Evidence supports the use of group therapy for symptom reduction and improving functioning in people with psychosis. However, research guidelines highlight the importance of establishing the feasibility of interventions. Adherence is an important indicator of feasibility and an essential step in supporting the development of the evidence base for group interventions. This review aims to estimate adherence, and possible barriers and facilitators, to psychotherapeutic groups in people with psychosis.

Embase, Ovid MEDLINE and PsycINFO databases were searched for cross-referencing terms related to group therapy and psychosis. Studies were assessed against inclusion criteria and methodological quality was evaluated. Data wasextracted from each paper including the average session attendance, demographic, clinical, study and therapy-related characteristics and the impact of these on adherence levels evaluated.

Fifty-nine original research papers were included, reporting on 52 independent studies which consisted of 66 therapy groups comprised of 2109 participants. Average adherence was 76.4% (s.d. = 17.4). Adherence was improved by receiving incentives and was higher in participants of older age. Study sample size was inversely associated with adherence levels. Study quality was variable with approximately 61.5% found to be at risk of bias. The results support the feasibility of group therapy and suggest that adherence in people with psychosis is not dissimilar to those for people experiencing common mental health difficulties. These findings, alongside efficacy evidence, support the use of group interventions in people with psychosis but also highlight the need for further high-quality research on the efficacy for these approaches.

Promulgating a continuum model of mental health and mental illness has been proposed as a way to reduce stigma by decreasing notions of differentness. This systematic review and meta-analysis examines whether continuum beliefs are associated with lower stigma, and whether continuum interventions reduce stigma.

Following a pre-defined protocol (PROSPERO: CRD42019123606), we searched three electronic databases (PubMed, Web of Science, and PsycINFO) yielding 6726 studies. After screening, we included 33 studies covering continuum beliefs, mental illness, and stigma. Of these, 13 studies were included in meta-analysis.

Continuum beliefs are consistently associated with lower stigma. Interventions were effective at manipulating continuum beliefs but differ in their effects on stigmatising attitudes.

We discuss whether and to what extent attitudes towards people with mental illness can be improved by providing information on a mental health-mental illness continuum. It appeared to be relevant whether interventions promoted a feeling of ‘us’ and a process of identification with the person with mental illness. We discuss implications for the design of future interventions.

Affective temperaments have been considered antecedents of major depressive disorder (MDD). However, little is known about how the covariation between alterations in brain activity and distinct affective temperaments work collaboratively to contribute to MDD. Here, we focus on the insular cortex, a critical hub for the integration of subjective feelings, emotions, and motivations, to examine the neural correlates of affective temperaments and their relationship to depressive symptom dimensions.

Twenty-nine medication-free patients with MDD and 58 healthy controls underwent magnetic resonance imaging scanning and completed the Temperament Evaluation of Memphis, Pisa, Paris and San Diego (TEMPS). Patients also received assessments of the Hamilton Depression Rating Scale (HDRS). We used multivariate analyses of partial least squares regression and partial correlation analyses to explore the associations among the insular activity, affective temperaments, and depressive symptom dimensions.

A profile (linear combination) of increased fractional amplitude of low-frequency fluctuations (fALFF) of the anterior insular subregions (left dorsal agranular–dysgranular insula and right ventral agranuar insula) was positively associated with an affective-temperament (depressive, irritable, anxious, and less hyperthymic) profile. The covariation between the insula-fALFF profile and the affective-temperament profile was significantly correlated with the sleep disturbance dimension (especially the middle and late insomnia scores) in the medication-free MDD patients.

The resting-state spontaneous activity of the anterior insula and affective temperaments collaboratively contribute to sleep disturbances in medication-free MDD patients. The approach used in this study provides a practical way to explore the relationship of multivariate measures in investigating the etiology of mental disorders.

Multiple studies have found a reduced reward positivity (RewP) among individuals with major depressive disorder (MDD). Event-related potential studies have also reported blunted neural responses to pleasant pictures in MDD as reflected by the late positive potential (LPP). These deficits have been interpreted broadly in terms of anhedonia and decreased emotional engagement characteristic of depression.

