Perceived discrimination is associated with worse mental health. Few studies have assessed whether perceived discrimination (i) is associated with the risk of psychotic disorders and (ii) contributes to an increased risk among minority ethnic groups relative to the ethnic majority.

We used data from the European Network of National Schizophrenia Networks Studying Gene-Environment Interactions Work Package 2, a population-based case−control study of incident psychotic disorders in 17 catchment sites across six countries. We calculated odds ratios (OR) and 95% confidence intervals (95% CI) for the associations between perceived discrimination and psychosis using mixed-effects logistic regression models. We used stratified and mediation analyses to explore differences for minority ethnic groups.

Reporting any perceived experience of major discrimination (e.g. unfair treatment by police, not getting hired) was higher in cases than controls (41.8% v. 34.2%). Pervasive experiences of discrimination (≥3 types) were also higher in cases than controls (11.3% v. 5.5%). In fully adjusted models, the odds of psychosis were 1.20 (95% CI 0.91–1.59) for any discrimination and 1.79 (95% CI 1.19–1.59) for pervasive discrimination compared with no discrimination. In stratified analyses, the magnitude of association for pervasive experiences of discrimination appeared stronger for minority ethnic groups (OR = 1.73, 95% CI 1.12–2.68) than the ethnic majority (OR = 1.42, 95% CI 0.65–3.10). In exploratory mediation analysis, pervasive discrimination minimally explained excess risk among minority ethnic groups (5.1%).

Pervasive experiences of discrimination are associated with slightly increased odds of psychotic disorders and may minimally help explain excess risk for minority ethnic groups.

The coronavirus [coronavirus disease 2019 (COVID-19)] pandemic has introduced extraordinary life changes and stress, particularly in adolescents and young adults. Initial reports suggest that depression and anxiety are elevated during COVID-19, but no prior study has explored changes at the within-person level. The current study explored changes in depression and anxiety symptoms from before the pandemic to soon after it first peaked in Spring 2020 in a sample of adolescents and young adults (N = 451) living in Long Island, New York, an early epicenter of COVID-19 in the U.S.

Depression (Children's Depression Inventory) and anxiety symptoms (Screen for Child Anxiety Related Symptoms) were assessed between December 2014 and July 2019, and, along with COVID-19 experiences, symptoms were re-assessed between March 27th and May 15th, 2020.

Across participants and independent of age, there were increased generalized anxiety and social anxiety symptoms. In females, there were also increased depression and panic/somatic symptoms. Multivariable linear regression indicated that greater COVID-19 school concerns were uniquely associated with increased depression symptoms. Greater COVID-19 home confinement concerns were uniquely associated with increased generalized anxiety symptoms, and decreased social anxiety symptoms, respectively.

Adolescents and young adults at an early epicenter of the COVID-19 pandemic in the U.S. experienced increased depression and anxiety symptoms, particularly amongst females. School and home confinement concerns related to the pandemic were independently associated with changes in symptoms. Overall, this report suggests that the COVID-19 pandemic is having multifarious adverse effects on the mental health of youth.

Agitated patients constitute 10% of all emergency psychiatric treatment. Management guidelines, the preferred treatment of clinicians differ in opinion and practice. In Lebanon, the use of the triple therapy haloperidol plus promethazine plus chlorpromazine (HPC) is frequently used but no studies involving this combination exists.

A pragmatic randomised open trial (September 2018–July 2019) in the Lebanese Psychiatric Hospital of the Cross in Beirut Lebanon involving 100 people requiring urgent intramuscular sedation due to aggressive behaviour were given intramuscular chlorpromazine 100 mg plus haloperidol 5 mg plus promethazine 25 mg (HPC) or intramuscular haloperidol 5 mg plus promethazine 25 mg

Primary outcome data were available for 94 (94%) people. People allocated to the haloperidol plus promethazine (HP) group showed no clear difference at 20 min compared with patients allocated to the HPC group [relative risk (RR) 0.84, 95% confidence interval (CI) 0.47–1.50].

Neither intervention consistently impacted the outcome of ‘calm’, or ‘asleep’ and had no discernible effect on the use of restraints, use of additional drugs or recurrence. If clinicians are faced with uncertainty on which of the two intervention combinations to use, the simpler HP is much more widely tested and the addition of chlorpromazine adds no clear benefit with a risk of additional adverse effects.

