There is inconsistent evidence regarding the influence of general cognitive abilities on the long-term course of depression.

To investigate the association between general childhood cognitive abilities and adult depression outcomes.

We conducted a cohort study using data from 633 participants in the New England Family Study with lifetime depression. Cognitive abilities at age 7 were measured using the Wechsler Intelligence Scale for Children. Depression outcomes were assessed using structured diagnostic interviews administered up to four times in adulthood between ages 17 and 49.

In analyses adjusting for demographic factors and parental psychiatric illness, low general cognitive ability (i.e. IQ<85 v. IQ>115) was associated with recurrent depressive episodes (odds ratio (OR) = 2.19, 95% CI 1.20–4.00), longer episode duration (rate ratio 4.21, 95% CI 2.24–7.94), admission to hospital for depression (OR = 3.65, 95% CI 1.34–9.93) and suicide ideation (OR = 3.79, 95% CI 1.79–8.02) and attempt (OR = 4.94, 95% CI 1.67–14.55).

Variation in cognitive abilities, predominantly within the normal range and established early in childhood, may confer long-term vulnerability for prolonged and severe depression. The mechanisms underlying this vulnerability need to be established to improve the prognosis of depression among individuals with lower cognitive abilities.

Mortality has been suggested to be increased in autism spectrum disorder (ASD).

To examine both all-cause and cause-specific mortality in ASD, as well as investigate moderating role of gender and intellectual ability.

Odds ratios (ORs) were calculated for a population-based cohort of ASD probands (n = 27 122, diagnosed between 1987 and 2009) compared with gender-, age- and county of residence-matched controls (n = 2 672 185).

During the observed period, 24 358 (0.91%) individuals in the general population died, whereas the corresponding figure for individuals with ASD was 706 (2.60%; OR = 2.56; 95% CI 2.38–2.76). Cause-specific analyses showed elevated mortality in ASD for almost all analysed diagnostic categories. Mortality and patterns for cause-specific mortality were partly moderated by gender and general intellectual ability.

Premature mortality was markedly increased in ASD owing to a multitude of medical conditions.

An essential element of mental health service scale up relates to an assessment of resource requirements and cost implications.

To assess the expected resource needs of scaling up services in five districts in sub-Saharan Africa and south Asia.

The resource quantities associated with each site's specified care package were identified and subsequently costed, both at current and target levels of coverage.

The cost of the care package at target coverage ranged from US$0.21 to 0.56 per head of population in four of the districts (in the higher-income context of South Africa, it was US$1.86). In all districts, the additional amount needed each year to reach target coverage goals after 10 years was below $0.10 per head of population.

Estimation of resource needs and costs for district-level mental health services provides relevant information concerning the financial feasibility of locally developed plans for successful scale up.

The aetiological boundary between obsessive–compulsive related disorders (OCRDs) including obsessive–compulsive disorder (OCD) and anxiety disorders is unclear and continues to generate debate.

To determine the genetic overlap and the pattern of causal relationships among OCRDs and anxiety disorders.

Multivariate twin modelling methods and a new regression analysis to infer causation were used, involving 2495 male and female twins.

The amount of common genetic liability observed for OCD symptoms was higher when considering anxiety disorders and OCRDs in the model v. modelling OCRD symptoms alone. OCD symptoms emerged as risk factors for the presence of generalised anxiety, panic and hoarding symptoms, whereas social phobia appeared as a risk factor for OCD symptoms.

OCD represents a complex phenotype that includes important shared features with anxiety disorders and OCRDs. The novel patterns of risk identified between OCD and anxiety disorder may help to explain their frequent co-occurrence.

Tailored psychosocial interventions can help families to manage behavioural and psychological symptoms in dementia (BPSD), but carer responses to their relative's behaviours contribute to the success of support programmes.

To understand why some family carers have difficulty in dealing with BPSD, in order to improve the quality of personalised care that is offered.

A systematic review and meta-ethnographic synthesis was conducted of high-quality quantitative and qualitative studies between 1980 and 2012.

We identified 25 high-quality studies and two main reasons for behaviours being reported as challenging by family carers: changes in communication and relationships, resulting in ‘feeling bereft’; and perceptions of transgressions against social norms associated with ‘misunderstandings about behaviour’ in the relative with dementia. The underlying belief that their relative had lost, or would inevitably lose, their identity to dementia was a fundamental reason why family carers experienced behaviour as challenging.

Family carers' perceptions of BPSD as challenging are associated with a sense of a declining relationship, transgressions against social norms and underlying beliefs that people with dementia inevitably lose their ‘personhood’. Interventions for the management of challenging behaviour in family settings should acknowledge unmet psychological need in family carers.