In the current study, a community-based sample of 83 participants with current MDD and 45 healthy individuals performed both a guessing task and a picture viewing paradigm with neutral and pleasant pictures to assess the RewP and the LPP, respectively.

We found that both RewP and LPP to pleasant pictures were reduced in the MDD group; moreover, RewP and LPP were both independent predictors of MDD status. Within the MDD group, a smaller RewP predicted impaired mood reactivity in younger but not older participants. Smaller LPP amplitudes were associated with increased anhedonia severity in the MDD group.

These data replicate and merge separate previous lines of research, and suggest that a blunted RewP and LPP reflect independent neural deficits in MDD – which could be used in conjunction to improve the classification of depression.

Accumulating evidence suggests that many psychiatric disorders etiologically represent the extreme end of dimensionally distributed features rather than distinct entities. The extent to which this applies to eating disorders (EDs) is unknown.

We investigated if there is similar etiology in (a) the continuous distribution of the Eating Disorder Inventory-2 (EDI-2), (b) the extremes of EDI-2 score, and (c) registered ED diagnoses, in 1481 female twin pairs at age 18 years (born 1992–1999). EDI-2 scores were self-reported at age 18. ED diagnoses were identified through the Swedish National Patient Register, parent-reported treatment and/or self-reported purging behavior of a frequency and duration consistent with DSM-IV criteria. We differentiated between anorexia nervosa (AN) and other EDs.

The heritability of the EDI-2 score was 0.65 (95% CI 0.61–0.68). The group heritabilities in DeFries–Fulker extremes analyses were consistent over different percentile-based extreme groups [0.59 (95% CI 0.37–0.81) to 0.65 (95% CI 0.55–0.75)]. Similarly, the heritabilities in liability threshold models were consistent over different levels of severity. In joint categorical-continuous models, the twin-based genetic correlation was 0.52 (95% CI 0.39–0.65) between EDI-2 score and diagnoses of other EDs, and 0.26 (95% CI 0.08–0.42) between EDI-2 score and diagnoses of AN. The non-shared environmental correlations were 0.52 (95% CI 0.32–0.70) and 0.60 (95% CI 0.38–0.79), respectively.

Our findings suggest that some EDs can partly be conceptualized as the extreme manifestation of continuously distributed ED features. AN, however, might be more distinctly genetically demarcated from ED features in the general population than other EDs.

Early irritability predicts a broad spectrum of psychopathology spanning both internalizing and externalizing disorders, rather than any particular disorder or group of disorders (i.e. multifinality). Very few studies, however, have examined the developmental mechanisms by which it leads to such phenotypically diverse outcomes. We examined whether variation in the diurnal pattern of cortisol moderates developmental pathways between preschool irritability and the subsequent emergence of internalizing and externalizing symptoms 9 years later.

When children were 3 years old, mothers were interviewed about children's irritability and completed questionnaires about their children's psychopathology. Six years later, children collected saliva samples at wake-up and bedtime on three consecutive days. Diurnal cortisol patterns were modeled as latent difference scores between evening and morning samples. When children were approximately 12 years old, mothers again completed questionnaires about their children's psychopathology.

Among children with higher levels of irritability at age 3, a steeper diurnal cortisol slope at age 9 predicted greater internalizing symptoms and irritability at age 12, whereas a blunted slope at age 9 predicted greater externalizing symptoms at age 12, adjusting for baseline and concurrent symptoms.

Our results suggest that variation in stress system functioning can predict and differentiate developmental trajectories of early irritability that are relatively more internalizing v. those in which externalizing symptoms dominate in pre-adolescence.

Lesbian, bisexual, or gay individuals (LBGs) have an increased risk for mental health problems compared to heterosexuals, but this association has sparsely been investigated for psychotic disorders. The aim of this study was: (1) to examine whether LBG sexual orientation is more prevalent in individuals with a non-affective psychotic disorder (NAPD) than in people without a psychotic disorder; and if so, (2) to explore possible mediating pathways.

Sexual orientation was assessed in the 6-year follow-up assessment of the Dutch Genetic Risk and Outcome of Psychosis study (GROUP), a case–control study with 1547 participants (582 patients with psychotic disorder, 604 siblings, and 361 controls). Binary logistic regression analyses were used to calculate the risk of patients with a psychotic disorder being LBG, compared to siblings and controls. Perceived discrimination, history of bullying, childhood trauma (CT), and sexual identity disclosure were investigated as potential mediating variables.

