Sleep disruption is a common precursor to deterioration and relapse in people living with psychotic disorders. Understanding the temporal relationship between sleep and psychopathology is important for identifying and developing interventions which target key variables that contribute to relapse.

We used a purpose-built digital platform to sample self-reported sleep and psychopathology variables over 1 year, in 36 individuals with schizophrenia. Once-daily measures of sleep duration and sleep quality, and fluctuations in psychopathology (positive and negative affect, cognition and psychotic symptoms) were captured. We examined the temporal relationship between these variables using the Differential Time-Varying Effect (DTVEM) hybrid exploratory-confirmatory model.

Poorer sleep quality and shorter sleep duration maximally predicted deterioration in psychosis symptoms over the subsequent 1–8 and 1–12 days, respectively. These relationships were also mediated by negative affect and cognitive symptoms. Psychopathology variables also predicted sleep quality, but not sleep duration, and the effect sizes were smaller and of shorter lag duration.

Reduced sleep duration and poorer sleep quality anticipate the exacerbation of psychotic symptoms by approximately 1–2 weeks, and negative affect and cognitive symptoms mediate this relationship. We also observed a reciprocal relationship that was of shorter duration and smaller magnitude. Sleep disturbance may play a causal role in symptom exacerbation and relapse, and represents an important and tractable target for intervention. It warrants greater attention as an early warning sign of deterioration, and low-burden, user-friendly digital tools may play a role in its early detection.

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.

Posttraumatic stress disorder (PTSD) is highly prevalent within prison settings, yet is often unidentified and undertreated. Complex PTSD (CPTSD) has been recently formally recognised in the International Classification of Diseases 11th revision (ICD-11) diagnostic framework but has never been explored in prison settings. We aimed to establish the prevalence of ICD-11 PTSD and CPTSD in a UK prison sample using a validated instrument (the International Trauma Questionnaire). We also explored the associations of these two diagnoses with their traumatic antecedents and psychiatric comorbidities.

Randomly selected male, sentenced prisoners in a large medium-security prison in south London (N = 221) took part in a clinical interview which assessed PTSD, CPTSD, trauma histories, and comorbid disorders. Multinomial logistic regression was performed to examine differences between those with PTSD or CPTSD, and those without symptoms.

A total of 7.7% (95% CI 4.5–12) of the male sentenced prisoners met diagnostic criteria for ICD-11 PTSD and 16.7% (95% CI 12.1–22.3) for CPTSD. A diagnosis of PTSD was associated with more recent traumatic exposure, comorbid generalised anxiety disorder, alcohol dependence, and Cluster B personality disorder. A diagnosis of CPTSD was associated with complex trauma exposure antecedents (developmental, interpersonal, repeated, or multiple forms), and comorbid with anxiety, depression, substance misuse, psychosis, and ADHD.

This study confirms that CPTSD is a very common and comorbid condition in male prisoners. There is an urgent need to develop trauma-informed care in prisons.

According to the cognitive neuropsychological model, antidepressants reduce symptoms of depression and anxiety by increasing positive relative to negative information processing. Most studies of whether antidepressants alter emotional processing use small samples of healthy individuals, which lead to low statistical power and selection bias and are difficult to generalise to clinical practice. We tested whether the selective serotonin reuptake inhibitor (SSRI) sertraline altered recall of positive and negative information in a large randomised controlled trial (RCT) of patients with depressive symptoms recruited from primary care.

The PANDA trial was a pragmatic multicentre double-blind RCT comparing sertraline with placebo. Memory for personality descriptors was tested at baseline and 2 and 6 weeks after randomisation using a computerised emotional categorisation task followed by a free recall. We measured the number of positive and negative words correctly recalled (hits). Poisson mixed models were used to analyse longitudinal associations between treatment allocation and hits.

A total of 576 participants (88% of those randomised) completed the recall task at 2 and 6 weeks. We found no evidence that positive or negative hits differed according to treatment allocation at 2 or 6 weeks (adjusted positive hits ratio = 0.97, 95% CI 0.90–1.05, p = 0.52; adjusted negative hits ratio = 0.99, 95% CI 0.90–1.08, p = 0.76).

