at: prevalence data, ward characteristics, patient and staff factors that are associated with aggressive behaviour and from this search 146 studies were included. Results The prevalence of aggressive behaviour on psychiatric wards varied (8–76%). Explanatory factors of aggressive behaviour were subdivided into patient, staff and ward factors. Patient risk factors were diagnosis of psychotic disorder or bipolar disorder, substance abuse, a history of aggression, younger age. Staff risk factors included male gender, unqualified or temporary staff, job strain, dissatisfaction with the job or management, burn-out and quality of the interaction between patients and staff. Staff protective factors were a good functioning team, good leadership and being involved in treatment decisions. Significant ward risk factors were a higher bed occupancy, busy places on the ward, walking rounds, an unsafe environment, a restrictive environment, lack of structure in the day, smoking and lack of privacy. Conclusion Despite a lack of prospective quantitative data, results did show that aggression arises from a combination of patient factors, staff factors and ward factors. Patient factors were studied most often, however, besides treatment, offering the least possibilities in prevention of aggression development. Future studies should focus more on the earlier stages of aggression such as agitation and on factors that are better suited for preventing aggression such as ward and staff factors. Management and clinicians could adapt staffing and ward in line with these results.

Aims Although attenuated psychotic symptoms in the psychosis clinical high-risk state (CHR-P) almost always occur in the context of a non-psychotic disorder (NPD), NPD is considered an undesired ‘comorbidity’ epiphenomenon rather than an integral part of CHR-P itself. Prospective work, however, indicates that much more of the clinical psychosis incidence is attributable to prior mood and drug use disorders than to psychosis clinical high-risk states per se. In order to examine this conundrum, we analysed to what degree the ‘risk’ in CHR-P is indexed by co-present NPD rather than attenuated psychosis per se. Methods We examined the incidence of early psychotic experiences (PE) with and without NPD (mood disorders, anxiety disorders, alcohol/drug use disorders), in a prospective general population cohort (n = 6123 at risk of incident PE at baseline). Four interview waves were conducted between 2007 and 2018 (NEMESIS-2). The incidence of PE, alone (PE-only) or with NPD (PE + NPD) was calculated, as were differential associations with schizophrenia polygenic risk score (PRS-Sz), environmental, demographical, clinical and cognitive factors. Results The incidence of PE + NPD (0.37%) was lower than the incidence of PE-only (1.04%), representing around a third of the total yearly incidence of PE. Incident PE + NPD was, in comparison with PE-only, differentially characterised by poor functioning, environmental risks, PRS-Sz, positive family history, prescription of antipsychotic medication and (mental) health service use. Conclusions The risk in ‘clinical high risk’ states is mediated not by attenuated psychosis per se but specifically the combination of attenuated psychosis and NPD. CHR-P/APS research should be reconceptualised from a focus on attenuated psychotic symptoms with exclusion of non-psychotic DSM-disorders, as the ‘pure' representation of a supposedly homotypic psychosis risk state, towards a focus on poor-outcome NPDs, characterised by a degree of psychosis admixture, on the pathway to psychotic disorder outcomes.

Clozapine is the most effective antipsychotic for patients with treatment-resistant schizophrenia. However, response is highly variable and possible genetic underpinnings of this variability remain unknown. Here, we performed polygenic risk score (PRS) analyses to estimate the amount of variance in symptom severity among clozapine-treated patients explained by PRSs (R2) and examined the association between symptom severity and genotype-predicted CYP1A2, CYP2D6, and CYP2C19 enzyme activity. Genome-wide association (GWA) analyses were performed to explore loci associated with symptom severity. A multicenter cohort of 804 patients (after quality control N=684) with schizophrenia spectrum disorder treated with clozapine were cross-sectionally assessed using the Positive and Negative Syndrome Scale and/or the Clinical Global Impression-Severity (CGI-S) scale. GWA and PRS regression analyses were conducted. Genotype-predicted CYP1A2, CYP2D6, and CYP2C19 enzyme activities were calculated. Schizophrenia-PRS was most significantly and positively associated with low symptom severity (p=1.03×10−3; R2=1.85). Cross-disorder-PRS was also positively associated with lower CGI-S score (p=0.01; R2=0.81). Compared to the lowest tertile, patients in the highest schizophrenia-PRS tertile had 1.94 times (p=6.84×10−4) increased probability of low symptom severity. Higher genotype-predicted CYP2C19 enzyme activity was independently associated with lower symptom severity (p=8.44×10−3). While no locus surpassed the genome-wide significance threshold, rs1923778 within NFIB showed a suggestive association (p=3.78×10−7) with symptom severity. We show that high schizophrenia-PRS and genotype-predicted CYP2C19 enzyme activity are independently associated with lower symptom severity among individuals treated with clozapine. Our findings open avenues for future pharmacogenomic projects investigating the potential of PRS and genotype-predicted CYP-activity in schizophrenia.