The proportion of individuals with LBG orientation was 6.8% in patients (n = 40), 4.3% in siblings (n = 26), and 2.5% in controls (n = 10). The age- and gender-adjusted odds ratio of LBG for patients was 1.57 (95% CI 1.08–2.27; p = 0.019), compared to siblings and controls. Discrimination, bullying, and CT all partially mediated this association.

Adverse social experiences related to sexual minority status may increase the risk for NAPD. Sexual identity, behavior, and difficulties need more attention in everyday clinical practice.

Early callous-unemotional (CU) behaviors identify children at risk for severe and persistent aggression and antisocial behavior. Recent work suggests that fearlessness and low social affiliation are implicated in the etiology of CU behaviors, although more research is needed to clarify these etiological pathways, as well as the role of parenting.

Using a sample of preschoolers (N = 620), we examined pathways between observed fear in response to social and non-social stimuli and observed social affiliation during social interactions at age 3 and increases child CU behaviors and oppositional-defiant behaviors from ages 3 to 5. To elucidate the role of parenting in exacerbating or buffering the relationships between low fear and social affiliation and CU behaviors, we tested whether parental harshness or low warmth moderated these pathways.

Fearlessness and low social affiliation uniquely predicted increases in CU behaviors, but not oppositional-defiant behaviors, from ages 3 to 5. Moreover, there was evidence for differential moderation of the fear pathway by harsh parenting, such that harsh parenting predicted increases in CU behaviors in fearless children but increases in oppositional-defiant behaviors in fearful children.

Fearlessness and low social affiliation contribute to the development of CU behaviors. Harsh parenting can exacerbate the risky fearlessness pathway. Preventative interventions aimed at reducing risk for CU behaviors and persistent aggression and antisocial behavior should target socioaffiliative processes and provide parents with strategies and training to manage and scaffold rule-compliant behavior when children show low fearful arousal.

Accurate perception of visual contours is essential for seeing and differentiating objects in the environment. Both the ability to detect visual contours and the influence of perceptual context created by surrounding stimuli are diminished in people with schizophrenia (SCZ). The central aim of the present study was to better understand the biological underpinnings of impaired contour integration and weakened effects of perceptual context. Additionally, we sought to determine whether visual perceptual abnormalities reflect genetic factors in SCZ and are present in other severe mental disorders.

We examined behavioral data and event-related potentials (ERPs) collected during the perception of simple linear contours embedded in similar background stimuli in 27 patients with SCZ, 23 patients with bipolar disorder (BP), 23 first-degree relatives of SCZ, and 37 controls.

SCZ exhibited impaired visual contour detection while BP exhibited intermediate performance. The orientation of neighboring stimuli (i.e. flankers) relative to the contour modulated perception across all groups, but SCZ exhibited weakened suppression by the perceptual context created by flankers. Late visual (occipital P2) and cognitive (centroparietal P3) neural responses showed group differences and flanker orientation effects, unlike earlier ERPs (occipital P1 and N1). Moreover, behavioral effects of flanker context on contour perception were correlated with modulation in P2 & P3 amplitudes.

In addition to replicating and extending findings of abnormal contour integration and visual context modulation in SCZ, we provide novel evidence that the abnormal use of perceptual context is associated with higher-order sensory and cognitive processes.

Experience of emotion is closely linked to valuation. Mood can be viewed as a bias to experience positive or negative emotions and abnormally biased subjective reward valuation and cognitions are core characteristics of major depression.

Thirty-four unmedicated subjects with major depressive disorder and controls estimated the probability that fractal stimuli were associated with reward, based on passive observations, so they could subsequently choose the higher of either their estimated fractal value or an explicitly presented reward probability. Using model-based functional magnetic resonance imaging, we estimated each subject's internal value estimation, with psychophysiological interaction analysis used to examine event-related connectivity, testing hypotheses of abnormal reward valuation and cingulate connectivity in depression.

