Data from an RCT of IAPT Norway (“Prompt Mental Health Care” [PMHC]) were linked to several administrative registers up to five years following the intervention. The aims were to (1) examine the effects of PMHC compared to treatment-as-usual (TAU) on work-related outcomes and health care use, (2) estimate the cost–benefit of PMHC, and (3) examine whether clinical outcomes at six-month follow-up explained the effects of PMHC on work−/cost–benefit-related outcomes.

RCTs with parallel assignment were conducted at two PMHC sites (N = 738) during 2016/2017. Eligible participants were considered for admission due to anxiety and/or depression. We used Bayesian estimation with 90% credibility intervals (CI) and posterior probabilities (PP) of effects in favor of PMHC. Primary outcome years were 2018–2022. The cost–benefit analysis estimated the overall economic gain expressed in terms of a benefit–cost ratio and the differences in overall public sector spending.

The PMHC group was more likely than the TAU group to be in regular work without receiving welfare benefits in 2019–2022 (1.27 ≤ OR ≤ 1.43). Some evidence was found that the PMHC group spent less on health care. The benefit–cost ratio in terms of economic gain relative to intervention costs was estimated at 5.26 (90%CI $ - $1.28, 11.8). The PP of PMHC being cost-beneficial for the economy as a whole was 85.9%. The estimated difference in public sector spending was small. PMHC effects on work participation and cost–benefit were largely explained by PMHC effects on mental health.

The results support the societal economic benefit of investing in IAPT-like services.

Population-level preventive interventions are urgently needed and may be effective for psychosis due to social determinants. We tested three syndemic models along pathways from childhood adversity (CA) to psychotic spectrum disorder (PSD) and their implications for prevention.

Cross-sectional data from 7461 British men surveyed in 5 population subgroups. We tested interactions on both additive and multiplicative scales for a syndemic of violence/criminality (VC), sexual behavior (SH), and substance misuse (SM) according to the presence of CA and adult traumatic life events; mediation analysis of path models; and partial least squares path modeling, with PSD as outcome.

Multiplicative synergistic interactions were found between VC, SH, and SM among men, who experienced CA and traumatic adult life events. However, when disaggregated, only SM mediated the pathway from CA to PSD. Path modeling showed traumatic life events acted on PSD through the syndemic and had no direct effect on PSD. Higher syndemic scores and living in areas of deprivation characterized men with PSD and CA.

Our findings support a broad division of PSD into cases due to (i) biological/inherent causes, and (ii) social determinants, the latter including a syndemic pathway determined by CA. Preventive strategies should focus primarily on preventing adverse effects of CA on developmental pathways which result in PSD. Single component prevention strategies may prevent triggering effects of SM on PSD during adolescence/early adulthood among vulnerable individuals due to CA. Future research should determine applicability and transferability of interventions based on these findings to different populations, specifically those experiencing syndemics.

Complex post-traumatic stress disorder (cPTSD) is a newly recognized condition characterized by core PTSD symptoms and disturbances in self-organization (DSO) that has been associated with psychotic-like experiences (PLEs). This study employs two psychopathology network approaches to identify which post-traumatic symptoms are related to PLEs in a sample of late adolescents. We propose that cPTSD symptoms play a crucial role in explaining the co-occurrence of trauma and PLEs.

A sample of 1010 late adolescents provided measures of post-traumatic symptomatology and PLEs. We estimated the Gaussian graphical network structure of PTSD/cPTSD symptoms and PLEs and assessed their bridge centrality indices. Bayesian network analysis was then used to estimate a directed acyclic graph (DAG). Gender was set as a moderator in both Gaussian and Bayesian models.

Results show that affect dysregulation, a cPTSD domain, presented the highest bridge connection with the PLE cluster. Bayesian network analysis identified a pathway going from cPTSD items of worthlessness and relational dysregulation, to PLE items of paranoia and social anxiety. Additionally, we found relevant gender differences in network connectivity, with females showing higher connectivity compared to males.

Our findings highlight the central role of affect dysregulation and negative self-concept in linking cPTSD to PLE symptoms, with specific differences according to gender. These insights underscore the need for targeted, gender-sensitive approaches in the prevention and treatment of PLEs among adolescents, emphasizing early intervention and tailored treatment strategies.

Poorer family functioning during childhood is associated with severe mental disorders in adulthood in the general population. However, family functioning is understudied in families with parental schizophrenia or bipolar disorder. We aimed to investigate family functioning in families with 11-year-old children of parents with schizophrenia or bipolar disorder compared with controls. Second, we aimed to examine associations between family functioning and levels of child psychopathology, child global functioning, and parental social functioning.

In this prospective, population-based cohort study, we included 160 families with parental schizophrenia, 95 families with parental bipolar disorder, and 177 control families. Family functioning was measured with the 12-item version of the McMaster Family Assessment Device – General Functional Scale.

Families with parental schizophrenia (Cohen’s d = 0.29; p = .002) and parental bipolar disorder (Cohen’s d = 0.34; p = .004) had significantly poorer family functioning and a significantly higher prevalence of clinically significant family dysfunction (Cohen’s d range = 0.29–0.34; p values = .007) than control families. Across study groups, poorer family functioning was associated with higher levels of child psychopathology and poorer social functioning of the primary caregiver (p values < .001).

Children in families with parental schizophrenia or bipolar disorder are at increased risk of experiencing family dysfunction, and poorer family functioning confers risk for more symptoms of child psychopathology and poorer parental social functioning. Future studies should investigate the potentially predictive value of family dysfunction in relation to later illness onset and other adverse outcomes in these populations.