The psychosis continuum implies that subclinical psychotic experiences (PEs) can be differentiated from clinically relevant expressions since they are not accompanied by a ‘need for care’.

Using data from Wave 2 of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC; N = 34 653), the current study examined variation in functioning, symptomology and aetiological risk across the psychosis phenotype [i.e. variation from (i) no PEs, ‘No PEs’ to (ii) non-distressing PEs, ‘PE-Experienced Only’ to (iii) distressing PEs, ‘PE-Impaired’ to (iv) clinically defined psychotic disorder, ‘Diagnosed’].

A graded trend was present such that, compared to those with no PEs, the Diagnosed group had the poorest functioning, followed by the PE-Impaired then PE-Experienced Only groups. In relation to symptom expression, the PE-Impaired group were more likely than the PE-Experienced Only and the Diagnosed groups to endorse most PEs. Predictors of group membership tended to vary quantitatively rather than qualitatively. Trauma, current mental health diagnoses (anxiety and depression) and drug use variables differentiated between all levels of the continuum, with the exception of the extreme end (PE-Impaired v. Diagnosed). Only a few variables distinguished groups at the upper end of the continuum: female sex, older age, unemployment, parental mental health hospitalisation and lower likelihood of having experienced physical assault.

The findings highlight the importance of continuum-based interpretations of the psychosis phenotype and afford valuable opportunities to consider if and how impairment, symptom expression and risk change along the continuum.

While cannabis use is a well-established risk factor for psychosis, little is known about any association between reasons for first using cannabis (RFUC) and later patterns of use and risk of psychosis.

We used data from 11 sites of the multicentre European Gene-Environment Interaction (EU-GEI) case–control study. 558 first-episode psychosis patients (FEPp) and 567 population controls who had used cannabis and reported their RFUC.

We ran logistic regressions to examine whether RFUC were associated with first-episode psychosis (FEP) case–control status. Path analysis then examined the relationship between RFUC, subsequent patterns of cannabis use, and case–control status.

Controls (86.1%) and FEPp (75.63%) were most likely to report ‘because of friends’ as their most common RFUC. However, 20.1% of FEPp compared to 5.8% of controls reported: ‘to feel better’ as their RFUC (χ2 = 50.97; p < 0.001). RFUC ‘to feel better’ was associated with being a FEPp (OR 1.74; 95% CI 1.03–2.95) while RFUC ‘with friends’ was associated with being a control (OR 0.56; 95% CI 0.37–0.83). The path model indicated an association between RFUC ‘to feel better’ with heavy cannabis use and with FEPp-control status.

Both FEPp and controls usually started using cannabis with their friends, but more patients than controls had begun to use ‘to feel better’. People who reported their reason for first using cannabis to ‘feel better’ were more likely to progress to heavy use and develop a psychotic disorder than those reporting ‘because of friends’.

Losing a parent or spouse in adulthood may result in prolonged grief disorder (PGD) symptoms. PGD levels in parents may affect PGD levels in their adult offspring and the other way around. However, research on transmission of PGD in parent–child dyads is lacking. Consequently, we aimed to examine temporal associations between PGD levels in parent and adult children.

In doing so, we analyzed longitudinal self-report data on PGD levels (using the PG-13) assessed at 2, 11, 18, and 26 months after loss in 257 adult parent–child dyads from Denmark. Cross-lagged panel modeling was used for data-analyses.

Changes in PGD levels in parents significantly predicted PGD levels in adult children, but not vice versa. Small through moderate cross-lagged effects (β = 0.05 through 0.07) were found for PGD levels in parents predicting PGD levels in adult children at a subsequent time-point. These cross-lagged effects were found while taking into account the association between PGD levels in parents and adult children at the same time-point as well as the associations between the same construct over time and relevant covariates.

Pending replication of these findings in clinical samples and younger families, our findings offer tentative support for expanding our focus in research and treatment of PGD from the individual to the family level.

Hospital-based biobanks are being increasingly considered as a resource for translating polygenic risk scores (PRS) into clinical practice. However, since these biobanks originate from patient populations, there is a possibility of bias in polygenic risk estimation due to overrepresentation of patients with higher frequency of healthcare interactions.