Reward value encoding in the hippocampus and rostral anterior cingulate was abnormal in depression. In addition, abnormal decision-making in depression was associated with increased anterior mid-cingulate activity and a signal in this region encoded the difference between the values of the two options. This localised decision-making and its impairment to the anterior mid-cingulate cortex (aMCC) consistent with theories of cognitive control. Notably, subjects with depression had significantly decreased event-related connectivity between the aMCC and rostral cingulate regions during decision-making, implying impaired communication between the neural substrates of expected value estimation and decision-making in depression.

Our findings support the theory that abnormal neural reward valuation plays a central role in major depressive disorder (MDD). To the extent that emotion reflects valuation, abnormal valuation could explain abnormal emotional experience in MDD, reflect a core pathophysiological process and be a target of treatment.

The trajectories of psychological distress differ between individuals, but these differences can be difficult to understand because the measures contain both consistent and situational features; however, in longitudinal studies these sources of information can be disentangled. In addition to occasion-specific features, interindividual differences can be decomposed into two sources of information: trait and carry-over effects between neighboring occasions that are not related to the trait (i.e. accumulated situational effects).

To disentangle these three sources of variance throughout adulthood, the consistency (trait and accumulated situational effects) and occasion specificity of nine indicators of psychological distress from the Malaise Inventory were examined in two birth cohorts, the 1958 National Child Development Study (NCDS58), and the 1970 British Cohort Study (BCS70).

The scale was administered at ages 23, 33, 42, and 50 in NCDS58 (n = 7147), and at ages 26, 30, 34, and 42 in BCS70 (n = 6859). For each psychological symptom, more variance was consistent than occasion-specific. The majority of the consistency was due to trait variance as opposed to accumulated situational effects, indicating that an individual predisposed to be distressed at the beginning of the study remained more likely to be distressed over the whole period. Symptoms of rage were notably more consistent among males than females in both cohorts (78.1% and 81.3% variance explained by trait in NCDS58 and BCS70, respectively), and among females in the NCDS58 (69%).

Symptoms of psychological distress exhibited high stability throughout adulthood, especially among men, due mostly to interindividual trait differences.

In the past decade, network analysis (NA) has been applied to psychopathology to quantify complex symptom relationships. This statistical technique has demonstrated much promise, as it provides researchers the ability to identify relationships across many symptoms in one model and can identify central symptoms that may predict important clinical outcomes. However, network models are highly influenced by node selection, which could limit the generalizability of findings. The current study (N = 6850) tests a comprehensive, cognitive–behavioral model of eating-disorder symptoms using items from two, widely used measures (Eating Disorder Examination Questionnaire and Eating Pathology Symptoms Inventory).

We used NA to identify central symptoms and compared networks across the duration of illness (DOI), as chronicity is one of the only known predictors of poor outcome in eating disorders (EDs).

Our results suggest that eating when not hungry and feeling fat were the most central symptoms across groups. There were no significant differences in network structure across DOI, meaning the connections between symptoms remained relatively consistent. However, differences emerged in central symptoms, such that cognitive symptoms related to overvaluation of weight/shape were central in individuals with shorter DOI, and behavioral central symptoms emerged more in medium and long DOI.

Our results have important implications for the treatment of individuals with enduring EDs, as they may have a different core, maintaining symptoms. Additionally, our findings highlight the importance of using comprehensive, theoretically- or empirically-derived models for NA.

We examine the performance of the Diagnostic and Statistical Manual of Mental Disorders-fifth edition (DSM-5) persistent complex bereavement-related disorder (PCBD) criteria in bereaved adults to identify prolonged grief cases determined prospectively.

Bereaved adults (n = 138) were assessed at 8, 21, 32, 67, and 90 months after the sudden death of a spouse or close relative. We used latent class growth analysis to identify the longitudinal trajectories of grief assessed using the Inventory for Complicated Grief. To validate the trajectory that corresponded to prolonged grief, we examined the baseline predictors of these trajectories and their relationship with functional impairment.