Examining social networks, characterized by interpersonal interactions across family, peer, school, and neighborhoods, offer alternative explanations to suicidal behaviors and shape effective suicide prevention. This study examines adolescent social networks predicting suicide ideation and attempt trajectories transitioning to adulthood, while revealing differences across racial/ethnic, sex, sexual identity, and socioeconomic status.

Participants included 9421 high school students (Mage = 15.30 years; 54.58% females, baseline) from Waves I–IV of the National Longitudinal Study of Adolescent to Adult Health, 1994–2008. Latent class growth analyses were conducted to identify suicide ideation and attempt trajectories. Multivariate multinomial logistic regressions examined the relationships between social network characteristics during adolescence and suicidal trajectories. Interaction terms between social networks and sociodemographic characteristics were included to test moderation effects.

Three suicidal ideation trajectories (low-stable, high-decreasing, moderate-decreasing-increasing) and two suicide attempt trajectories (low-stable, moderate-decreasing) were identified. Greater family cohesion significantly reduced the probability of belonging to high-decreasing (Trajectory 2) and moderate-decreasing-increasing (Trajectory 3) suicidal ideation trajectories, and moderate-decreasing (Trajectory 2) suicide attempt trajectory. Race/ethnicity, sex, and sexual identity significantly moderated the associations between social networks (household size, peer network density, family cohesion, peer support, neighborhood support) and suicidal trajectories.

Social networks during adolescence influenced the odds of belonging to distinct suicidal trajectories. Family cohesion protected youth from being in high-risk developmental courses of suicidal behaviors. Social networks, especially quality of interactions, may improve detecting adolescents and young adults at-risk for suicide behaviors. Network-based interventions are key to prevent suicidal behaviors over time and suicide intervention programming.

Despite evidence for the general effectiveness of psychological therapies, there exists substantial heterogeneity in patient outcomes. We aimed to identify factors associated with baseline severity of depression and anxiety symptoms, rate of symptomatic change over the course of therapy, and symptomatic recovery in a primary mental health care setting.

Using data from a service evaluation involving 35 527 patients in England's psychological and wellbeing [Improving Access to Psychological Therapies (IAPT)] services, we applied latent growth models to explore which routinely-collected sociodemographic, clinical, and therapeutic variables were associated with baseline symptom severity and rate of symptomatic change. We used a multilevel logit model to determine variables associated with symptomatic recovery.

Being female, younger, more functionally impaired, and more socioeconomically disadvantaged was associated with higher baseline severity of both depression and anxiety symptoms. Being older, less functionally impaired, and having more severe baseline symptomatology was associated with more rapid improvement of both depression and anxiety symptoms (male gender and greater socioeconomic disadvantage were further associated with rate of change for depression only). Therapy intensity and appointment frequency seemed to have no correlation with rate of symptomatic improvement. Patients with lower baseline symptom severity, less functional impairment, and older age had a greater likelihood of achieving symptomatic recovery (as defined by IAPT criteria).

We must continue to investigate how best to tailor psychotherapeutic interventions to fit patients’ needs. Patients who begin therapy with more severe depression and/or anxiety symptoms and poorer functioning merit special attention, as these characteristics may negatively impact recovery.

Cognitive impairment is common in late-life depression, which may increase Alzheimer disease (AD) risk. Therefore, we aimed to investigate whether late-life major depressive disorder (MDD) has worse cognition and increases the characteristic AD neuropathology. Furthermore, we carried out a comparison between treatment-resistant depression (TRD) and non-TRD. We hypothesized that patients with late-life depression and TRD may have increased β-amyloid (Aβ) deposits in brain regions responsible for global cognition.

We recruited 81 subjects, including 54 MDD patients (27 TRD and 27 non-TRD) and 27 matched healthy controls (HCs). Neurocognitive tasks were examined, including Mini-Mental State Examination and Montreal Cognitive Assessment to detect global cognitive functions. PET with Pittsburgh compound-B and fluorodeoxyglucose were used to capture brain Aβ pathology and glucose use, respectively, in some patients.