Hypotheses about the link between cannabis use and psychosis apply to the within-person level but have been tested mostly at the between-person level. We used a within-person design, in which a person serves as his own control, thus removing the need to consider confounding by any fixed (genetic and nongenetic) characteristic to study the prospective association between cannabis use and the incidence of attenuated psychotic experiences, and vice versa, adjusted for time-varying confounders. We combined 2 general population cohorts (at baseline: Early Developmental Stages of Psychopathology Study, n = 1395; Netherlands Mental Health Survey and Incidence Study-2, n = 6603), which applied a similar methodology to study cannabis use and attenuated psychotic experiences with repeated interviews (T0, T1, T2, and T3) over a period of approximately 10 years. The Hausman test was significant for the adjusted models, indicating the validity of the fixed-effects model. In the adjusted fixed-effects model, prior cannabis use was associated with psychotic experiences (aOR = 7.03, 95% CI: 2.39, 20.69), whereas prior psychotic experiences were not associated with cannabis use (aOR = 0.59, 95% CI: 0.21, 1.71). Longitudinal studies applying random-effects models to study associations between risk factors and mental health outcomes, as well as reverse causality, may not yield precise estimates. Cannabis likely impacts causally on psychosis but not the other way round.

BackgroundEvidence suggests that cannabis use, childhood adversity, and urbanicity, in interaction with proxy measures of genetic risk, may facilitate onset of psychosis in the sense of early affective dysregulation becoming ‘complicated’ by, first, attenuated psychosis and, eventually, full-blown psychotic symptoms.MethodsData were derived from three waves of the second Netherlands Mental Health Survey and Incidence Study (NEMESIS-2). The impact of environmental risk factors (cannabis use, childhood adversity, and urbanicity) was analyzed across severity levels of psychopathology defined by the degree to which affective dysregulation was ‘complicated’ by low-grade psychotic experiences (‘attenuated psychosis’ – moderately severe) and, overt psychotic symptoms leading to help-seeking (‘clinical psychosis’ – most severe). Familial and non-familial strata were defined based on family history of (mostly) affective disorder and used as a proxy for genetic risk in models of family history × environmental risk interaction.ResultsIn proxy gene–environment interaction analysis, childhood adversity and cannabis use, and to a lesser extent urbanicity, displayed greater-than-additive risk if there was also evidence of familial affective liability. In addition, the interaction contrast ratio grew progressively greater across severity levels of psychosis admixture (none, attenuated psychosis, clinical psychosis) complicating affective dysregulation.ConclusionKnown environmental risks interact with familial evidence of affective liability in driving the level of psychosis admixture in states of early affective dysregulation in the general population, constituting an affective pathway to psychosis. There is interest in decomposing family history of affective liability into the environmental and genetic components that underlie the interactions as shown here.

BackgroundThe jumping to conclusions (JTC) reasoning bias and decreased working memory performance (WMP) are associated with psychosis, but associations with affective disturbances (i.e. depression, anxiety, mania) remain inconclusive. Recent findings also suggest a transdiagnostic phenotype of co-occurring affective disturbances and psychotic experiences (PEs). This study investigated whether JTC bias and decreased WMP are associated with co-occurring affective disturbances and PEs.MethodsData were derived from the second Netherlands Mental Health Survey and Incidence Study (NEMESIS-2). Trained interviewers administered the Composite International Diagnostic Interview (CIDI) at three time points in a general population sample (N = 4618). The beads and digit-span task were completed to assess JTC bias and WMP, respectively. CIDI was used to measure affective disturbances and an add-on instrument to measure PEs.ResultsCompared to individuals with neither affective disturbances nor PEs, the JTC bias was more likely to occur in individuals with co-occurring affective disturbances and PEs [moderate psychosis (1–2 PEs): adjusted relative risk ratio (RRR) 1.17, 95% CI 0.98–1.41; and high psychosis (3 or more PEs or psychosis-related help-seeking behaviour): adjusted RRR 1.57, 95% CI 1.19–2.08], but not with affective disturbances and PEs alone, whereas decreased WMP was more likely in all groups. There was some evidence of a dose–response relationship, as JTC bias and decreased WMP were more likely in individuals with affective disturbances as the level of PEs increased or help-seeking behaviour was reported.ConclusionThe findings suggest that JTC bias and decreased WMP may contribute to a transdiagnostic phenotype of co-occurring affective disturbances and PEs.