In the largest individual placebo-controlled trial of an antidepressant not funded by the pharmaceutical industry, we found no evidence that sertraline altered positive or negative recall early in treatment. These findings challenge some assumptions of the cognitive neuropsychological model of antidepressant action.

Cognitive mechanisms that characterize or precede depressive symptoms are poorly understood. We investigated cross-sectional and longitudinal associations between risk taking to obtain reward and adolescent depressive symptoms in a large prospective cohort, using the Cambridge Gambling Task (CGT). We also explored sex differences.

The Millennium Cohort Study (MCS) is an ongoing UK study, following the lives of 19 000 individuals born 2000/02. The CGT was completed at ages 11 (n = 12 355) and 14 (n = 10 578). Our main exposure was the proportion of points gambled, when the odds of winning were above chance (risk-taking to obtain reward). Outcomes were emotional symptoms (Strengths and Difficulties Questionnaire, SDQ) at age 11 and depressive symptoms (short Mood and Feelings Questionnaire, sMFQ) at age 14. We calculated cross-sectional and longitudinal associations, using linear regressions.

In univariable models, there was evidence of cross-sectional associations between risk-taking and SDQ/sMFQ scores, but these associations disappeared after we adjusted for sex. Longitudinally, there was weak evidence of an association between risk-taking and depressive symptoms in females only [a 20-point increase in risk-taking at age 11 was associated with a reduction of 0.31 sMFQ points at age 14 (95% CI −0.60 to −0.02)]. At both time-points, females were less risk-taking than males.

We found no convincing evidence of a relationship between risk-taking to obtain reward and depressive symptoms. There were large sex differences in risk-taking, but these do not appear to contribute to the female preponderance of depressive symptoms in adolescence.

The prefrontal deficits in psychiatric disorders have been investigated using functional neuroimaging tools; however, no studies have tested the related characteristics across psychiatric disorders considering various demographic and clinical confounders.

We analyzed 1558 functional brain measurements using a functional near-infrared spectroscopy during a verbal fluency task from 1200 participants with three disease spectra [196 schizophrenia, 189 bipolar disorder (BPD), and 394 major depressive disorder (MDD)] and 369 healthy controls along with demographic characteristics (age, gender, premorbid IQ, and handedness), task performance during the measurements, clinical assessments, and medication equivalent doses (chlorpromazine, diazepam, biperiden, and imipramine) in a consistent manner. The association between brain functions and demographic and clinical variables was tested using a general linear mixed model (GLMM). Then, the direction of relationship between brain activity and symptom severity, controlling for any other associations, was estimated using a model comparison of structural equation models (SEMs).

The GLMM showed a shared functional deficit of brain activity and a schizophrenia-specific delayed activity timing in the prefrontal cortex (false discovery rate-corrected p < 0.05). Comparison of SEMs showed that brain activity was associated with the global assessment of functioning scores in the left inferior frontal gyrus opercularis (IFGOp) in BPD group and the bilateral superior temporal gyrus and middle temporal gyrus, and the left superior frontal gyrus, inferior frontal gyrus triangularis, and IFGOp in MDD group.

This cross-disease large-sample neuroimaging study with high-quality clinical data reveals a robust relationship between prefrontal function and behavioral outcomes across three major psychiatric disorders.

This study examined the associations between accelerometer-derived sedentary time (ST), lower intensity physical activity (LPA), higher intensity physical activity (HPA) and the incidence of depressive symptoms over 4 years of follow-up.

We included 2082 participants from The Maastricht Study (mean ± s.d. age 60.1 ± 8.0 years; 51.2% men) without depressive symptoms at baseline. ST, LPA and HPA were measured with the ActivPAL3 activity monitor. Depressive symptoms were measured annually over 4 years of follow-up with the 9-item Patient Health Questionnaire (PHQ-9). Cox regression analysis was performed to examine the associations between ST, LPA, HPA and incident depressive symptoms (PHQ-9 ⩾ 10). Analyses were adjusted for total waking time per day, age, sex, education level, type 2 diabetes mellitus, body mass index, total energy intake, smoking status and alcohol use.