Healthcare access and outcomes in cancer patients with schizophrenia remain unclear.

To investigate the likelihood of early diagnosis and treatment in patients with schizophrenia who have cancer and their prognosis.

A retrospective matched-pair cohort of gastrointestinal cancer patients was identified using a national in-patient database in Japan. Multivariable ordinal/binary logistic regressions was modelled to compare cancer stage at admission, invasive treatments and 30-day in-hospital mortality between patients with schizophrenia (n = 2495) and those without psychiatric disorders (n = 9980).

The case group had a higher proportion of stage IV cancer (33.9% v. 18.1%), a lower proportion of invasive treatment (56.5% v. 70.2%, odds ratio (OR) = 0.77, 95% CI 0.69–0.85) and higher in-hospital mortality (4.2% v. 1.8%, OR = 1.35, 95% CI 1.04–1.75).

Patients with schizophrenia who had gastrointestinal cancer had more advanced cancer, a lower likelihood of invasive treatment and higher in-hospital mortality than those without psychiatric disorders.

People born in densely populated areas have a higher risk of developing schizophrenia, bipolar disorder and autism.

The purpose of this study was to investigate whether urban–rural differences in place of birth influence a broad range of mental disorders.

Population-based cohort study of everyone born in Denmark between 1955 and 2006 (n = 2 894 640). Main outcome measures were incidence rate ratios for five levels of urbanisation and summary estimates contrasting birth in the capital with birth in rural areas.

For all psychiatric disorders, except intellectual disability (ICD-10 ‘mental retardation’) and behavioural and emotional disorders with onset in childhood, people born in the capital had a higher incidence than people born in rural areas.

Birth in an urban environment is associated with an increased risk for mental illness in general and for a broad range of specific psychiatric disorders. Given this new evidence that urban–rural differences in incidence are not confined to the well-studied psychotic disorders, further work is needed to identify the underlying aetiopathogenic mechanisms.

Attention-deficit hyperactivity disorder (ADHD) persists in around two-thirds of individuals in adolescence and early adulthood.

To examine the cognitive and neurophysiological processes underlying the persistence or remission of ADHD.

Follow-up data were obtained from 110 young people with childhood ADHD and 169 controls on cognitive, electroencephalogram frequency, event-related potential (ERP) and actigraph movement measures after 6 years.

ADHD persisters differed from remitters on preparation-vigilance measures (contingent negative variation, delta activity, reaction time variability and omission errors), IQ and actigraph count, but not on executive control measures of inhibition or working memory (nogo-P3 amplitudes, commission errors and digit span backwards).

Preparation-vigilance measures were markers of remission, improving concurrently with ADHD symptoms, whereas executive control measures were not sensitive to ADHD persistence/remission. For IQ, the present and previous results combined suggest a role in moderating ADHD outcome. These findings fit with previously identified aetiological separation of the cognitive impairments in ADHD. The strongest candidates for the development of non-pharmacological interventions involving cognitive training and neurofeedback are the preparation-vigilance processes that were markers of ADHD remission.

Evidence suggests a link between sedentary behaviours and depressive symptoms. Mechanisms underlying this relationship are not understood, but inflammatory processes may be involved. Autonomic and inflammatory responses to stress may be heightened in sedentary individuals contributing to risk, but no study has experimentally investigated this.

To examine the effect of sedentary time on mood and stress responses using an experimental design.

Forty-three individuals were assigned to a free-living sedentary condition and to a control condition (usual activity) in a cross-over, randomised fashion and were tested in a psychophysiology laboratory after spending 2 weeks in each condition. Participants completed mood questionnaires (General Health Questionnaire and Profile of Mood States) and wore a motion sensor for 4 weeks.

Sedentary time increased by an average of 32 min/day (P = 0.01) during the experimental condition compared with control. Being sedentary resulted in increases in negative mood independent of changes in moderate to vigorous physical activity (δGHQ= 6.23, δPOMS= 2.80). Mood disturbances were associated with greater stress-induced inflammatory interleukin-6 (IL-6) responses (β = 0.37).

Two weeks of exposure to greater free-living sedentary time resulted in mood disturbances independent of reduction in physical activity. Stress-induced IL-6 responses were associated with changes in mood.

Early-life adversity is a risk for obsessive–compulsive disorder (OCD), but the impact at the neural level is less clear.

To investigate the association between brain volumes and early-life adversity in individuals with a diagnosis of OCD only.