Introduction Antipsychotics are associated with bodyweight gain and metabolic disturbance. Previous meta-analyses were limited to mainly antipsychotic switch studies in patients with a diagnosis of schizophrenia or psychosis with short follow-up periods. The present meta-analysis aimed to analyse the impact of weight change in antipsychotic-naive and antipsychotics switch patients and whether body weight change depended on diagnosis. Method We performed a meta-analysis of clinical trials of antipsychotics that reported weight change, irrespective of psychiatric diagnosis. Outcome measure was body weight change. Studies were classified into antipsychotic-naive and antipsychotic-switch. Forest plots stratified by antipsychotic and the duration of antipsychotic use were generated and results were summarised in figures. Results In total, 404 articles were included for the quantitative synthesis. 58 articles were on antipsychotic naive patients. In the antipsychotic naive group, all antipsychotics resulted in body weight gain. In the antipsychotic switch group, most antipsychotics likewise resulted in bodyweight gain, with exception of amisulpride, aripiprazole and ziprasidone that showed no body weight gain or even some weight loss after switching antipsychotics. Diagnosis was not a discriminating factor of antipsychotic induced weight change. Conclusion Antipsychotic use resulted in substantial increase in body weight in antipsychotic-naive patients. In antipsychotic-switch patients the weight gain was mild and not present in amisulpride, aripiprazole and ziprasidone. In both groups, weight gain was irrespective of the psychiatric diagnosis.

Background Antipsychotic-induced Weight Gain (AiWG) is a debilitating and common adverse effect of antipsychotics. AiWG negatively impacts life expectancy, quality of life, treatment adherence, likelihood of developing type-2 diabetes and readmission. Treatment of AiWG is currently challenging, and there is no consensus on the optimal management strategy. In this study, we aim to evaluate the use of metformin for the treatment of AiWG by comparing metformin with placebo in those receiving treatment as usual, which includes a lifestyle intervention. Methods In this randomized, double-blind, multicenter, placebo-controlled, pragmatic trial with a follow-up of 52 weeks, we aim to include 256 overweight participants (Body Mass Index (BMI) > 25 kg/m2) of at least 16 years of age. Patients are eligible if they have been diagnosed with schizophrenia spectrum disorder and if they have been using an antipsychotic for at least three months. Participants will be randomized with a 1:1 allocation to placebo or metformin, and will be treated for a total of 26 weeks. Metformin will be started at 500 mg b.i.d. and escalated to 1000 mg b.i.d. 2 weeks thereafter (up to a maximum of 2000 mg daily). In addition, all participants will undergo a lifestyle intervention as part of the usual treatment consisting of a combination of an exercise program and dietary consultations. The primary outcome measure is difference in body weight as a continuous trait between the two arms from treatment inception until 26 weeks of treatment, compared to baseline. Secondary outcome measures include: 1) Any element of metabolic syndrome (MetS); 2) Response, defined as ≥5% body weight loss at 26 weeks relative to treatment inception; 3) Quality of life; 4) General mental and physical health; and 5) Cost-effectiveness. Finally, we aim to assess whether genetic liability to BMI and MetS may help estimate the amount of weight reduction following initiation of metformin treatment. Discussion The pragmatic design of the current trial allows for a comparison of the efficacy and safety of metformin in combination with a lifestyle intervention in the treatment of AiWG, facilitating the development of guidelines on the interventions for this major health problem. Trial registration This trial was registered in the Netherlands Trial Register (NTR) at https://www.trialregister.nl/trial/8440 as NTR NL8840 on March 8, 2020.

BackgroundAlcohol consumption, smoking and mood disorders are leading contributors to the global burden of disease and are highly comorbid. Yet, their interrelationships have remained elusive. The aim of this study was to examine the multi-cross-sectional and longitudinal associations between (change in) smoking and alcohol use and (change in) number of depressive symptoms.MethodsIn this prospective, longitudinal study, 6646 adults from the general population were included with follow-up measurements after 3 and 6 years. Linear mixed-effects models were used to test multi-cross-sectional and longitudinal associations, with smoking behaviour, alcohol use and genetic risk scores for smoking and alcohol use as independent variables and depressive symptoms as dependent variables.ResultsIn the multi-cross-sectional analysis, smoking status and number of cigarettes per day were positively associated with depressive symptoms (p < 0.001). Moderate drinking was associated with less symptoms of depression compared to non-use (p = 0.011). Longitudinally, decreases in the numbers of cigarettes per day and alcoholic drinks per week as well as alcohol cessation were associated with a reduction of depressive symptoms (p = 0.001–0.028). Results of genetic risk score analyses aligned with these findings.ConclusionsWhile cross-sectionally smoking and moderate alcohol use show opposing associations with depressive symptoms, decreases in smoking behaviour as well as alcohol consumption are associated with improvements in depressive symptoms over time. Although we cannot infer causality, these results open avenues to further investigate interventions targeting smoking and alcohol behaviours in people suffering from depressive symptoms.