During 7812.81 person-years of follow-up, 203 (9.8%) participants developed incident depressive symptoms. No significant associations [Hazard Ratio (95% confidence interval)] were found between sex-specific tertiles of ST (lowest v. highest tertile) [1.13 (0.76–1.66], or HPA (highest v. lowest tertile) [1.14 (0.78–1.69)] and incident depressive symptoms. LPA (highest v. lowest tertile) was statistically significantly associated with incident depressive symptoms in women [1.98 (1.19–3.29)], but not in men (p-interaction <0.01).

We did not observe an association between ST or HPA and incident depressive symptoms. Lower levels of daily LPA were associated with an increased risk of incident depressive symptoms in women. Future research is needed to investigate accelerometer-derived measured physical activity and ST with incident depressive symptoms, preferably stratified by sex.

Sedentary behaviour is potentially a modifiable risk factor for anxiety disorders, a major source of global disability that typically starts during adolescence. This is the first prospective study of associations between repeated, device-based measures of sedentary behaviour and anxiety symptoms in adolescents.

A UK cohort with 4257 adolescents aged 12 at baseline (56% female). Main exposures were sedentary behaviour and physical activity measured using accelerometers for 7-days at ages 12, 14, and 16. Primary outcome was anxiety symptom scores at age 18 from a Clinical Interview Schedule-Revised. We used adjusted negative binomial regression and iso-temporal substitution methods to analyse the data.

We found a positive association between sedentary behaviour at ages 12, 14, and 16, with anxiety symptoms at age 18, independent of total physical activity volume. Theoretically replacing an hour of daily sedentary behaviour for light activity at ages 12, 14, and 16, was associated with lower anxiety symptoms by age 18 by 15.9% (95% CI 8.7–22.4), 12.1% (95% CI 3.4–20.1), and 14.7% (95% CI 4–24.2), respectively. Whereas, theoretically replacing an hour of sedentary behaviour with moderate-to-vigorous physical activity was not associated with differences in anxiety symptoms. These results were robust to a series of sensitivity analyses.

Sedentary behaviour is a possible risk factor for increasing anxiety symptoms during adolescence, independent of total physical activity volume. Instead of focusing on moderate-to-vigorous activity, replacing daily sedentary behaviour with light activity during adolescence could be a more suitable method of reducing future anxiety symptoms.

Experience of early-life socioeconomic deprivation (ELSD) may increase the risk of mental disorders in young adulthood. This association may be mediated by structural and functional alterations of the hippocampus.

We conducted a prospective cohort study on 122 participants of the European Longitudinal Study of Pregnancy and Childhood. Information about ELSD was collected via questionnaire from mothers during the first 18 months of participants’ lives. At age 23–24, participants underwent examination by structural magnetic resonance imaging, resting-state functional connectivity and assessment of depressive symptoms (Mood and Feelings Questionnaire) and anxiety (Spielberger State-Trait Anxiety Inventory). The association of ELSD with brain outcomes in young adulthood was assessed with correlations, linear regression (adjusting for sex, socioeconomic position and mother's mental health) and moderated mediation analysis.

Higher ELSD was associated with greater depressive symptoms (B = 0.22; p = 0.001), trait anxiety (B = 0.07; p = 0.02) and lower global connectivity of the right hippocampus (B = −0.01; p = 0.02). These associations persisted when adjusted for covariates. In women, lower global connectivity of the right hippocampus was associated with stronger trait anxiety (B = −4.14; p = 0.01). Global connectivity of the right hippocampus as well as connectivity between the right hippocampus and the left middle temporal gyrus mediated the association between ELSD and trait anxiety in women. Higher ELSD correlated with a lower volume of the right hippocampus in men, but the volume of the right hippocampus was not related to mental health.

