Autoimmune-mediated basal ganglia dysfunction is implicated in the pathophysiology of neuropsychiatric disorders commonly manifesting with obsessive–compulsive features (e.g. Sydenham chorea). The relationship between autoimmunity and primary obsessive–compulsive disorder (OCD), however, is less clear.

To pool data on serum and cerebrospinal fluid (CSF) anti-basal ganglia antibody (ABGA) positivity in primary OCD (without neurological or autoimmune comorbidity) relative to controls or neuropsychiatric disorders previously associated with increased odds of ABGA positivity.

We performed electronic database and hand-searches for studies meeting pre-specified eligibility criteria from which we extracted data using a standardised form. We calculated pooled estimates of ABGA positivity using a random-effects model.

Seven case–control studies totalling 844 participants met the eligibility criteria. Meta-analysis showed that a significantly greater proportion of those with primary OCD were ABGA seropositive compared with various controls (odds ratio (OR) = 4.97, 95% CI 2.88–8.55, P<0.00001). This effect was not associated with heterogeneity or publication bias, and remained significant after stratifying the analysis by age, gender, disease severity, illness duration, immunostaining methodology, study quality, publication type, kind of control group, and sample size. There were no significant differences in ABGA seropositivity for comparisons between primary OCD and Tourette syndrome, attention-deficit hyperactivity disorder or paediatric acute-onset neuropsychiatric syndrome. Results of one study testing CSF samples showed that a significantly greater proportion of participants with primary OCD were ABGA CSF-positive compared with healthy controls (OR = 5.60, 95% CI 1.04–30.20, P = 0.045).

Odds of ABGA seropositivity are increased fivefold in primary OCD compared with controls, but are comparable to those associated with disorders previously associated with ABGA, providing circumstantial evidence of autoimmunity in a subset of those with primary OCD. Further experimental studies are needed to ascertain whether this relationship is causal.

Pathways from early-life conduct problems to young adult depression remain poorly understood.

To test developmental pathways from early-life conduct problems to depression at age 18.

Data (n = 3542) came from the Avon Longitudinal Study of Parents and Children (ALSPAC). Previously derived conduct problem trajectories (ages 4–13 years) were used to examine associations with depression from ages 10 to 18 years, and the role of early childhood factors as potential confounders.

Over 43% of young adults with depression in the ALSPAC cohort had a history of child or adolescent conduct problems, yielding a population attributable fraction of 0.15 (95% CI 0.08–0.22). The association between conduct problems and depression at age 18 was considerable even after adjusting for prior depression (odds ratio 1.55, 95% CI 1.24–1.94). Early-onset persistent conduct problems carried the highest risk for later depression. Irritability characterised depression for those with a history of conduct problems.

Early-life conduct problems are robustly associated with later depressive disorder and may be useful targets for early intervention.

Obesity has been shown to be associated with depression and it has been suggested that higher body mass index (BMI) increases the risk of depression and other common mental disorders. However, the causal relationship remains unclear and Mendelian randomisation, a form of instrumental variable analysis, has recently been employed to attempt to resolve this issue.

To investigate whether higher BMI increases the risk of major depression.

Two instrumental variable analyses were conducted to test the causal relationship between obesity and major depression in RADIANT, a large case–control study of major depression. We used a single nucleotide polymorphism (SNP) in FTO and a genetic risk score (GRS) based on 32 SNPs with well-established associations with BMI.

Linear regression analysis, as expected, showed that individuals carrying more risk alleles of FTO or having higher score of GRS had a higher BMI. Probit regression suggested that higher BMI is associated with increased risk of major depression. However, our two instrumental variable analyses did not support a causal relationship between higher BMI and major depression (FTO genotype: coefficient −0.03, 95% CI −0.18 to 0.13, P = 0.73; GRS: coefficient −0.02, 95% CI −0.11 to 0.07, P = 0.62).

Our instrumental variable analyses did not support a causal relationship between higher BMI and major depression. The positive associations of higher BMI with major depression in probit regression analyses might be explained by reverse causality and/or residual confounding.

Early identification of patients with bipolar disorder during their first depressive episode is beneficial to the outcome of the disorder and treatment, but traditionally this has been a great challenge to clinicians. Recently, brain-derived neurotrophic factor (BDNF) has been suggested to be involved in the pathophysiology of bipolar disorder and major depressive disorder (MDD), but it is not clear whether BDNF levels can be used to predict bipolar disorder among patients in their first major depressive episode.

To explore whether BDNF levels can differentiate between MDD and bipolar disorder in the first depressive episode.

A total of 203 patients with a first major depressive episode as well as 167 healthy controls were recruited. After 3 years of bi-annual follow-up, 164 patients with a major depressive episode completed the study, and of these, 21 were identified as having bipolar disorder and 143 patients were diagnosed as having MDD. BDNF gene expression and plasma levels at baseline were compared among the bipolar disorder, MDD and healthy control groups. Logistic regression and decision tree methods were applied to determine the best model for predicting bipolar disorder at the first depressive episode.

At baseline, patients in the bipolar disorder and MDD groups showed lower BDNF mRNA levels (P<0.001 and P = 0.02 respectively) and plasma levels (P = 0.002 and P = 0.01 respectively) compared with healthy controls. Similarly, BDNF levels in the bipolar disorder group were lower than those in the MDD group. These results showed that the best model for predicting bipolar disorder during a first depressive episode was a combination of BDNF mRNA levels with plasma BDNF levels (receiver operating characteristics (ROC) = 0.80, logistic regression; ROC = 0.84, decision tree).