BackgroundAlthough hallucinations have been studied in terms of prevalence and its associations with psychopathology and functional impairment, very little is known about sensory modalities other than auditory (i.e. haptic, visual and olfactory), as well the incidence of hallucinations, factors predicting incidence and subsequent course.MethodsWe examined the incidence, course and risk factors of hallucinatory experiences across different modalities in two unique prospective general population cohorts in the same country using similar methodology and with three interview waves, one over the period 1996–1999 (NEMESIS) and one over the period 2007–2015 (NEMESIS-2).ResultsIn NEMESIS-2, the yearly incidence of self-reported visual hallucinations was highest (0.33%), followed by haptic hallucinations (0.31%), auditory hallucinations (0.26%) and olfactory hallucinations (0.23%). Rates in NEMESIS-1 were similar (respectively: 0.35%, 0.26%, 0.23%, 0.22%). The incidence of clinician-confirmed hallucinations was approximately 60% of the self-reported rate. The persistence rate of incident hallucinations was around 20–30%, increasing to 40–50% for prevalent hallucinations. Incident hallucinations in one modality were very strongly associated with occurrence in another modality (median OR = 59) and all modalities were strongly associated with delusional ideation (median OR = 21). Modalities were approximately equally strongly associated with the presence of any mental disorder (median OR = 4), functioning, indicators of help-seeking and established environmental risk factors for psychotic disorder.ConclusionsHallucinations across different modalities are a clinically relevant feature of non-psychotic disorders and need to be studied in relation to each other and in relation to delusional ideation, as all appear to have a common underlying mechanism.

Background: The observed link between positive psychotic experiences (PE) and psychosis spectrum disorder (PSD) may be stronger depending on concomitant presence of PE with other dimensions of psychopathology. We examined whether the effect of common risk factors for PSD on PE is additive and whether the impact of risk factors on the occurrence of PE depends on the co-occurrence of other symptom dimensions (affective dysregulation, negative symptoms, and cognitive alteration).Method: Data from the Netherlands Mental Health Survey and Incidence Study 2 were used. Risk factors included childhood adversity, cannabis use, urbanicity, foreign born, hearing impairment, and family history of affective disorders. Logistic regression models were applied to test (1) the additive effect of risk factors (4 levels) on PE and (2) the moderating effects of symptom dimensions on the association between risk factors (present/absent) and PE, using additive interaction, expressed as the interaction contrast ratio.Results: Risk factors were additive: the greater the number of risk factors, the greater the odds of PE. Furthermore, concomitant presence of the other symptom dimensions all increased the impact of risk factors on PE. After controlling for age, sex, and education, only affective dysregulation and negative symptoms remained significant moderators; only affective dysregulation remained a significant moderator if all dimensions were adjusted for each other.Conclusions: Risk factors may not be directly associated with PE but additively give rise to a multidimensional subthreshold state anticipating the multidimensional clinical syndrome. Early motivational and cognitive impairments in the context of PE may be reducible to affective dysregulation.

BackgroundThe experience sampling method (ESM) builds an intensive time series of experiences and contexts in the flow of daily life, typically consisting of around 70 reports, collected at 8-10 random time points per day over a period of up to 10 days.MethodsWith the advent of widespread smartphone use, ESM can be used in routine clinical practice. Multiple examples of ESM data collections across different patient groups and settings are shown and discussed, varying from an ESM evaluation of a 6-week randomized trial of mindfulness, to a twin study on emotion dynamics in daily life.ResultsResearch shows that ESM-based self-monitoring and feedback can enhance resilience by strengthening the capacity to use natural rewards. Personalized trajectories of starting or stopping medication can be more easily initiated and predicted if sensitive feedback data are available in real time. In addition, personalized trajectories of symptoms, cognitive abilities, symptoms impacting on other symptoms, the capacity of the dynamic system of mental health to bounce back from disturbance, and patterns of environmental reactivity yield uniquely personal data to support shared decision making and prediction in clinical practice. Finally, ESM makes it possible to develop insight into previous implicit patterns of thought, experience, and behavior, particularly if rapid personalized feedback is available.ConclusionsESM enhances clinical practice and research. It is empowering, providing co-ownership of the process of diagnosis, treatment evaluation, and routine outcome measurement. Blended care, based on a mix of face-to-face and ESM-based outside-the-office treatment, may reduce costs and improve outcomes.