Early preventive strategies targeted at children from socioeconomically deprived families may yield long-lasting benefits for the mental health of the population.

Traumatic experiences are associated with a higher risk of psychotic illnesses, but little is known about potentially modifiable mechanisms underlying this relationship. This study aims to examine whether post-traumatic stress disorder (PTSD) symptoms mediate the relationship between trauma and psychotic experiences (PEs).

We used data from the Avon Longitudinal Study of Parents and Children to examine whether: PTSD symptoms mediate the relationships between (a) childhood trauma and adolescent PEs (study of adolescent PEs; n = 2952), and (b) childhood/adolescent trauma and PEs in early adulthood (study of adult PEs; n = 2492). We examined associations between variables using logistic regression, and mediation using the parametric g-computation formula.

Exposure to trauma was associated with increased odds of PEs (adolescent PEs: ORadjusted 1.48, 95% CI 1.23–1.78; adult PEs: ORadjusted 1.57, 95% CI 1.25–1.98) and PTSD symptoms (adolescent PTSD: ORadjusted 1.59, 95% CI 1.31–1.93; adult PTSD: ORadjusted 1.50, 95% CI 1.36–1.65). The association between PTSD symptoms and PE was stronger in adolescence (ORadjusted 4.63, 95% CI 2.34–9.17) than in adulthood (ORadjusted 1.62, 95% CI 0.80–3.25). There was some evidence that PTSD symptoms mediated the relationship between childhood trauma and adolescent PEs (proportion mediated 14%), though evidence of mediation was weaker for adult PEs (proportion mediated 8%).

These findings are consistent with the hypothesis that PTSD symptoms partly mediate the association between trauma exposure and PEs. Targeting PTSD symptoms might help prevent the onset of psychotic outcomes.

Depression treatment might be enhanced by ecological momentary interventions (EMI) based on self-monitoring and person-specific feedback. This study is the first to examine the efficacy of two different EMI modules for depression in routine clinical practice.

Outpatients starting depression treatment at secondary mental health services (N = 161; MIDS−DEPRESSION = 35.9, s.d. = 10.7; MAGE = 32.8, s.d. = 12.1; 46% male) participated in a pragmatic randomized controlled trial with three arms. Two experimental groups engaged in 28 days of systematic self-monitoring (5 times per day), and received weekly feedback on either positive affect and activities (Do-module) or negative affect and thinking patterns (Think-module). The control group received no additional intervention. Participants completed questionnaires on depressive symptoms (primary outcome), social functioning, and empowerment before and after the intervention period, and at four measurements during a 6-month follow-up period.

Of the 90 (out of 110) participants who completed the intervention, 86% would recommend it. However, the experimental groups did not show significantly more or faster changes over time than the control group in terms of depressive symptoms, social functioning, and empowerment. Furthermore, the trajectories of the two EMI modules were very similar.

We did not find statistical evidence that this type of EMI augments the efficacy of regular depression treatment, regardless of module content. We cannot rule out that EMIs have a positive impact on other domains or provide a more efficient way of delivering care. Nonetheless, EMI's promise of effectiveness has not materialized yet.

Over the past two decades, early detection and early intervention in psychosis have become essential goals of psychiatry. However, clinical impressions are insufficient for predicting psychosis outcomes in clinical high-risk (CHR) individuals; a more rigorous and objective model is needed. This study aims to develop and internally validate a model for predicting the transition to psychosis within 10 years.

Two hundred and eight help-seeking individuals who fulfilled the CHR criteria were enrolled from the prospective, naturalistic cohort program for CHR at the Seoul Youth Clinic (SYC). The least absolute shrinkage and selection operator (LASSO)-penalized Cox regression was used to develop a predictive model for a psychotic transition. We performed k-means clustering and survival analysis to stratify the risk of psychosis.