MDD patients performed worse in Montreal Cognitive Assessment (p = 0.003) and had more Aβ deposits than HCs across the brain (family-wise error-corrected p < 0.001), with the most significant finding in the left middle frontal gyrus. Significant negative correlations between global cognition and prefrontal Aβ deposits existed in MDD patients, whereas positive correlations were noted in HCs. TRD patients had significantly more deposits in the left-sided brain regions (corrected p < 0.001). The findings were not explained by APOE genotypes. No between-group fluorodeoxyglucose difference was detected.

Late-life depression, particularly TRD, had increased brain Aβ deposits and showed vulnerability to Aβ deposits. A detrimental role of Aβ deposits in global cognition in patients with late-onset or non-late-onset MDD supported the theory that late-life MDD could be a risk factor for AD.

MRI-derived cortical folding measures are an indicator of largely genetically driven early developmental processes. However, the effects of genetic risk for major mental disorders on early brain development are not well understood.

We extracted cortical complexity values from structural MRI data of 580 healthy participants using the CAT12 toolbox. Polygenic risk scores (PRS) for schizophrenia, bipolar disorder, major depression, and cross-disorder (incorporating cumulative genetic risk for depression, schizophrenia, bipolar disorder, autism spectrum disorder, and attention-deficit hyperactivity disorder) were computed and used in separate general linear models with cortical complexity as the regressand. In brain regions that showed a significant association between polygenic risk for mental disorders and cortical complexity, volume of interest (VOI)/region of interest (ROI) analyses were conducted to investigate additional changes in their volume and cortical thickness.

The PRS for depression was associated with cortical complexity in the right orbitofrontal cortex (right hemisphere: p = 0.006). A subsequent VOI/ROI analysis showed no association between polygenic risk for depression and either grey matter volume or cortical thickness. We found no associations between cortical complexity and polygenic risk for either schizophrenia, bipolar disorder or psychiatric cross-disorder when correcting for multiple testing.

Changes in cortical complexity associated with polygenic risk for depression might facilitate well-established volume changes in orbitofrontal cortices in depression. Despite the absence of psychopathology, changed cortical complexity that parallels polygenic risk for depression might also change reward systems, which are also structurally affected in patients with depressive syndrome.

Considering the heterogeneity of depression, distinct depressive symptom dimensions may be differentially associated with more objective actigraphy-based estimates of physical activity (PA), sleep and circadian rhythm (CR). We examined the association between PA, sleep, and CR assessed with actigraphy and symptom dimensions (i.e. mood/cognition, somatic/vegetative, sleep).

Fourteen-day actigraphy data of 359 participants were obtained from the Netherlands Study of Depression and Anxiety. PA, sleep, and CR estimates included gross motor activity (GMA), sleep duration (SD), sleep efficiency (SE), relative amplitude between daytime and night-time activity (RA) and sleep midpoint. The 30-item Inventory of Depressive Symptomatology was used to assess depressive symptoms, which were categorised in three depression dimensions: mood/cognition, somatic/vegetative, and sleep.

GMA and RA were negatively associated with higher score on all three symptom dimensions: mood/cognition (GMA: β = −0.155, p < 0.001; RA: β = −0.116, p = 0.002), somatic/vegetative (GMA: β = −0.165, p < 0.001; RA: β = −0.133, p < 0.001), sleep (GMA: β = −0.169, p < 0.001; RA: β = −0.190, p < 0.001). The association with sleep was more pronounced for two depression dimensions: longer SD was linked to somatic/vegetative (β = 0.115, p = 0.015) dimension and lower SE was linked to sleep (β = −0.101, p = 0.011) dimension.

As three symptom dimensions were associated with actigraphy-based low PA and dampened CR, these seem to be general indicators of depression. Sleep disturbances appeared more linked to the somatic/vegetative and sleep dimensions; the effectiveness of sleep interventions in patients reporting somatic/vegetative symptoms may be explored, as well as the potential of actigraphy to monitor treatment response to such interventions.

Whether smoking should be regarded as a risk factor for mental disorders remains unresolved. Prescribed psychotropic drugs can be used as indications for mental disorders. We investigated how smoking was prospectively related to prescription of antipsychotics, mood stabilizers, antidepressants, and anxiolytics.