Background Despite their efficacy, antipsychotic drugs appear to be associated with metabolic side effects such as impaired lipid metabolism and an increased risk for developing metabolic syndrome. The association between individual antipsychotics with a stratification for different durations of exposure and mean changes in the complete lipid profile has not yet been the focus of a meta-analysis. Aim of this meta-analysis was to examine the association between changes in lipid parameters in adults using an antipsychotic drug, irrespective of diagnostic indication. Methods This meta-analysis follows the PRISMA guidelines and a protocol has been published in PROSPERO. A systematic search was performed using the databases PubMed, EMBASE, Cochrane, and PsycINFO. Eligible RCTs were identified and no restriction was made regarding diagnosis or publication date. Statistical analysis was based on a random effects model from which forest plots were generated. Effect sizes were reported as the standardized mean difference (SMD) with 95% confidence intervals (CI). Results were presented stratified by four exposure categories, namely < 6 weeks, 6–16 weeks, 16–38 weeks, and ≥ 38 weeks. Outcome measures include mean change from baseline in total cholesterol, high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL) and triglyceride levels. Results The search strategy identified 1144 citations. Of these, 746 abstracts were excluded as being off-topic. A total of 398 full-text articles were assessed for eligibility and 135 RCT’s fulfilled the inclusion criteria. Preliminary results show an overall significant association between olanzapine and mildly elevated triglyceride levels (SMD 0.40, 95% CI 0.02–0.77), risperidone and elevated LDL levels (SMD 0.07, 95% CI 0.01–0.13) and clozapine with elevated total cholesterol and triglyceride levels (SMD 0.59 95% CI 0.26-0.02 and SMD 0.44 95% CI 0.35–0.53, respectively). Final results stratified by exposure category will be presented at the SIRS congress. Discussion The preliminary findings of this meta-analysis build upon previous literature and do confirm an association between the use of an antipsychotic drug and changes in lipid parameters. However, changes in the different lipid parameters do not seem to be consistent for each antipsychotic. Tentatively, we may suggest that the duration of exposure to an antipsychotic drug is correlated to the extent of lipid abnormalities. It should be noted that the majority of included studies had a short study duration (< 6 weeks). Monitoring over short periods might give misleading results. Furthermore, literature suggests that the role of lipids should not be seen independently, and interplay exists between lipid metabolism and changes in weight. For example, previous studies suggest that there is a positive association between increases in triglyceride levels and increases in weight, and that once weight has stabilised, triglyceride levels decrease. Further analysis should focus on including longer-term studies in which changes in body weight in relation to changes in lipids should be taken into account. We expect the findings of this study to be of clinical relevance in the management and monitoring of antipsychotic treatment. The knowledge of whether duration of exposure is associated with different lipid changes could provide interesting results benefiting individualised choices, appropriate prevention and early management.

Background In recent years, antipsychotic-induced weight gain (AIWG) has gained more attention in research. Although interventions to prevent weight gain are currently being investigated, AIWG remains a major problem for both patients and clinicians and often results in poor treatment adherence, a decrease in quality of life. Furthermore, schizophrenia is associated with higher mortality rates and a decreased life expectancy. Recently, some new antipsychotic drugs have been introduced that are hypothesised to entail no or low incidences of clinically relevant weight gain (CRWG), and high incidences of clinically relevant weight loss (CRWL). Here ‘clinically relevant’ is defined as >7% weight change. In this meta-analysis, we aim to give a complete overview of both CRWG and CRWL, including these newer antipsychotics. Methods We searched Pubmed, Embase and Psychinfo for randomized clinical trials of antipsychotics that reported 7% weight change in study populations aged 18 years or older. We performed meta-analyses stratified by study duration (38 weeks) with a random effects model. Results The search yielded in total 941 articles. Ninety-two articles could be included in the meta-analysis, resulting in 341 records in the data set. All data were related to AP switch patients, no data on AP-naïve patients were found. During SIRS final results will be presented. Preliminary results showed that haloperidol, paliperidone and quetiapine had relatively low CRWG (16.6%, 18.7% and 18.4%, respectively), aripiprazole and risperidone had relatively high percentages of CRWG (25.4% and 24.0%, respectively). Olanzapine (29.5%) and lurasidone (7.4%) resulted in respectively the highest and lowest CRWG at >38 weeks of treatment. In the placebo group, CRWG was 3.8%. Incidences of CRWG continued to rise even after 38 weeks of treatment in most treatment groups. CRWL occurred with all antipsychotic drugs; at 6–16 weeks aripiprazole (7.9%) and ziprasidone (7.1%) had CRWL similar to placebo (8.7%). We found insufficient data on CRWL in the long term (>38 weeks) to draw any conclusions. Discussion All antipsychotics can result in both weight gain and weight loss. Previous research showed that patients more often gain weight than lose weight (Bak, 2014) and this is replicated in the present meta-analysis. Proportions CRWG and CRWL seem different between the antipsychotics. Future network meta-analysis are needed to test statistical significance of those differences. It appears, however, that CRWG is higher in patients receiving antipsychotics drugs compared to placebo. No conclusions can be drawn on CRWL due to insufficient data. It is clear that after >38 weeks of treatment, no ‘plateau’ phase is reached as CRWG continued to increase. More future research is needed on long-term weight effects on both CRWG and CRWL to give a clear overview on the ‘real’ effects on weight, as the majority of studies had a duration of less than 26 weeks. Furthermore, more research is needed on the long-term dose-response relationship in CRWG, as this could prove to be a method for managing weight in some patients.

