The COVID-19 pandemic and nationally mandated restrictions to control the virus have been associated with increased mental health issues. However, the differential impact of the pandemic and lockdown on groups of individuals, and the personal characteristics associated with poorer outcomes are unknown.

Data from 21 938 adults in England who participated in a stratified cohort study were analysed. Trajectories of depression and anxiety symptoms were identified using growth mixture modelling. Multinomial and logistic regression models were constructed to identify sociodemographic and personality-related risk factors associated with trajectory class membership.

Four trajectories of depression and five for anxiety were identified. The most common group presented with low symptom severity throughout, other classes were identified that showed: severe levels of symptoms which increased; moderate symptoms throughout; worsening mental health during lockdown but improvements after lockdown ended; and for anxiety only, severe initial anxiety that decreased quickly during lockdown. Age, gender, ethnicity, income, previous diagnoses, living situation, personality factors and sociability were associated with different trajectories.

Nearly 30% of participants experienced trajectories with symptoms in the clinical range during lockdown, and did not follow the average curve or majority group, highlighting the importance of differential trajectories. Young, female, outgoing and sociable people and essential workers experienced severe anxiety around the announcement of lockdown which rapidly decreased. Younger individuals with lower incomes and previous mental health diagnoses experienced higher and increasing levels of symptoms. Recognising the likely symptom trajectories for such groups may allow for targeted care or interventions.

This meta-analysis on peripheral blood compounds in drug-naïve first-episode patients with either schizophrenia or major depressive disorder (MDD) examined which compounds change following psychopharmacological treatment.

The Embase, PubMed and PsycINFO databases were systematically searched for longitudinal studies reporting measurements of blood compounds in drug-naïve first-episode schizophrenia or MDD.

For this random-effects meta-analysis, we retrieved a total of 31 studies comprising 1818 schizophrenia patients, and 14 studies comprising 469 MDD patients. Brain-derived neurotrophic factor (BDNF) increased following treatment in schizophrenia (Hedges' g (g): 0.55; 95% confidence interval (CI) 0.39–0.70; p < 0.001) and MDD (g: 0.51; CI 0.06–0.96; p = 0.027). Interleukin (IL)-6 levels decreased in schizophrenia (g: −0.48; CI −0.85 to −0.11; p = 0.011), and for MDD a trend of decreased IL-6 levels was observed (g: −0.39; CI −0.87 to 0.09; p = 0.115). Tumor necrosis factor alpha (TNFα) also decreased in schizophrenia (g: −0.34; CI −0.68 to −0.01; p = 0.047) and in MDD (g: −1.02; CI −1.79 to −0.25; p = 0.009). Fasting glucose levels increased only in schizophrenia (g: 0.26; CI 0.07–0.44; p = 0.007), but not in MDD. No changes were found for C-reactive protein, IL-1β, IL-2 and IL-4.

Psychopharmacological treatment has modulating effects on BDNF and TNFα in drug-naïve first-episode patients with either schizophrenia or MDD. These findings support efforts for further research into transdiagnostic preventive strategies and augmentation therapy for those with immune dysfunctions.

Altered expression of the complement component C4A gene is a known risk factor for schizophrenia. Further, predicted brain C4A expression has also been associated with memory function highlighting that altered C4A expression in the brain may be relevant for cognitive and behavioral traits.

We obtained genetic information and performance measures on seven cognitive tasks for up to 329 773 individuals from the UK Biobank, as well as brain imaging data for a subset of 33 003 participants. Direct genotypes for variants (n = 3213) within the major histocompatibility complex region were used to impute C4 structural variation, from which predicted expression of the C4A and C4B genes in human brain tissue were predicted. We investigated if predicted brain C4A or C4B expression were associated with cognitive performance and brain imaging measures using linear regression analyses.

We identified significant negative associations between predicted C4A expression and performance on select cognitive tests, and significant associations with MRI-based cortical thickness and surface area in select regions. Finally, we observed significant inconsistent partial mediation of the effects of predicted C4A expression on cognitive performance, by specific brain structure measures.

These results demonstrate that the C4 risk locus is associated with the central endophenotypes of cognitive performance and brain morphology, even when considered independently of other genetic risk factors and in individuals without mental or neurological disorders.

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.

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.

COVID-19 physical distancing measures can potentially increase the likelihood of mental disorders. It is unknown whether these measures are associated with depression and anxiety.