We found three distinct trajectories of grief reactions. One of these trajectories (13.8%) showed high and sustained grief reactions that persisted for almost 7.5 years after the death. Participants with prolonged grief showed greater functional impairment [relative risk ratio (RRR) = 0.82, 95% confidence interval (CI): 0.70 to −0.97; p = 0.02] and higher self-reported depression (RRR = 1.21, 95% CI 1.09 to 1.96; p = 0.001) than participants whose grief reactions subsided over time. The original PCBD (requiring 6 criterion C symptoms) criteria correctly identified cases (57.9–94.7%) with perfect specificity (100%) but low to high sensitivity (5.6–81.3%); however, its sensitivity increased when revising criterion C to require ⩾3 (45.5–94.1%). The dimensional approach showed high sensitivity (0.50–1) and specificity (0.787–0.97).

We recommend revisions to the PCBD criteria, which are overly restrictive and may exclude cases with clinically significant grief-related distress and impairment. In the meantime, clinicians need to monitor grief symptoms over time using available dimensional approaches to reduce the burden of grief.

The dopamine transporter gene (DAT1), striatal network dysfunction, and visual memory deficits have been consistently reported to be associated with attention-deficit/hyperactivity disorder (ADHD). This study aimed to examine the effects of the DAT1 rs27048 (C)/rs429699 (T) haplotype on striatal functional connectivity and visual memory performance in youths with ADHD.

After excluding those who had excessive head motion, a total of 96 drug-naïve youths with ADHD and 114 typically developing (TD) youths were assessed with the resting-state functional magnetic resonance imaging and the delayed matching to sample (DMS) task for visual memory. We examined the effects of ADHD, DAT1 CT haplotype, and the ADHD × CT haplotype interaction on the functional connectivity of five striatal seeds. We also correlated visual memory performance with the functional connectivity of striatal subregions, which showed significant diagnosis × genotype interactions.

Compared with TD youths, ADHD youths showed significant hypoconnectivity of the left dorsal caudate (DC) with bilateral sensorimotor clusters. Significant diagnosis × genotype interactions were found in the connectivity between the left DC and the right sensorimotor cluster, and between the right DC and the left dorsolateral prefrontal/bilateral anterior cingulate clusters. Furthermore, the connectivity of the left DC showing significant diagnosis × genotype interactions was associated with DMS performance in youths with ADHD who carried the DAT1 CT haplotype.

A novel gene-brain-behavior association between the left DC functional connectivity and visual memory performance in ADHD youths with the DAT1 rs27048 (C)/rs429699 (T) haplotype suggests a differential effect of DAT1 genotype altering specific brain function causing neuropsychological dysfunction in ADHD.

We sought to quantify and investigate the causal nature of the association between resilience at age 18 and future drug abuse (DA).

In a national sample of Swedish men (n = 1 392 800), followed for a mean of 30.3 years, resilience was assessed during military conscription and DA defined from medical, criminal and pharmacy registers. For causal inference, we utilized three methods: (i) instrumental variable analyses with the month of birth as the instrument; (ii) co-relative analyses using the general population, cousins, siblings and monozygotic twins; and (iii) propensity scoring on a subsample (n = 48 548) with strong resilience predictors. Cox proportional hazards models were utilized to examine survival time till DA diagnosis.

Low resilience was most robustly predicted from internalizing symptoms. Lower levels of standardized resilience strongly predicted the risk for DA (HR = 2.31, 95% CIs 2.28–2.33). In instrumental, co-relative, and propensity score analyses, the association between resilience and DA was estimated at HR = 3.06 (2.44–3.85), 1.34 (1.28–1.39), and 1.40 (1.28–1.53), respectively. Sensitivity analyses suggested that our instrument was weak and, despite our large sample, likely under-estimated confounding.

Low resilience strongly predicts DA risk. Three different causal analysis methods, with divergent assumptions, concurred in estimating that an appreciable proportion of this association was causal, probably around 40%, with the remainder arising from confounding variables many of which are likely familial. Consistent with prior interventions focused on substance use prevention, our results suggest that prevention programs that increase resilience in adolescence should meaningfully reduce the long-term risk for DA.