Our findings suggest that BDNF levels may serve as a potential differential diagnostic biomarker for bipolar disorder in a patient's first depressive episode.

Although manic episodes reportedly contribute to cognitive deficits in bipolar I disorder, the contribution of depressive episodes is poorly researched.

We investigated the impact of depressive episodes on cognitive function early in the course of bipolar I disorder.

A total of 68 patients and 38 controls from the Systematic Treatment Optimization Programme for Early Mania (STOP-EM) first-episode mania programme were examined. We conducted (a) a cross-sectional analysis of the impact of prior depressive episodes on baseline cognitive function and (b) a prospective analysis assessing the contribution of depression recurrence within 1 year following a first episode of mania on cognitive functioning.

The cross-sectional analysis showed no significant differences between patients with past depressive episodes compared with those without, on overall or individual domains of cognitive function (all P>0.09). The prospective analysis failed to reveal a significant group×time interaction for cognitive decline from baseline to 1 year (P = 0.99) in patients with a recurrence of depressive episodes compared with those with no recurrence. However, impaired verbal memory at baseline was associated with a depression recurrence within 1 year.

Although deficits in all domains of cognitive function are seen in patients early in the course of bipolar disorder, depressive episodes do not confer additional burden on cognitive function. However, poorer verbal memory may serve as a marker for increased susceptibility to depression recurrence early in the course of illness.

All antipsychotic medications carry warnings of increased mortality for older adults, but little is known about comparative mortality risks between individual agents.

To estimate the comparative mortality risks of commonly prescribed antipsychotic agents in older people living in the community.

A retrospective, claims-based cohort study was conducted of people over 65 years old living in the community who had been newly prescribed risperidone, olanzapine, quetiapine, haloperidol, aripiprazole or ziprasidone (n = 136 393). Propensity score-adjusted Cox proportional hazards models assessed the 180-day mortality risk of each antipsychotic compared with risperidone.

Risperidone, olanzapine and haloperidol showed a dose–response relation in mortality risk. After controlling for propensity score and dose, mortality risk was found to be increased for haloperidol (hazard ratio (HR) = 1.18, 95% CI 1.06–1.33) and decreased for quetiapine (HR = 0.81, 95% CI 0.73–0.89) and olanzapine (HR = 0.82, 95% CI 0.74–0.90).

Significant variation in mortality risk across commonly prescribed antipsychotics suggests that antipsychotic selection and dosing may affect survival of older people living in the community.

Psychoeducation programmes for people with schizophrenia are shown to reduce relapses but few studies have indicated significant improvements in patients' illness awareness and insight, functioning, symptom severity or rates of readmission to hospital.

To examine the effects of a mindfulness-based psychoeducation programme for Chinese people with schizophrenia.

A multisite randomised controlled trial was conducted with 107 out-patients with schizophrenia: 36 and 35 received a 6-month mindfulness-based psychoeducation and a conventional psychoeducation programme, respectively, and 35 received routine care alone. Patient outcome measures were psychiatric symptom severity, psychosocial functioning, social support, insight into illness/treatment, and frequency and duration of readmissions to hospital (ClinicalTrials.gov: trial registration NCT01667601).

The mindfulness-based psychoeducation group reported significantly greater improvements in psychiatric symptoms, psychosocial functioning, insight into illness/treatment and duration of readmissions to hospital over 24 months when compared with the other two groups.

Mindfulness-based psychoeducation appears to be a promising approach to treatment for Chinese patients with schizophrenia.

Increasing evidence shows attachment security influences symptom expression and adaptation in people diagnosed with schizophrenia and other psychoses.

To describe the distribution of secure and insecure attachment in a cohort of individuals with first-episode psychosis, and to explore the relationship between attachment security and recovery from positive and negative symptoms in the first 12 months.

The study was a prospective 12-month cohort study. The role of attachment, duration of untreated psychosis (DUP), baseline symptoms and insight in predicting and mediating recovery from symptoms was investigated using multiple regression analysis and path analysis.

Of the 79 participants, 54 completed the Adult Attachment Interview (AAI): 37 (68.5%) were classified as insecure, of which 26 (48.1%) were insecure/dismissing and 11 (20.4%) insecure preoccupied. Both DUP and insight predicted recovery from positive symptoms at 12 months. Attachment security, DUP and insight predicted recovery from negative symptoms at 12 months.

Attachment is an important construct contributing to understanding and development of interventions promoting recovery following first-episode psychosis.

Optimisation of the process and outcomes of service user involvement in research is dependent on understanding current practice, challenges and opportunities.

To describe activities, roles and experiences of service users involved in mental health research.

National cross-sectional online questionnaire survey, using snowball sampling. Descriptive statistics and framework analysis undertaken collaboratively with a service user reference group.

The survey revealed a previously undescribed, highly qualified service user research workforce. Positioned within and alongside mainstream research, respondents reported drawing on extensive service use, and passion for service improvement to challenge perceived clinical academic dominance of research. The support of peers was crucial to involvement, which typically enhanced mental health but for some, pervasive stigma and scrutiny undermined self-confidence and practical difficulties challenged equitable participation.

Recognition of the service user research workforce will support the constructive amalgamation of academic and experiential expertise needed to shape and realise investment in mental health research.