PRS for schizophrenia, bipolar disorder, and depression were calculated using summary statistics from the largest available genomic studies for a sample of 24 153 European ancestry participants in the Mass General Brigham (MGB) Biobank. To correct for selection bias, we fitted logistic regression models with inverse probability (IP) weights, which were estimated using 1839 sociodemographic, clinical, and healthcare utilization features extracted from electronic health records of 1 546 440 non-Hispanic White patients eligible to participate in the Biobank study at their first visit to the MGB-affiliated hospitals.

Case prevalence of bipolar disorder among participants in the top decile of bipolar disorder PRS was 10.0% (95% CI 8.8–11.2%) in the unweighted analysis but only 6.2% (5.0–7.5%) when selection bias was accounted for using IP weights. Similarly, case prevalence of depression among those in the top decile of depression PRS was reduced from 33.5% (31.7–35.4%) to 28.9% (25.8–31.9%) after IP weighting.

Non-random selection of participants into volunteer biobanks may induce clinically relevant selection bias that could impact implementation of PRS in research and clinical settings. As efforts to integrate PRS in medical practice expand, recognition and mitigation of these biases should be considered and may need to be optimized in a context-specific manner.

Childhood maltreatment (CM) exerts long-lasting psychological and biological alterations in affected individuals and might also affect the endocannabinoid (eCB) system which modulates inflammation and the endocrine stress response. Here, we investigated the eCB system of women with and without CM and their infants using hair samples representing eCB levels accumulated during the last trimester of pregnancy and 10–12 months postpartum.

CM exposure was assessed with the Childhood Trauma Questionnaire. At both timepoints, 3 cm hair strands were collected from mothers and children (N = 170 resp. 150) to measure anandamide (AEA), 2/1-arachidonoylglycerol (2-AG/1-AG), stearoylethanolamide (SEA), oleoylethanolamide (OEA), and palmitoylethanolamide (PEA).

Maternal hair levels of 2-AG/1-AG increased and SEA levels decreased from late pregnancy to one year postpartum. Maternal CM was associated with lower SEA levels in late pregnancy, but not one year later. In the children's hair, levels of 2-AG/1-AG increased while levels of SEA, OEA, and PEA decreased from late pregnancy to one year later. Maternal CM was not consistently associated with the eCB levels measured in children's hair.

We provide first evidence for longitudinal change in the eCB system of mothers and infants from pregnancy to one year later. While maternal CM influenced the maternal eCB system, we found no consistent intergenerational effects on early regulation of the eCB system in children. Longitudinal research on the importance of the eCB system for the course and immunoregulation of pregnancy as well as for the children's development.

Are genetic risk factors for current depressive symptoms good proxies for genetic risk factors for syndromal major depression (MD)?

In over 9000 twins from the population-based Virginia Adult Twin Study of Psychiatric and Substance Use Disorders, the occurrence of all nine DSM symptomatic criteria for MD in the last year was assessed at personal interview and then grouped by their temporal co-occurrence. The DSM criteria which occurred outside (OUT) v. inside of (IN) MD episodes were then separated. We calculated tetrachoric correlations for OUT and IN depressive criteria in monozygotic (MZ) and dizygotic (DZ) pairs and fitted univariate and bivariate ACE twin models using OpenMx.

The mean twin correlations (±95% CIs) for IN depressive criteria were substantially higher than for OUT depressive criteria in both MZ [+0.35 (0.32–0.38) v. 0.20 (0.17–0.24)] and DZ pairs [0.20 (0.17–0.24) v. 0.10 (0.04–0.16]. The mean IN–OUT cross-correlation in MZ and DZ pairs was modest [+0.15 (0.07–0.24) and +0.07 (0.03–0.12)]. The mean heritability estimates for the nine In v. Out depressive criteria was 0.31 (0.22–0.41) and 0.15 (0.08–0.21), in MZ and DZ pairs, respectively. The mean genetic correlation between the nine IN and OUT depressive criteria was +0.07 (−0.07 to 0.21).

Depressive criteria occurring outside depressive episodes are less heritable than those occurring within. These two ways criteria can manifest are not closely genetically related. Current depressive symptoms – most of which are occurring outside of depressive episodes – are not, for genetic studies, good proxies for MD.