Self-administered questionnaires are widely used in primary care and other clinical settings to assess the severity of depressive symptoms and monitor treatment outcomes. Qualitative studies have found that changes in questionnaire scores might not fully capture patients' experience of changes in their mood but there are no quantitative studies of this issue. We examined the extent to which changes in scores from depression questionnaires disagreed with primary care patients' perceptions of changes in their mood and investigated factors influencing this relationship.

Prospective cohort study assessing patients on four occasions, 2 weeks apart. Patients (N = 554) were recruited from primary care surgeries in three UK sites (Bristol, Liverpool and York) and had reported depressive symptoms or low mood in the past year [68% female, mean age 48.3 (s.d. 12.6)]. Main outcome measures were changes in scores on patient health questionnaire (PHQ-9) and beck depression inventory (BDI-II) and the patients' own ratings of change.

There was marked disagreement between clinically important changes in questionnaire scores and patient-rated change, with disagreement of 51% (95% CI 46–55%) on PHQ-9 and 55% (95% CI 51–60%) on BDI-II. Patients with more severe anxiety were less likely, and those with better mental and physical health-related quality of life were more likely, to report feeling better, having controlled for depression scores.

Our results illustrate the limitations of self-reported depression scales to assess clinical change. Clinicians should be cautious in interpreting changes in questionnaire scores without further clinical assessment.

Social anxiety disorder (SAD) has been linked to academic underachievement, but previous studies had methodological limitations. We investigated the association between SAD and objective indicators of educational performance, controlling for a number of covariates and unmeasured confounders shared between siblings.

This population-based birth cohort study included 2 238 837 individuals born in Sweden between 1973 and 1997, followed-up until 2013. Within the cohort, 15 755 individuals had a recorded ICD-10 diagnosis of SAD in the Swedish National Patient Register. Logistic regression models tested the association between SAD and educational performance. We also identified 6488 families with full siblings discordant for SAD.

Compared to unexposed individuals, individuals diagnosed with SAD were less likely to pass all subjects in the last year of compulsory education [adjusted odds ratios (aOR) ranging from 0.19 to 0.44] and less likely to be eligible for a vocational or academic programme in upper secondary education [aOR = 0.31 (95% confidence interval [CI] 0.30–0.33) and aOR = 0.52 (95% CI 0.50–0.55), respectively], finish upper secondary education [aOR = 0.19 (95% CI 0.19–0.20)], start a university degree [aOR = 0.47 (95% CI 0.45–0.49)], obtain a university degree [aOR = 0.35 (95% CI 0.33–0.37)], and finish postgraduate education [aOR = 0.58 (95% CI 0.43–0.80)]. Results were attenuated but remained statistically significant in adjusted sibling comparison models. When psychiatric comorbidities were taken into account, the results were largely unchanged.

Treatment-seeking individuals with SAD have substantially impaired academic performance throughout the formative years. Early detection and intervention are warranted to minimise the long-term socioeconomic impact of the disorder.

Among the most disabling and fatal psychiatric illnesses, eating disorders (EDs) often manifest early in life, which encourages investigations into in utero and perinatal environmental risk factors. The objective of this study was to determine whether complications during pregnancy and birth and perinatal conditions are associated with later eating disorder risk in offspring and whether these associations are unique to EDs.

All individuals born in Denmark to Danish-born parents 1989–2010 were included in the study and followed from their 6th birthday until the end of 2016. Exposure to factors related to pregnancy, birth, and perinatal conditions was determined using national registers, as were hospital-based diagnoses of anorexia nervosa (AN), bulimia nervosa, and eating disorder not otherwise specified during follow-up. For comparison, diagnoses of depressive, anxiety, and obsessive-compulsive disorders were also included. Cox regression was used to compare hazards of psychiatric disorders in exposed and unexposed individuals.

1 167 043 individuals were included in the analysis. We found that similar to the comparison disorders, prematurity was associated with increased eating disorder risk. Conversely, patterns of increasing risks of EDs, especially in AN, with increasing parental ages differed from the more U-shaped patterns observed for depressive and anxiety disorders.

Our results suggest that pregnancy and early life are vulnerable developmental periods when exposures may influence offspring mental health, including eating disorder risk, later in life. The results suggest that some events pose more global transdiagnostic risk whereas other patterns, such as increasing parental ages, appear more specific to EDs.