Psychiatric disorders and homelessness are related, but temporal associations are unclear. We aimed to explore the overlap between hospital-based psychiatric disorders and sheltered homelessness.

This population-based cohort study was conducted using the Danish registers e.g., the Danish Homeless Register and the Danish National Patient Register. The study cohort included all individuals aged 15 years or older, living in Denmark at least one day during 2002–2021 (born 1984–2006). First psychiatric diagnosis was used to define psychiatric disorder and first homeless shelter contact to define homelessness. Adjusted incidence rate ratios (IRRs) and cumulative incidences were estimated.

Among 1 530 325 individuals accounting for 16 787 562 person-years at risk aged 15–38 years, 11 433 (0.8%) had at least one homeless shelter contact. Among 1 406 410 individuals accounting for 14 131 060 person-years at risk, 210 730 had at least one psychiatric disorder. People with any psychiatric disorder had increased risk of sheltered homelessness relative to individuals with no psychiatric disorder [IRR 9.2, 95% confidence interval (CI) 8.8–9.6]. Ten years after first psychiatric disorder, 3.0% (95% CI 2.9–3.1) had at least one homeless shelter contact. Individuals experiencing homelessness had increased risk of any psychiatric disorder compared to individuals with no homeless shelter contact (IRR 7.0, 95% CI 6.7–7.4). Ten years after first homeless shelter contact, 47.1% (45.3–48.0) had received a hospital-based psychiatric diagnosis.

Strong bidirectional associations between psychiatric disorders and homelessness were identified. Health and social care professionals should be aware of and address these high risks of accumulated psychiatric and social problems.

Major depressive disorder (MDD) is one of the growing human mental health challenges facing the global health care system. In this study, the structural connectivity between symptoms of MDD is explored using two different network modeling approaches.

Data are from ‘the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders (VATSPSUD)’. A cohort of N = 2163 American Caucasian female-female twins was assessed as part of the VATSPSUD study. MDD symptoms were assessed using personal structured clinical interviews. Two network analyses were conducted. First, an undirected network model was estimated to explore the connectivity between the MDD symptoms. Then, using a Bayesian network, we computed a directed acyclic graph (DAG) to investigate possible directional relationships between symptoms.

Based on the results of the undirected network, the depressed mood symptom had the highest centrality value, indicating its importance in the overall network of MDD symptoms. Bayesian network analysis indicated that depressed mood emerged as a plausible driving symptom for activating other symptoms. These results are consistent with DSM-5 guidelines for MDD. Also, somatic weight and appetite symptoms appeared as the strongest connections in both networks.

We discuss how the findings of our study might help future research to detect clinically relevant symptoms and possible directional relationships between MDD symptoms defining major depression episodes, which would help identify potential tailored interventions. This is the first study to investigate the network structure of VATSPSUD data using both undirected and directed network models.

To better understand the associations of childhood trauma and childhood disorder with past-year suicidality (thoughts, plans or attempts), we compared male military and civilian populations aged 18–60 years old.

Data derived from the 2010 Australian Defence Force (ADF) Mental Health Prevalence and Wellbeing Study and the 2007 Australian Bureau of Statistics Australian National Survey of Mental Health and Wellbeing were compared using logistic regression and Generalized Structural Equation Modelling (GSEM).

A greater proportion of the ADF experienced suicidality than civilians. Those who experienced childhood trauma that was not interpersonal in nature were not at increased odds of suicidality, in either population. A higher proportion of the ADF experienced three or more types of trauma in childhood and first experienced three or more types of trauma in adulthood. Both were associated with suicidality in the ADF and civilians. Childhood anxiety had a strong and independent association with suicidality in the ADF (controlling for demographics and childhood trauma, adult trauma and adult onset disorder). Childhood anxiety fully mediated the relationship between childhood trauma and suicidality in the ADF, but not in civilians.

These data highlight the need to take a whole life approach to understanding suicidality, and the importance of categorizing the nature of childhood trauma exposure. Importantly, childhood anxiety was not only associated with suicidality, it fully mediated the relationship between childhood trauma and suicidality in the more trauma exposed (military) population only. These findings have the potential to inform the development of strategies for suicide prevention.

Social anxiety disorder (SAD) is common, first-line treatments are often only partially effective, and reliable predictors of treatment response are lacking. Here, we assessed resting state functional connectivity (rsFC) at pre-treatment and during early treatment as a potential predictor of response to a novel attention bias modification procedure, gaze-contingent music reward therapy (GC-MRT).

Thirty-two adults with SAD were treated with GC-MRT. rsFC was assessed with multi-voxel pattern analysis of fMRI at pre-treatment and after 2–3 weeks. For comparison, 20 healthy control (HC) participants without treatment were assessed twice for rsFC over the same time period. All SAD participants underwent clinical evaluation at pre-treatment, early-treatment (week 2–3), and post-treatment.