Information about smoking, including the Fagerström Test for Nicotine Dependence, and relevant confounders, were obtained from the population-based Young in Norway Study (N = 2602), with four data collection waves between 1992 and 2006. These survey data were linked with information on prescriptions for psychotropic drugs from the comprehensive, nationwide Norwegian Prescription Database from 2007 to 2015.

Daily smoking with high dependence in 2006 at age 28.5 (s.d. = 2.0) was associated with filling prescriptions of antipsychotics (OR, 6.57, 95% CI 2.19–19.70, p = 0.001), mood stabilizers (OR, 7.11, 95% CI 2.51–20.15, p < 0.001) and antidepressants (OR, 1.91, 95% CI 1.13–3.23, p = 0.016) 1–9 years later. Associations remained significant after adjustment for a variety of potential confounders measured before the assessment of smoking, including sociodemographic background, conduct problems, cannabis use, mental distress, and previous prescriptions for psychotropic medications. The association between smoking and prescription of anxiolytics was weaker and more unstable.

In this study of young adults, daily smoking with high dependence was associated with later prescriptions of antipsychotics, mood stabilizers and antidepressants, indicating smoking as a risk factor for mental disorders treated with these drugs.

Childhood adversity (CA) is commonly associated with an increased risk of subsequent psychopathology. It is important to identify potential mediators of this relationship which can allow for the development of interventions. In a large population-based cohort study we investigated the relationship between CA and late adolescent psychopathology and early adolescent candidate mediators of this relationship.

We used data from three waves (n = 6039) of Cohort 98′ of the Growing up in Ireland Study (age 9, 13 and 17). We used doubly robust counterfactual analyses to investigate the relationship between CA (reported at age-9) with psychopathology (internalizing and externalizing problems), measured using the Strengths and Difficulties Questionnaire at age-17. Counterfactual and traditional mediation was used to investigate the mediating effects of the parent-child relationship, peer relations, self-concept, computer usage and physical activity.

CA was associated with an increased risk of internalizing and externalizing problems at age-17. Parent-child conflict mediated 35 and 42% of the relationship between CA and late adolescent externalizing problems and internalizing problems, respectively. Self-concept and physical activity mediated an additional proportion of the relationship between CA and internalizing problems. These results were robust to unmeasured confounding.

Parent-child conflict explains more than a third of the relationship between CA and later psychopathology. Self-concept and physical activity explain the additional proportion of the relationship between CA and internalizing problems. This suggests that these factors may be good targets for intervention in young people who have experienced CA to prevent subsequent psychopathology.

Schizophrenia (SZ) is associated with thalamic dysconnectivity. Compared to healthy controls (HCs), individuals with SZ have hyperconnectivity with sensory regions, and hypoconnectivity with cerebellar, thalamic, and prefrontal regions. Despite replication of this pattern in chronically ill individuals, less is known about when these abnormalities emerge in the illness course and if they are present prior to illness onset.

Resting-state functional magnetic resonance imaging data were collected from psychosis risk syndrome (PRS) youth (n = 45), early illness SZ (ESZ) (n = 74) patients, and HCs (n = 85). Age-adjusted functional connectivity, seeded from the thalamus, was compared among the groups.

Significant effects of group were observed in left and right middle temporal regions, left and right superior temporal regions, left cerebellum, and bilateral thalamus. Compared to HCs, ESZ demonstrated hyperconnectivity to all temporal lobe regions and reduced connectivity with cerebellar, anterior cingulate, and thalamic regions. Compared to HCs, PRS demonstrated hyperconnectivity with the left and right middle temporal regions, and hypoconnectivity with the cerebellar and other thalamic regions. Compared to PRS participants, ESZ participants were hyperconnected to temporal regions, but did not differ from PRS in hypoconnectivity with cerebellar and thalamic regions. Thalamic dysconnectivity was unrelated to positive symptom severity in ESZ or PRS groups.

PRS individuals demonstrated an intermediate level of thalamic dysconnectivity, whereas ESZ showed a pattern consistent with prior observations in chronic samples. These cross-sectional findings suggest that thalamic dysconnectivity may occur prior to illness onset and become more pronounced in early illness stages.

The etiology of schizophrenia (SZ) is proposed to include an interplay between a genetic risk for disease development and the biological environment of pregnancy and birth, where early adversities may contribute to the poorer developmental outcome. We investigated whether a history of birth asphyxia (ASP) moderates the relationship between intracranial volume (ICV) and intelligence in SZ, bipolar disorder (BD) and healthy controls (HC).