Introduction:Non-pharmacological interventions preferably precede pharmacological interventions in acute agitation. Reviews of pharmacological interventions remain descriptive or compare only one compound with several other compounds. The goal of this study is to compute a systematic review and meta-analysis of the effect on restoring calmness after a pharmacological intervention, so a more precise recommendation is possible.Method:A search in Pubmed and Embase was done to isolate RCT’s considering pharmacological interventions in acute agitation. The outcome is reaching calmness within maximum of 2 h, assessed by the psychometric scales of PANSS-EC, CGI or ACES. Also the percentages of adverse effects was assessed.Results:Fifty-three papers were included for a systematic review and meta-analysis. Most frequent studied drug is olanzapine. Changes on PANNS-EC and ACES at 2 h showed the strongest changes for haloperidol plus promethazine, risperidon, olanzapine, droperidol and aripiprazole. However, incomplete data showed that the effect of risperidon is overestimated. Adverse effects are most prominent for haloperidol and haloperidol plus lorazepam.Conclusion:Olanzapine, haloperidol plus promethazine or droperidol are most effective and safe for use as rapid tranquilisation. Midazolam sedates most quickly. But due to increased saturation problems, midazolam is restricted to use within an emergency department of a general hospital.

Background Antipsychotic (AP) medication is associated with metabolic dysregulation, increasing the risk for weight gain. Previously, we showed that all antipsychotics are related with body weight gain and there was a time effect, the longer the AP was taken the more the weight gain was (Bak, Fransen, Janssen, van Os, & Drukker, 2014). This study included data from 1999–2013. The aim of this study is to up-date the previous study on weight gain by extending the search from 1960 – July 2019. So, older studies of before 2000 were in included as well as studies on AP’s after 2014. The differences in weight change between the various AP’s were calculated. Methods A systematic search was performed using the databases PubMed and EMBASE. Eligible RCTs were identified and no restriction was made regarding diagnosis or publication date. Statistical analysis was based on a random effects model from which forest plots were generated. Effect sizes were reported as the standardized mean difference (SMD) with 95% confidence intervals (CI). Results were presented stratified by four exposure categories, namely < 6 weeks, 6–16 weeks, 16–38 weeks, and ≥ 38 weeks. Furthermore, that results are divided in AP naive patients (patients who had no AP previously) and patient in whom AP were switched from at least one other AP. Patients >17 years of age were excluded and all diagnostic categories were included. Results In total 3488 papers were found. Following PRSIMA guidelines in total 472 papers were eligible for inclusion. Preliminary results. For the longer term 16–38 & >38 wks all AP-naive patients showed an increase in weight of > 5 kg, except for aripiprazole (< 6wks, 0.46kg; 6-16wks, 2.04kg; 16-38wks, 4.5kg; >38 wks, 3.31kg), paliperidone (< 6wks, 1.24kg; 6-16wks, 1.69kg; 16-38wks, -0.3kg; >38wks 0.2kg), quetiapine (< 6wks, 2.51kg; 6-16wks, 2.69kg; 16-38wks, 3.02kg; >38wks 6.14kg) and ziprasidone (< 6wks, 0.06kg; 6-16wks, 0.32kg; 16-38wks, 0.51kg; >38wks 2.18kg). The result of the switch studies shows that clozapine and olanzapine result in most weight gain after switch. Other AP result in modest weight gain to weight loss over the various time periods: amisulpride (range -0.76 and 1.40), aripriprazole (range -0.81 and 0.81), asenapine (-0.99 – 1.14), haloperidol (0.49 – 1.31) and ziprasidone (-1.18 – -0.38). During SIRS final results will be presented. Discussion The number of studies in AP naif patients is limited. Most RCT’s discuses medication evaluation after switch into a new compound. Here, metabolic changes may interact with evaluation of changes in weight. However, switching an AP because after severe weight gain needs to be considered with caution as it does not result in considerable weight loss. The AP-naive show that all AP lead to weight gain. Given only patient older than 17years were included, this might explain the limited number of available studies. However, younger age seems to be associated were an increased risk of weight gain. Reference Bak, M., Fransen, A., Janssen, J., van Os, J., & Drukker, M. (2014). Almost all antipsychotics result in weight gain: a meta-analysis. PLoS One, 9(4), e94112. doi:10.1371/journal.pone.0094112