To investigate meta-analytic global levels of depression and anxiety during the COVID-19 pandemic and how the implementation of mitigation strategies (i.e. public transportation closures, stay-at-home orders, etc.) impacted such disorders.

PubMed, MEDLINE, Web of Science, BIOSIS Citation Index, Current Content Connect, PsycINFO, CINAHL, medRxiv, and PsyArXiv databases for depression and anxiety prevalences; Oxford Covid-19 Government Response Tracker for the containment and closure policies indexes; Global Burden of Disease Study for previous levels of depression and anxiety.

Original studies conducted during COVID-19 pandemic, which assessed categorical depression and anxiety, using PHQ-9 and GAD-7 scales (cutoff ⩾10).

General population, healthcare providers, students, and patients. National physical distancing measures.

Meta-analysis and meta-regression.

In total, 226 638 individuals were assessed within the 60 included studies. Global prevalence of both depression and anxiety during the COVID-19 pandemic was 24.0% and 21.3%, respectively. There were differences in the prevalence of both anxiety and depression reported across regions and countries. Asia (17.6% and 17.9%), and China (16.2% and 15.5%) especially, had the lowest prevalence of both disorders. Regarding the impact of mitigation strategies on mental health, only public transportation closures increased the prevalence of anxiety, especially in Europe.

Country-level data on physical distancing measures and previous anxiety/depression may not necessarily reflect local (i.e. city-specific) contexts.

Mental health concerns should not be viewed only as a delayed consequence of the COVID-19 pandemic, but also as a concurrent epidemic. Our data provide support for policy-makers to consider real-time enhanced mental health services, and increase initiatives to foster positive mental health outcomes.

Previous results have been mixed regarding the role of the apolipoprotein E e4 (APOE e4) allele in later-life depression: some studies note that carriers experience greater symptoms and increased risk while others find no such association. However, there are few prospective, population-based studies of the APOE e4-depression association and fewer that examine depressive symptom trajectory and depression risk longitudinally. We examined the association between APOE e4 allele status and longitudinal change in depressive symptoms and depression risk in later-life, over a 12-year follow-up period.

We used data from 690 participants of the Lothian Birth Cohort 1936 who took part in the Scottish Mental Survey 1947 (aged 11) and were followed-up in later-life over five waves from 2004 to 2019 (aged 70–82). We used APOE e4 allele status to predict longitudinal change in depressive symptom scores and risk of depression (defined by a symptom score threshold or use of depression-related medication). Models were adjusted for sex, childhood cognitive ability, childhood social class, education, adult social class, smoking status and functional limitations at baseline.

Depressive symptom scores increased with age. Once adjusted for covariates, APOE e4 allele status did not significantly predict symptom score trajectories or depression risk. Greater functional limitations at baseline significantly predicted poorer symptom score trajectories and increased depression risk (defined by medications). APOE e4 allele status did not significantly moderate the contribution of sex, education or functional limitations.

There was no evidence that APOE e4 carriers experience an increased risk for later-life depression.

Expressive writing about a traumatic event is promising in treating posttraumatic stress disorder (PTSD) symptoms in adult trauma survivors. To date, the comparative efficacy and acceptability of this approach is uncertain. Therefore, we aimed to examine the comparative efficacy and acceptability of expressive writing treatments.

We included 44 RCTs with 7724 participants contributing 54 direct comparisons between expressive writing (EW), enhanced writing (i.e. including additional therapist contact or individualized writing assignments; EW+), PTSD psychotherapies (PT), neutral writing (NW), and waiting-list control (WL).

EW, EW+, PT, and NW were statistically significantly more efficacious than WL at the longest available follow-up, with SMDs (95% CI) of −0.78 (−1.10 to −0.46) for PT, −0.81 (−1.02 to −0.61) for EW+ , −0.43 (−0.65 to −0.21) for EW, and −0.37 (−0.61 to −0.14) for NW. We found small to moderate differences between the active treatments. At baseline mean PTSD severity was significantly lower in EW+ compared with WL. We found considerable heterogeneity and inconsistency and we found elevated risk of bias in at least one of the bias dimensions in all studies. When EW+-WL comparisons were excluded from the analyses EW+ was no longer superior compared with EW.

The summarized evidence confirms that writing treatments may contribute to improving PTSD symptoms in medium to long-term. Methodological issues in the available evidence hamper definite conclusions regarding the comparative efficacy and acceptability of writing treatments. Adequately sized comparative randomized controlled trials preferably including all four active treatment approaches, reporting long-term data, and including researchers with balanced preferences are needed.