Two hundred seventy-nine adult patients (18–42 years) on the SZ and BD spectrums and 216 HC were evaluated for ASP based on information from the Medical Birth Registry of Norway. Participants underwent structural magnetic resonance imaging (MRI) to estimate ICV and intelligence quotient (IQ) assessment using the Wechsler Abbreviated Scale of Intelligence (WASI). Multiple linear regressions were used for analyses.

We found a significant three-way interaction (ICV × ASP × diagnosis) on the outcome variable, IQ, indicating that the correlation between ICV and IQ was stronger in patients with SZ who experienced ASP compared to SZ patients without ASP. This moderation by ASP was not found in BD or HC groups. In patients with SZ, the interaction between ICV and a history of the ASP was specifically related to the verbal subcomponent of IQ as measured by WASI.

The significant positive association between ICV and IQ in patients with SZ who had experienced ASP might indicate abnormal neurodevelopment. Our findings give support for ICV together with verbal intellectual abilities as clinically relevant markers that can be added to prediction tools to enhance evaluations of SZ risk.

Two prominent risk factors for major depressive disorder (MDD) are childhood maltreatment (CM) and familial risk for MDD. Despite having these risk factors, there are individuals who maintain mental health, i.e. are resilient, whereas others develop MDD. It is unclear which brain morphological alterations are associated with this kind of resilience. Interaction analyses of risk and diagnosis status are needed that can account for complex adaptation processes, to identify neural correlates of resilience.

We analyzed brain structural data (3T magnetic resonance imaging) by means of voxel-based morphometry (CAT12 toolbox), using a 2 × 2 design, comparing four groups (N = 804) that differed in diagnosis (healthy v. MDD) and risk profiles (low-risk, i.e. absence of CM and familial risk v. high-risk, i.e. presence of both CM and familial risk). Using regions of interest (ROIs) from the literature, we conducted an interaction analysis of risk and diagnosis status.

Volume in the left middle frontal gyrus (MFG), part of the dorsolateral prefrontal cortex (DLPFC), was significantly higher in healthy high-risk individuals. There were no significant results for the bilateral superior frontal gyri, frontal poles, pars orbitalis of the inferior frontal gyri, and the right MFG.

The healthy high-risk group had significantly higher volumes in the left DLPFC compared to all other groups. The DLPFC is implicated in cognitive and emotional processes, and higher volume in this area might aid high-risk individuals in adaptive coping in order to maintain mental health. This increased volume might therefore constitute a neural correlate of resilience to MDD in high risk.

The hyper-function of the striatal dopamine system has been suggested to underlie key pathophysiological mechanisms in schizophrenia. Moreover, patients have been observed to present a significant elevation of dopamine receptor availability compared to healthy controls. Although it is difficult to measure dopamine levels directly in humans, neurochemical imaging techniques such as single-photon emission computed tomography (SPECT) provide indirect indices of in vivo dopamine synthesis and release, and putative synaptic levels.

We focused on the role of dopamine postsynaptic regulation using [123I] iodobenzamide (IBZM) SPECT. We compared D2/3 receptor availability between 53 healthy controls and 21 medication-naive patients with recent-onset schizophrenia.

The mean specific striatal binding showed no significant difference between patients and controls (estimated difference = 0.001; 95% CI −0.11 to 0.11; F = 0.00, df = 1, 69; p = 0.99). There was a highly significant effect of age whereby IBZM binding declined with advancing age [estimated change per decade of age = −0.01(binding ratio); 95% CI −0.01 to −0.004; F = 11.5, df = 1, 69; p = 0.001]. No significant correlations were found between the mean specific striatal binding and psychopathological or cognitive rating scores.

Medication-naïve patients with recent-onset schizophrenia have similar D2/3 receptor availability to healthy controls. We suggest that, rather than focusing exclusively on postsynaptic receptors, future treatments should target the presynaptic control of dopamine synthesis and release.

Maternal age has progressively increased in industrialized countries. Most studies focus on the consequences of delayed motherhood for women's physical and mental health, but little is known about potential effects on infants' neurodevelopment. This prospective study examines the association between maternal age and offspring neurodevelopment in terms of both psychomotor development (Ages & Stages Questionnaires-3) and emotional competences (Early Childhood Behavior Questionnaire).