Background Evidence suggests that the impact of adult stressful life events (SLE) on health depends on an individual’s environmental and genetic predisposition to psychopathology. However, the influence of the genomic and exposomic (the sum of exposures) liabilities for schizophrenia on the association between SLE and health outcomes in the general population has not been studied. The current longitudinal study therefore aims to evaluate whether the association of recent SLE with mental as well as physical health is moderated by polygenic risk score for schizophrenia (PRS-S) and the exposome score for schizophrenia (ES-S, an aggregated environmental exposure score, akin to PRS-S). Methods Data from four waves of the Netherlands Mental Health Survey and Incidence Study-II (NEMESIS-II), a prospective survey in the Dutch general population aged 18 – 64, was used. The baseline data (T0) of NEMESIS-II, including 6646 participants, were collected from 2007 to 2009 and were followed up at year 3 (T1), year 6 (T2), and year 9 (T3). The Short-Form-36 Health Survey was used to repeatedly assess mental and physical health. Repeated assessment of SLE were based on the Brugha Life events section. Guided by our previous work, ES-S was constructed as the weighted sum of important baseline environmental factors, which were previously associated with schizophrenia. A subsample of 3099 participants (at T0) were genotyped and PRS-S was trained on the latest Psychiatric Genetics Consortium schizophrenia meta-analysis, adjusted for the first three population principal components. The analyses were conducted using random intercept multilevel regression models with age, sex, and education included as a priori covariates. Models were clustered for multiple assessments per individual, and the random intercept of mental or physical health at T-1 was added to the model to control for previous health status. We evaluated the main effects of SLE, ES-S, and PRS-S, and tested the moderating effects of ES-S and PRS-S on the impact of SLE on physical and mental health. As sensitivity analyses, we repeated the analyses using lagged SLE at T-1. Results SLE and ES-S were associated with decreased mental (SLE: β = -2.53, P Discussion In support of the diathesis-stress model, we have provided novel evidence showing that exposure to adult SLE, particularly in individuals with high ES-S, is associated with decreased mental health. However, we did not find evidence for a gene-environment interaction in the context of SLExPRS-S. Our findings also add to the literature showing that genomic and exposomic liability for schizophrenia is pleiotropically associated with health outcomes in the general population.

Objective: A plethora of data deriving from single studies as well as meta-analyses demonstrates that weight gain is associated with the exposure to the majority of antipsychotics (AP). However, potential sex differences have widely evaded the attention of AP treatment trials. It is hypothesised that female patients gain more weight compared with male patients due to their enhanced susceptibility to adverse drug reactions. Method: A meta-analysis was conducted using clinical trials of AP that reported weight change separately for female and male patients. Duration of AP use was stratified in four categories: 38 weeks. Forest plots were generated for men and women separately, stratified by AP as well as by duration of use. Sex differences were tested by performing meta-regression. Results: Data of 26 studies were used in the present analysis because sufficient data were available only for olanzapine, risperidone and the no-medication group. Both female and male patients showed considerable weight gain after switch or initiate of olanzapine or risperidone, but meta-regression analyses did not show significant sex differences. Conclusion: The present meta-analysis revealed that sex differences in AP-related weight gain have been under investigated hampering the detection of sex-specific patterns. In chronic patients switching to olanzapine or risperidone receiving short-or middle-term treatment, AP were associated with weight gain in both sex subgroups and no significant differences were reported.

In hoofdstuk 1 is besproken hoe psychische problemen het beste te begrijpen zijn. Het uitgangspunt is dat klachten en symptomen, en de ziekten die we daaronder zien, dynamisch zijn in ernst, frequentie en impact. Dit hebben we vervat in een dynamisch stress-kwetsbaarheidsmodel; een continuummodel van klachten, symptomen en dus ook ziekten, gebaseerd op drie onderliggende (biologische, psychologische en contextuele) kernmechanismen van kwetsbaarheid en weerbaarheid.

Ook dit hoofdstuk gaat over zorg. Meer specifiek over de organisatie van zorg. Een inkijkje in de organisatiekunde is daartoe onontbeerlijk. De lezer zal merken dat het loont om daar iets van te begrijpen. Want een goede of slechte organisatie van zorg heeft een enorme impact op de kwaliteit van zorg.