The predictive model, which includes clinical and cognitive variables, identified the following six baseline variables as important predictors: 1-year percentage decrease in the Global Assessment of Functioning score, IQ, California Verbal Learning Test score, Strange Stories test score, and scores in two domains of the Social Functioning Scale. The predictive model showed a cross-validated Harrell's C-index of 0.78 and identified three subclusters with significantly different risk levels.

Overall, our predictive model showed a predictive ability and could facilitate a personalized therapeutic approach to different risks in high-risk individuals.

Our aim was to estimate provisional willingness to receive a coronavirus 2019 (COVID-19) vaccine, identify predictive socio-demographic factors, and, principally, determine potential causes in order to guide information provision.

A non-probability online survey was conducted (24th September−17th October 2020) with 5,114 UK adults, quota sampled to match the population for age, gender, ethnicity, income, and region. The Oxford COVID-19 vaccine hesitancy scale assessed intent to take an approved vaccine. Structural equation modelling estimated explanatory factor relationships.

71.7% (n=3,667) were willing to be vaccinated, 16.6% (n=849) were very unsure, and 11.7% (n=598) were strongly hesitant. An excellent model fit (RMSEA=0.05/CFI=0.97/TLI=0.97), explaining 86% of variance in hesitancy, was provided by beliefs about the collective importance, efficacy, side-effects, and speed of development of a COVID-19 vaccine. A second model, with reasonable fit (RMSEA=0.03/CFI=0.93/TLI=0.92), explaining 32% of variance, highlighted two higher-order explanatory factors: ‘excessive mistrust’ (r=0.51), including conspiracy beliefs, negative views of doctors, and need for chaos, and ‘positive healthcare experiences’ (r=−0.48), including supportive doctor interactions and good NHS care. Hesitancy was associated with younger age, female gender, lower income, and ethnicity, but socio-demographic information explained little variance (9.8%). Hesitancy was associated with lower adherence to social distancing guidelines.

COVID-19 vaccine hesitancy is relatively evenly spread across the population. Willingness to take a vaccine is closely bound to recognition of the collective importance. Vaccine public information that highlights prosocial benefits may be especially effective. Factors such as conspiracy beliefs that foster mistrust and erode social cohesion will lower vaccine up-take.

Freeman et al. (2020a, Psychological Medicine, 21, 1–13) argue that there is widespread support for coronavirus conspiracy theories in England. We hypothesise that their estimates of prevalence are inflated due to a flawed research design. When asking respondents to their survey to agree or disagree with pro-conspiracy statements, they used a biased set of response options: four agree options and only one disagree option (and no ‘don't know’ option). We also hypothesise that due to these flawed measures, the Freeman et al. approach under-estimates the strength of the correlation between conspiracy beliefs and compliance. Finally, we hypothesise that, due to reliance on bivariate correlations, Freeman et al. over-estimate the causal connection between conspiracy beliefs and compliance.

In a pre-registered study, we conduct an experiment embedded in a survey of a representative sample of 2057 adults in England (fieldwork: 16−19 July 2020).

Measured using our advocated ‘best practice’ approach (balanced response options, with a don't know option), prevalence of support for coronavirus conspiracies is only around five-eighths (62.3%) of that indicated by the Freeman et al. approach. We report mixed results on our correlation and causation hypotheses.

To avoid over-estimating prevalence of support for coronavirus conspiracies, we advocate using a balanced rather than imbalanced set of response options, and including a don't know option.

The COVID-19 pandemic in the UK and subsequent lockdown may have affected the mental health of the population. This study examines whether there was an increase in the prevalence and incidence of common mental disorders (CMD) in the UK adult population during the first months of lockdown and whether changes in CMD were associated with stressors related to the pandemic and lockdown.

Longitudinal data from the UK Household Longitudinal Study waves 10–11: 2019–2020 and waves 1–4 of the COVID-19 monthly surveys in April (n = 17 761) to July 2020 (n = 13 754), a representative sample of UK adult population, were analysed. CMD was measured using the 12-item General Health Questionnaire (GHQ-12) (cut-off >2). Changes in CMD were analysed in relation to COVID-19 and social stressors.