SAD and depressive symptoms improved significantly from pre-treatment to post-treatment. After 2–3 weeks of treatment, decreased connectivity between the executive control network (ECN) and salience network (SN), and increased connectivity within the ECN predicted improvement in SAD and depressive symptoms at week 8. Increased connectivity between the ECN and default mode network (DMN) predicted greater improvement in SAD but not depressive symptoms at week 8. Connectivity within the DMN decreased significantly after 2–3 weeks of treatment in the SAD group, while no changes were found in HC over the same time interval.

We identified early changes in rsFC during a course of GC-MRT for SAD that predicted symptom change. Connectivity changes within the ECN, ECN-DMN, and ECN-SN may be related to mechanisms underlying the clinical effects of GC-MRT and warrant further study in controlled trials.

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

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

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

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

Excessive worry is a common phenomenon. Our research group has previously developed an online intervention for excessive worry based on operant principles of extinction (IbET; internet-based extinction therapy) and tested it against a waiting-list. The aim of this study was to evaluate IbET against an active control comparator (CTRL).

A 10-week parallel participant blind randomised controlled trial with health-economical evaluation and mediation analyses. Participants (N = 311) were randomised (ratio 4.5:4.5:1) to IbET, to CTRL (an internet-based stress-management training program) or to waiting-list. The nation-wide trial included self-referred adults with excessive worry. The primary outcome was change in worry assessed with the Penn State Worry Questionnaire from baseline to 10 weeks.

IbET had greater reductions in worry compared to CTRL [−3.6 point difference, (95% CI −2.4 to −4.9)] and also a significantly larger degree of treatment responders [63% v. 51%; risk ratio = 1.24 (95% CI 1.01–1.53)]. Both IbET and CTRL made large reductions in worry compared to waiting-list and effects were sustained up to 1 year. Treatment credibility, therapist attention, compliance and working alliance were equal between IbET and CTRL. Data attrition was 4% at the primary endpoint. The effects of IbET were mediated by the hypothesized causal mechanism (reduced thought suppression) but not by competing mediators. Health-economical evaluation indicated that IbET had a 99% chance of being cost-effective compared to CTRL given societal willingness to pay of 1000€.

IbET is more effective than active comparator to treat excessive worry. Replication and extensions to real-world setting are warranted.

Previous literature supports antipsychotics’ (AP) efficacy in acute first-episode psychosis (FEP) in terms of symptomatology and functioning but also a cognitive detrimental effect. However, regarding functional recovery in stabilised patients, these effects are not clear. Therefore, the main aim of this study is to investigate dopaminergic/anticholinergic burden of (AP) on psychosocial functioning in FEP. We also examined whether cognitive impairment may mediate these effects on functioning.

A total of 157 FEP participants were assessed at study entry, and at 2 months and 2 years after remission of the acute episode. The primary outcomes were social functioning as measured by the functioning assessment short test (FAST). Cognitive domains were assessed as potential mediators. Dopaminergic and anticholinergic AP burden on 2-year psychosocial functioning [measured with chlorpromazine (CPZ) and drug burden index] were independent variables. Secondary outcomes were clinical and socio-demographic variables.

Mediation analysis found a statistical but not meaningful contribution of dopaminergic receptor blockade burden to worse functioning mediated by cognition (for every 600 CPZ equivalent points, 2-year FAST score increased 1.38 points). Regarding verbal memory and attention, there was an indirect effect of CPZ burden on FAST (b = 0.0045, 95% CI 0.0011–0.0091) and (b = 0.0026, 95% CI 0.0001–0.0006) respectively. However, only verbal memory post hoc analyses showed a significant indirect effect (b = 0.009, 95% CI 0.033–0.0151) adding premorbid IQ as covariate. We did not find significant results for anticholinergic burden.

CPZ dose effect over functioning is mediated by verbal memory but this association appears barely relevant.

Recent research has emphasized the importance of within-person transactions between situational perceptions and borderline symptomatology. The current study extends current evidence by evaluating a broad range of situational perceptions and their transactions with borderline symptomatology across both private and professional contexts. Additionally, it explores whether early experiences of parental harsh punishment and emotional support during childhood, two well-established etiological factors in developmental theories of borderline symptomatology, influence the effect of daily situation perception in adulthood on borderline symptom presentation.

N = 131 young adults (Mage = 20.97, s.d.age = 1.64) completed end-of-day diaries of their borderline symptoms and perceptions of the home and school or work environment for 14 days. During their mid-childhood, reports of maternal strategies of harsh punishment and emotional support were collected.