Psychiatrie is een prachtvak. In 150 jaar is ook eindeloos veel kennis vergaard. En we hebben slimme structuren bedacht voor het optimaliseren van hulpverlening. Maar zijn we inmiddels niet verdwaald in onze goede bedoelingen? Zien we elk afzonderlijk individu met psychische problemen nog wel staan?Dit leerboek heeft een focus. De patiënt.De zestig auteurs die hebben meegewerkt staan natuurlijk op de schouders van de groten uit het psychiatrische vak.Ze hoeven het wiel niet uit te vinden. Maar ze hebben wel even adem gehaald voordat ze hun kennis en ervaring in een didactisch verantwoorde vorm goten.Om de mens met psychische problemen echt centraal te kunnen stellen bleek het noodzakelijk om in eerste instantie veel te schiften. Er is teveel classificatie. Een overmaat aan diagnostische varianten helpt de patiënt meestal niet verder. Het volgen van protocollen vergt veel tijd die ten koste gaat van effectieve therapie.Na bestudering van dit boek zal het vak misschien wat afgeslankt lijken: minder verfijnde diagnostiek, een overzichtelijk aantal syndromen in de plaats van eindeloos veel symptomen. Minder bewegwijzerde zorgpaden.Maar het vak wordt ook verrijkt: met ‘persoonlijke psychiatrie’. Hoe organiseer je persoonlijke aandacht voor elke individuele patiënt? Hoe profiteert de cliënt van het inzicht dat psychische problemen gewoon kleinere of grotere verschuivingen zijn in de verhouding van stressoren en kwetsbaarheden? En vooral: hoe wordt een cliënt praktisch en steeds opnieuw geholpen op de weg naar herstel?Noem het een nieuw paradigma. Noem het ‘nieuwe ggz’. Maar het gaat beslist niet om oude wijn in nieuwe zakken. Deze publicatie maakt bestaande literatuur niet obsoleet. Wel beoogt dit leerboek uitdrukkelijk het, opnieuw, scherp stellen van de (persoonsgerichte) psychiatrische missie.

Objective Previous work has shown that across different patient samples, patients with childhood trauma are more likely to have co-occurrence of affective, anxious and psychosis symptoms than non-traumatized patients. However, the clinical relevance of trauma-related admixture remains to be established. Method We examined patients with mood disorder (NEMESIS-2; n = 1260), anxiety disorder (NEMESIS-2; n = 896) or psychotic disorder (GROUP; n = 532) in terms of symptom profiles, quality of life (QOL) and social functioning. Results Results showed that mood disorder patients with both trauma and co-occurrence of affective, anxious and psychosis symptoms had a lower QOL (B-12.6, 95% CI −17.7 to −7.5, P

Background: Different psychological models of trauma-induced psychosis have been postulated, often based on the observation of specific associations between particular types of childhood trauma (CT) and particular psychotic symptoms or the co-occurrence of delusions and hallucinations. However, the actual specificity of these associations remains to be tested. Methods: In 2 population-based studies with comparable methodology (Netherlands Mental Health Survey and Incidence Study-1 [NEMESIS-1] and NEMESIS-2, N 13 722), trained interviewers assessed CT, psychotic symptoms, and other psychopathology. Specificity of associations was assessed with mixed-effects regression models with multiple outcomes, a statistical method suitable to examine specificity of associations in case of multiple correlated outcomes. Results: Associations with CT were strong and significant across the entire range of psychotic symptoms, without evidence for specificity in the relationship between particular trauma variables and particular psychotic experiences (PEs). Abuse and neglect were both associated with PEs (ORabuse: 2.12, P

Background There is robust evidence that reasoning biases such as a tendency of jumping to conclusions (JTC) as well as cognitive deficits are associated with psychosis, but evidence on their association with affective disturbances remains inconclusive. Recent findings also suggest a transdiagnostic phenotype of co-occurring affective disturbances and psychotic experiences. This study aimed to investigate whether JTC bias and decreased working memory performance are associated with the co-occurrence of affective disturbances, psychotic experiences (PEs), and psychosis-related help-seeking behaviour (HS) in the general population. Methods The second Netherlands Mental Health Survey and Incidence Study (NEMESIS-2). Trained interviewers administered the Composite International Diagnostic Interview (CIDI) at three time points in a representative general population sample, with N=4.596 individuals who completed all assessments. The beads task and digit-span task were completed to assess JTC bias and working memory performance, respectively. CIDI was used to measure affective disturbances (i.e. depression, anxiety, mania) and an add-on instrument to measure PEs and HS. Results We found that, compared to individuals with neither affective disturbances nor PEs, JTC bias was more likely to be present in individuals with co-occurring affective disturbances, PEs, and HS (moderate psychosis [1–2 PEs]: relative risk ratio [RRR]=1.23, 95% CI 1.03 – 1.48, p=0.023; high psychosis [3 or more PEs or HS]: RRR=1.66, 95% CI 1.26 – 2.19, p