Individuals with depression often experience widespread and persistent cognitive deficits, which might be due to brain atrophy and cerebral small vessel disease (CSVD). We therefore studied the associations between depression, markers of brain atrophy and CSVD, and cognitive functioning.

We used cross-sectional data from the population-based Maastricht study (n = 4734; mean age 59.1 ± 8.6 years, 50.2% women), which focuses on type 2 diabetes. A current episode of major depressive disorder (MDD, n = 151) was assessed by the Mini-International Neuropsychiatric Interview. Volumes of cerebral spinal fluid, white matter, gray matter and white matter hyperintensities, presence of lacunar infarcts and cerebral microbleeds, and total CSVD burden were assessed by 3 T magnetic resonance imaging. Multiple linear and logistic regression analyses tested the associations between MDD, brain markers and cognitive functioning in memory, information processing speed, and executive functioning & attention, and presence of cognitive impairment. Structural equation modeling was used to test mediation.

In fully adjusted models, MDD was associated with lower scores in information processing speed [mean difference = −0.18(−0.28;−0.08)], executive functioning & attention [mean difference = −0.13(−0.25;−0.02)], and with higher odds of cognitive impairment [odds ratio (OR) = 1.60(1.06;2.40)]. MDD was associated with CSVD in participants without type 2 diabetes [OR = 1.65(1.06;2.56)], but CSVD or other markers of brain atrophy or CSVD did not mediate the association with cognitive functioning.

MDD is associated with more impaired information processing speed and executive functioning & attention, and overall cognitive impairment. Furthermore, MDD was associated with CSVD in participants without type 2 diabetes, but this association did not explain an impaired cognitive profile.

Previous research on the depression scale of the Patient Health Questionnaire (PHQ-9) has found that different latent factor models have maximized empirical measures of goodness-of-fit. The clinical relevance of these differences is unclear. We aimed to investigate whether depression screening accuracy may be improved by employing latent factor model-based scoring rather than sum scores.

We used an individual participant data meta-analysis (IPDMA) database compiled to assess the screening accuracy of the PHQ-9. We included studies that used the Structured Clinical Interview for DSM (SCID) as a reference standard and split those into calibration and validation datasets. In the calibration dataset, we estimated unidimensional, two-dimensional (separating cognitive/affective and somatic symptoms of depression), and bi-factor models, and the respective cut-offs to maximize combined sensitivity and specificity. In the validation dataset, we assessed the differences in (combined) sensitivity and specificity between the latent variable approaches and the optimal sum score (⩾10), using bootstrapping to estimate 95% confidence intervals for the differences.

The calibration dataset included 24 studies (4378 participants, 652 major depression cases); the validation dataset 17 studies (4252 participants, 568 cases). In the validation dataset, optimal cut-offs of the unidimensional, two-dimensional, and bi-factor models had higher sensitivity (by 0.036, 0.050, 0.049 points, respectively) but lower specificity (0.017, 0.026, 0.019, respectively) compared to the sum score cut-off of ⩾10.

In a comprehensive dataset of diagnostic studies, scoring using complex latent variable models do not improve screening accuracy of the PHQ-9 meaningfully as compared to the simple sum score approach.

Fibromyalgia is a chronic condition characterised by widespread musculoskeletal pain. Although accumulating evidence suggests that exposure to stressful events increases the risk for this complex disorder, this is the first meta-analysis to compare the impact of a full range of lifetime stressors (e.g. physical trauma through to emotional neglect) on adult fibromyalgia.

This review was performed in accordance with PRISMA guidelines. Random-effects models examined associations between different stressor exposures and fibromyalgia status with meta-regression investigating the effects of publication year and study quality on effect sizes.

Nineteen studies were included in the meta-analysis. Significant associations with fibromyalgia status were observed for all six exposure types examined: odds ratios (OR) were highest for physical abuse (OR 3.23, 95% confidence interval 1.99–5.23) and total abuse (3.06, 1.71–5.46); intermediate for sexual abuse (2.65, 1.85–3.79) and smaller for medical trauma (1.80, 1.19–2.71), other lifetime stressors (1.70, 1.31–2.20), and emotional abuse (1.52, 1.27–1.81). Results were not significantly changed when childhood, as opposed to adult, exposures were used in studies that reported both. Meta-regression analyses demonstrated no effect of publication year or study quality on effect sizes.