We evaluated a cohort of healthy pregnant women aged 20–41 years and their offspring, assessed at 38 weeks gestation (n = 131) and 24 months after birth (n = 101). Potential age-related variables were considered (paternal age, education level, parity, social support, maternal cortisol levels, and maternal anxiety and depressive symptoms). Bayesian ordinal regression models were performed for each neurodevelopmental outcome.

Maternal age was negatively associated with poor child development in terms of personal-social skills [odds ratio (OR) −0.13, 95% confidence interval (CI) 0.77–0.99] and with difficult temperament in terms of worse emotional regulation (OR −0.13, 95% CI 0.78–0.96) and lower positive affect (OR 0.16, 95% CI 0.75–0.95). As for age-related variables, whereas maternal anxiety symptoms and cortisol levels were also correlated with poor child development and difficult temperament, maternal social support and parental educational level were associated with better psychomotor and emotional competences.

Increasing maternal age may be associated with child temperament difficulties and psychomotor delay in terms of social interaction skills. Early detection of neurodevelopment difficulties in these babies would allow preventive psychosocial interventions to avoid future neuropsychiatric disorders.

One putative psychological mechanism through which momentary stress impacts on psychosis in individuals with increased liability to the disorder is via affective disturbance. However, to date, this has not been systematically tested. We aimed to investigate whether (i) cross-sectional and temporal effects of momentary stress on psychotic experiences via affective disturbance, and (ii) the reverse pathway of psychotic experiences on stress via affective disturbance were modified by familial liability to psychosis.

The Experience Sampling Method was used in a pooled data set of six studies with three groups of 245 individuals with psychotic disorder, 165 unaffected first-degree relatives, and 244 healthy control individuals to index familial liability. Multilevel moderated mediation models were fitted to investigate indirect effects across groups cross-sectionally and multilevel cross-lagged panel models to investigate temporal effects in the proposed pathways across two measurement occasions.

Evidence on indirect effects from cross-sectional models indicated that, in all three groups, effects of stress on psychotic experiences were mediated by negative affect and, vice versa, effects of psychotic experiences on stress were mediated by negative affect, with all indirect effects being weakest in relatives. Longitudinal modelling of data provided no evidence of temporal priority of stress in exerting its indirect effects on psychotic experiences via affective disturbance or, vice versa.

Our findings tentatively suggest a rapid vicious cycle of stress impacting psychotic experiences via affective disturbances, which does, however, not seem to be consistently modified by familial liability to psychosis.

Preliminary evidence suggests beneficial effects of cognitive remediation in depression. An update of the current evidence is needed. The aim was to systematically assess the effectiveness of cognitive remediation in depression on three outcomes.

The meta-analysis was pre-registered on PROSPERO (CRD42019124316). PubMed, PsycINFO, Embase and Cochrane Library were searched on 2 February 2019 and 8 November 2020 for peer-reviewed published articles. We included randomized and non-randomized clinical trials comparing cognitive remediation to control conditions in adults with primary depression. Random-effects models were used to calculate Hedges' g, and moderators were assessed using mixed-effects subgroup analyses and meta-regression. Main outcome categories were post-treatment depressive symptomatology (DS), cognitive functioning (CF) and daily functioning (DF).

We identified 5221 records and included 21 studies reporting on 24 comparisons, with 438 depressed patients receiving cognitive remediation and 540 patients in a control condition. We found a small effect on DS (g = 0.28, 95% CI 0.09–0.46, I2 40%), a medium effect on CF (g = 0.60, 95% CI 0.37–0.83, I2 44%) and a small effect on DF (g = 0.22, 95% CI 0.06–0.39, I2 3%). There were no significant effects at follow-up. Confounding bias analyses indicated possible overestimation of the DS and DF effects in the original studies.

Cognitive remediation in depression improves CF in the short term. The effects on DS and DF may have been overestimated. Baseline depressive symptom severity should be considered when administering cognitive remediation.

It has been suggested that individual differences in temperament could be involved in the (non-)response to antidepressant (AD) treatment. However, how neurobiological processes such as brain glucose metabolism may relate to personality features in the treatment-resistant depressed (TRD) state remains largely unclear.