Findings revealed that on the same day, borderline symptoms were associated with more negative and stressful, and less positive perceptions of both the private and professional context. Additionally, borderline symptoms predicted more negative and stressful perceptions of school/work on subsequent days. Finally, while early harsh punishment predicted overall increases in daily borderline symptoms 10 years later, emotionally supportive parenting in childhood predicted decreases in borderline symptom expression in less positive and more stressful contexts.

The current study points to the importance of managing BPD symptoms to reduce subsequent negative perceptions of the environment, and also indicates the relevance of exploring adult person-situation processes based on early parenting experiences.

The neuropsychological origins of negative syndrome of schizophrenia remain elusive. Evidence from behavioural studies, which utilised emotion-inducing pictures to elicit motivated behaviour generally reported that that schizophrenia patients experienced similar affective experience as healthy individuals but failed to translate emotional salience to motivated behaviour, a phenomenon called emotion–behaviour decoupling. However, a few studies have examined emotion–behaviour decoupling in non-psychotic high-risk populations, who are relatively unaffected by medication effects.

In this study, we examined the nature and extent of emotion–behaviour decoupling in in three independent samples (65 schizophrenia patients v. 63 controls; 40 unaffected relatives v. 45 controls; and 32 individuals with social anhedonia v. 32 controls). We administered an experimental task to examine their affective experience and its coupling with behaviour, using emotion-inducing slides, and allowed participants to alter stimulus exposure using button-pressing to seek pleasure or avoid aversion.

Schizophrenia patients reported similar affective experiences as their controls, while their unaffected relatives and individuals with high levels of social anhedonia exhibited attenuated affective experiences, in particular in the arousal aspect. Compared with their respective control groups, all of the three groups showed emotion–behaviour decoupling.

Our findings support that both genetically and behaviourally high-risk groups exhibit emotion–behaviour decoupling. The familial association apparently supports its role as a putative trait marker for schizophrenia.

The neurodevelopmental model of psychosis was established over 30 years ago; however, the developmental influence on psychotic symptom expression – how age affects clinical presentation in first-episode psychosis – has not been thoroughly investigated.

Using generalized additive modeling, which allows for linear and non-linear functional forms of age-related change, we leveraged symptom data from a large sample of antipsychotic-naïve individuals with first-episode psychosis (N = 340, 12–40 years, 1–12 visits), collected at the University of Pittsburgh from 1990 to 2017. We examined relationships between age and severity of perceptual and non-perceptual positive symptoms and negative symptoms. We tested for age-associated effects on change in positive or negative symptom severity following baseline assessment and explored the time-varying relationship between perceptual and non-perceptual positive symptoms across adolescent development.

Perceptual positive symptom severity significantly decreased with increasing age (F = 7.0, p = 0.0007; q = 0.003) while non-perceptual positive symptom severity increased with age (F = 4.1, p = 0.01, q = 0.02). Anhedonia severity increased with increasing age (F = 6.7, p = 0.00035; q = 0.0003), while flat affect decreased in severity with increased age (F = 9.8, p = 0.002; q = 0.006). Findings remained significant when parental SES, IQ, and illness duration were included as covariates. There were no developmental effects on change in positive or negative symptom severity (all p > 0.25). Beginning at age 18, there was a statistically significant association between severity of non-perceptual and perceptual symptoms. This relationship increased in strength throughout adulthood.

These findings suggest that as maturation proceeds, perceptual symptoms attenuate while non-perceptual symptoms are enhanced. Findings underscore how pathological brain–behavior relationships vary as a function of development.

We need to better understand the frequency and predictors of opioid use disorder (OUD) after first opioid prescription (OP).

We followed 1 516 392 individuals from the Swedish population born 1980–2000, from 1 July 2007, until 31 Dec 2017. We examined putative risk predictors with univariable and multivariable Cox Models and the potential causal effects of predictors by propensity score and co-sibling analyses.

Of the individuals in our cohort, 24.8% (375 404) received a first OP, of whom 3034 (0.90%) developed a subsequent first OUD. The hazard ratio (HR) (± 95% CIs) for OUD after OP equaled 7.10 (6.75–7.46), with a mean time to onset of 3.41 (2.39) years. The strongest putative risk factors for development of OUD after OP were prior psychiatric and substance use disorders, criminal behavior, parental divorce/death, poor school performance, current community deprivation, divorce, and male sex. Few predictors differed across sexes. OP renewal was associated with a HR of 3.66 (3.41–3.93) for OUD. Co-sibling and propensity score analyses suggested that at least a moderate proportion of the risk factor-OUD association was likely causal. A risk score to predict OUD after OP had an AUC of 0.85, where nearly 60% of cases scoring in the top decile.

In a general population sample, an OP represents a substantial risk factor for subsequent OUD. Many of the risk factors for OUD after OP can be readily assessed at the time of potential OP, permitting clinicians to evaluate the risk of iatrogenic OUD.