This study confirmed a significant association between stressor exposure and adult fibromyalgia with the strongest associations observed for physical abuse. Limitations related to current available literature were identified; we provide several suggestions for how these can be addressed in future studies. Stressors are likely to be one of many risk factors for fibromyalgia which we argue is best approached from a biopsychosocial perspective.

Mood plays an important role in our life which is illustrated by the disruptive impact of aberrant mood states in depression. Although vagus nerve stimulation (VNS) has been shown to improve symptoms of depression, the exact mechanism is still elusive, and it is an open question whether non-invasive VNS could be used to swiftly and robustly improve mood.

Here, we investigated the effect of left- and right-sided transcutaneous auricular VNS (taVNS) v. a sham control condition on mood after the exertion of physical and cognitive effort in 82 healthy participants (randomized cross-over design) using linear mixed-effects and hierarchical Bayesian analyses of mood ratings.

We found that 90 min of either left-sided or right-sided taVNS improved positive mood [b = 5.11, 95% credible interval, CI (1.39–9.01), 9.6% improvement relative to the mood intercept, BF10 = 7.69, pLME = 0.017], yet only during the post-stimulation phase. Moreover, lower baseline scores of positive mood were associated with greater taVNS-induced improvements in motivation [r = −0.42, 95% CI (−0.58 to −0.21), BF10 = 249].

We conclude that taVNS boosts mood after a prolonged period of effort exertion with concurrent stimulation and that acute motivational effects of taVNS are partly dependent on initial mood states. Collectively, our results show that taVNS may help quickly improve affect after a mood challenge, potentially by modulating interoceptive signals contributing to the reappraisal of effortful behavior. This suggests that taVNS could be a useful add-on to current behavioral therapies.

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.

Risk is an essential trait of most daily decisions. Our behaviour when faced with risks involves evaluation of many factors including the outcome probabilities, the valence (gains or losses) and past experiences. Several psychiatric disorders belonging to distinct diagnostic categories, including pathological gambling and addiction, show pathological risk-taking and implicate abnormal dopaminergic, opioidergic and serotonergic neurotransmission. In this study, we adopted a transdiagnostic approach to delineate the neurochemical substrates of decision making under risk.

We recruited 39 participants, including 17 healthy controls, 15 patients with pathological gambling and seven binge eating disorder patients, who completed an anticipatory risk-taking task. Separately, participants underwent positron emission tomography (PET) imaging with three ligands, [18F]fluorodopa (FDOPA), [11C]MADAM and [11C]carfentanil to assess presynaptic dopamine synthesis capacity and serotonin transporter and mu-opioid receptor binding respectively.

Risk-taking behaviour when faced with gains positively correlated with dorsal cingulate [11C]carfentanil binding and risk-taking to losses positively correlated with [11C]MADAM binding in the caudate and putamen across all subjects.

We show distinct neurochemical substrates underlying risk-taking with the dorsal cingulate cortex mu-opioid receptor binding associated with rewards and dorsal striatal serotonin transporter binding associated with losses. Risk-taking and goal-directed control appear to dissociate between dorsal and ventral fronto-striatal systems. Our findings thus highlight the potential role of pharmacological agents or neuromodulation on modifying valence-specific risk-taking biases.

Interpersonal processes influence our physiological states and associated affect. Physiological arousal dysregulation, a core feature of anxiety disorders, has been identified in children of parents with elevated anxiety. However, little is understood about how parent–infant interpersonal regulatory processes differ when the dyad includes a more anxious parent.

We investigated moment-to-moment fluctuations in arousal within parent-infant dyads using miniaturised microphones and autonomic monitors. We continually recorded arousal and vocalisations in infants and parents in naturalistic home settings across day-long data segments.

Our results indicated that physiological synchrony across the day was stronger in dyads including more rather than less anxious mothers. Across the whole recording epoch, less anxious mothers showed responsivity that was limited to ‘peak’ moments in their child's arousal. In contrast, more anxious mothers showed greater reactivity to small-scale fluctuations. Less anxious mothers also showed behaviours akin to ‘stress buffering’ – downregulating their arousal when the overall arousal level of the dyad was high. These behaviours were absent in more anxious mothers.

Our findings have implications for understanding the differential processes of physiological co-regulation in partnerships where a partner is anxious, and for the use of this understanding in informing intervention strategies for dyads needing support for elevated levels of anxiety.