To examine how brainstem metabolism in the TRD state may predict Cloninger's temperament dimensions Harm Avoidance (HA), Novelty Seeking (NS), and Reward Dependence (RD), we collected 18fluorodeoxyglucose positron emission tomography (18FDG PET) scans in 40 AD-free TRD patients. All participants were assessed with the Temperament and Character Inventory (TCI). We applied a multiple kernel learning (MKL) regression to predict the HA, NS, and RD from brainstem metabolic activity, the origin of respectively serotonergic, dopaminergic, and noradrenergic neurotransmitter (NT) systems.

The MKL model was able to significantly predict RD but not HA and NS from the brainstem metabolic activity. The MKL pattern regression model identified increased metabolic activity in the pontine nuclei and locus coeruleus, the medial reticular formation, the dorsal/median raphe, and the ventral tegmental area that contributed to the predictions of RD.

The MKL algorithm identified a likely metabolic marker in the brainstem for RD in major depression. Although 18FDG PET does not investigate specific NT systems, the predictive value of brainstem glucose metabolism on RD scores however indicates that this temperament dimension in the TRD state could be mediated by different monoaminergic systems, all involved in higher order reward-related behavior.

Coronavirus-related conspiracy theories (CT) have been found to be associated with fewer pandemic containment-focused behaviors. It is therefore important to evaluate associated cognitive factors. We aimed to obtain first endorsement rate estimates of coronavirus-related conspiracy beliefs in a German-speaking general population sample and investigate whether delusion-related reasoning biases and paranoid ideation are associated with such beliefs.

We conducted a cross-sectional non-probability online study, quota-sampled for age and gender, with 1684 adults from Germany and German-speaking Switzerland. We assessed general and specific coronavirus conspiracy beliefs, reasoning biases [jumping-to-conclusions bias (JTC), liberal acceptance bias (LA), bias against disconfirmatory evidence (BADE), possibility of being mistaken (PM)], and paranoid ideation, using established experimental paradigms and self-report questionnaires.

Around 10% of our sample endorsed coronavirus-related CT beliefs at least strongly, and another 20% to some degree. Overall endorsement was similar to levels observed in a UK-based study (Freeman et al., 2020b). Higher levels of conspiracy belief endorsement were associated with greater JTC, greater LA, greater BADE, higher PM, and greater paranoid ideation. Associations were mostly small to moderate and best described by non-linear relationships.

A noticeable proportion of our sample recruited in Germany and German-speaking Switzerland endorsed coronavirus conspiracy beliefs strongly or to some degree. These beliefs are associated with reasoning biases studied in delusion research. The non-probability sampling approach limits the generalizability of findings. Future longitudinal and experimental studies investigating conspiracy beliefs along the lines of reasoning are encouraged to validate reasoning aberrations as risk factors.

The symptoms of obsessive−compulsive disorder (OCD) are highly heterogeneous and it is unclear what is the optimal way to conceptualize this heterogeneity. This study aimed to establish a comprehensive symptom structure model of OCD across the lifespan using factor and network analytic techniques.

A large multinational cohort of well-characterized children, adolescents, and adults diagnosed with OCD (N = 1366) participated in the study. All completed the Dimensional Yale-Brown Obsessive−Compulsive Scale, which contains an expanded checklist of 87 distinct OCD symptoms. Exploratory and confirmatory factor analysis were used to outline empirically supported symptom dimensions, and interconnections among the resulting dimensions were established using network analysis. Associations between dimensions and sociodemographic and clinical variables were explored using structural equation modeling (SEM).

Thirteen first-order symptom dimensions emerged that could be parsimoniously reduced to eight broad dimensions, which were valid across the lifespan: Disturbing Thoughts, Incompleteness, Contamination, Hoarding, Transformation, Body Focus, Superstition, and Loss/Separation. A general OCD factor could be included in the final factor model without a significant decline in model fit according to most fit indices. Network analysis showed that Incompleteness and Disturbing Thoughts were most central (i.e. had most unique interconnections with other dimensions). SEM showed that the eight broad dimensions were differentially related to sociodemographic and clinical variables.

Future research will need to establish if this expanded hierarchical and multidimensional model can help improve our understanding of the etiology, neurobiology and treatment of OCD.