The Childhood Trauma Questionnaire (CTQ-28) was used to assess early-life adversity in 21 participants with OCD and 25 matched healthy controls. The relationship between global and regional brain volume and early-life adversity was measured using voxel-based morphometry (VBM). All data were corrected for multiple comparisons using family-wise error (FWE) at P<0.05.

In the OCD group, correlations with total CTQ scores were positively associated with a larger right orbitofrontal cortex volume. Physical neglect was higher in the OCD group than in controls and was positively associated with larger right cerebellum volume in the OCD group only.

Larger brain volumes may reflect underlying developmental neuropathology in adults with OCD who also have experience of childhood trauma.

Bipolar disorder is a highly heritable polygenic disorder. Recent enrichment analyses suggest that there may be true risk variants for bipolar disorder in the expression quantitative trait loci (eQTL) in the brain.

We sought to assess the impact of eQTL variants on bipolar disorder risk by combining data from both bipolar disorder genome-wide association studies (GWAS) and brain eQTL.

To detect single nucleotide polymorphisms (SNPs) that influence expression levels of genes associated with bipolar disorder, we jointly analysed data from a bipolar disorder GWAS (7481 cases and 9250 controls) and a genome-wide brain (cortical) eQTL (193 healthy controls) using a Bayesian statistical method, with independent follow-up replications. The identified risk SNP was then further tested for association with hippocampal volume (n = 5775) and cognitive performance (n = 342) among healthy individuals.

Integrative analysis revealed a significant association between a brain eQTL rs6088662 on chromosome 20q11.22 and bipolar disorder (log Bayes factor = 5.48; bipolar disorder P = 5.85×10–5). Follow-up studies across multiple independent samples confirmed the association of the risk SNP (rs6088662) with gene expression and bipolar disorder susceptibility (P = 3.54×10–8). Further exploratory analysis revealed that rs6088662 is also associated with hippocampal volume and cognitive performance in healthy individuals.

Our findings suggest that 20q11.22 is likely a risk region for bipolar disorder; they also highlight the informative value of integrating functional annotation of genetic variants for gene expression in advancing our understanding of the biological basis underlying complex disorders, such as bipolar disorder.

People with severe mental illness (SMI) have high rates of chronic disease and premature death.

To explore the strength of evidence for interventions to reduce risk of mortality in people with SMI.

In a meta-review of 16 systematic reviews of controlled studies, mortality was the primary outcome (8 reviews). Physiological health measures (body mass index, weight, glucose levels, lipid profiles and blood pressure) were secondary outcomes (14 reviews).

Antipsychotic and antidepressant medications had some protective effect on mortality, subject to treatment adherence. Integrative community care programmes may reduce physical morbidity and excess deaths, but the effective ingredients are unknown. Interventions to improve unhealthy lifestyles and risky behaviours can improve risk factor profiles, but longer follow-up is needed. Preventive interventions and improved medical care for comorbid chronic disease may reduce excess mortality, but data are lacking.

Improved adherence to pharmacological and physical health management guidelines is indicated.

The monoamine oxidase A (MAOA) gene has been shown to moderate the impact of maltreatment on antisocial behaviour. Replication efforts have, however, yielded inconsistent results.

To investigate whether the interaction between the MAOA gene and violence is present across the full distribution of violence or emerges at higher levels of exposure.

Participants were 327 male members of the Québec Longitudinal Study of Kindergarten Children. Exposure to violence comprised retrospective reports of mother's and father's maltreatment, sexual and physical abuse. Conduct disorder and antisocial personality symptoms were assessed in semi-structured interviews and partner violence, property-violent crimes and arrest were self-reported.

Non-linear interactions between the MAOA gene and violence were detected, suggesting that the genetic moderation may come about once a certain level of violence is experienced.

Future studies should investigate the mechanisms translating substantial violence exposure, which could, subsequently, trigger the expression of genetically based differences in antisocial behaviour.

Numerous studies describe the occurrence of post-traumatic stress disorder following disasters, but less is known about the risk of major depression.

To review the risk of depressive disorder in people surviving disasters and in soldiers returning from military deployment.

A systematic literature search combined with reference screening identified 23 controlled epidemiological studies. We used random effects models to compute pooled odds ratios (ORs).

The average OR was significantly elevated following all types of exposures: natural disaster OR = 2.28 (95% CI 1.30–3.98), technological disaster OR = 1.44 (95% CI 1.21–1.70), terrorist acts OR = 1.80 (95% CI 1.38–2.34) and military combat OR = 1.60 (95% CI 1.09–2.35). In a subset of ten high-quality studies OR was 1.41 (95% CI 1.06–1.87).

Disasters and combat experience substantially increase the risk of depression. Whether psychological trauma per se or bereavement is on the causal path is unresolved.