Around 29% of adults without CMD less than a year earlier had a CMD in April 2020. However, by July 2020, monthly incidence of CMD had reduced to 9%. Most employment, financial and psychological ‘shocks’ were at their highest levels in April and reduced steadily in later months. Despite the lifting of some lockdown conditions by July, stressors related to loneliness, unemployment, financial problems and domestic work continued to influence CMD.

Some COVID-19 policy responses such as furloughing may have been effective in mitigating the increase in CMD for some groups of employees. Despite some reduction in levels of pandemic and lockdown-related stressors by the middle of 2020, loneliness and financial stressors remained key determinants of incidence in CMD among the UK adult population.

Symptoms of attention deficit hyperactivity disorder (ADHD) and trait impulsivity have been associated with disordered eating but are seldom assessed in community studies, or longitudinally and little is known about the mediating mechanisms.

We tested associations between ADHD symptoms and disordered eating cross-sectionally and between trait impulsivity and disordered eating longitudinally. We utilised data from a normative cohort of young adults (642 participants: 65% female, Mage = 23 years). Participants were classified as high risk or low risk for disordered eating using the SCOFF instrument. In the first two steps of both cross-sectional and longitudinal hierarchical logistic regression models, demographics and covariates were entered. For the cross-sectional regression, Adult ADHD self-report scale (ASRS) scores, separated into inattentive and hyperactive/impulsive symptoms, were entered in the third step. In a separate longitudinal model, Barratt impulsivity scale subscales (attentional, motor and non-planning impulsivity) were entered in the third step. Depression, as assessed by the moods and feelings questionnaire (MFQ), was examined as a mediator.

Cross-sectionally, sex, MFQ score and inattentive symptoms predicted disordered eating risk (model R2 = 20%). Longitudinally, sex, MFQ score and attentional impulsivity predicted disordered eating risk (model R2 = 16%). The relationship between inattentive symptoms and the disordered eating risk was partially mediated by MFQ score, whereas the relationship between attentional impulsivity and the disordered eating risk was fully mediated by MFQ scores.

These data highlight (1) a specific role for inattentive symptoms of ADHD and (2) the importance of both depression and impulsivity in predicting eating disorder risk.

Family-based treatment (FBT) is an efficacious intervention for adolescents with an eating disorder. Evaluated to a lesser degree among adolescents, enhanced cognitive-behavior therapy (CBT-E) has shown promising results. This study compared the relative effectiveness of FBT and CBT-E, and as per manualized CBT-E, the sample was divided into a lower weight [<90% median body mass index (mBMI)], and higher weight cohort (⩾90%mBMI).

Participants (N = 97) aged 12–18 years, with a DSM-5 eating disorder diagnosis (largely restrictive, excluding Avoidant Restrictive Food Intake Disorder), and their parents, chose between FBT and CBT-E. Assessments were administered at baseline, end-of-treatment (EOT), and follow-up (6 and 12 months). Treatment comprised of 20 sessions over 6 months, except for the lower weight cohort where CBT-E comprised 40 sessions over 9–12 months. Primary outcomes were slope of weight gain and change in Eating Disorder Examination (EDE) Global Score at EOT.

Slope of weight gain at EOT was significantly higher for FBT than for CBT-E (lower weight, est. = 0.597, s.e. = 0.096, p < 0.001; higher weight, est. = 0.495, s.e. = 0.83, p < 0.001), but not at follow-up. There were no differences in the EDE Global Score or most secondary outcome measures at any time-point. Several baseline variables emerged as potential treatment effect moderators at EOT. Choosing between FBT and CBT-E resulted in older and less well participants opting for CBT-E.

Results underscore the efficiency of FBT to facilitate weight gain among underweight adolescents. FBT and CBT-E achieved similar outcomes in other domains assessed, making CBT-E a viable treatment for adolescents with an eating disorder.

Treatment Outcome in Eating Disorders; https://clinicaltrials.gov/; NCT03599921.