Families express a need for information to support people with severe anorexia nervosa.

To examine the impact of the addition of a skills training intervention for caregivers (Experienced Caregivers Helping Others, ECHO) to standard care.

Patients over the age of 12 (mean age 26 years, duration 72 months illness) with a primary diagnosis of anorexia nervosa and their caregivers were recruited from 15 in-patient services in the UK. Families were randomised to ECHO (a book, DVDs and five coaching sessions per caregiver) or treatment as usual. Patient (n=178) and caregiver (n=268) outcomes were measured at discharge and 6 and 12 months after discharge.

Patients with caregivers in the ECHO group had reduced eating disorder psychopathology (EDE-Q) and improved quality of life (WHO-Quol; both effects small) and reduced in-patient bed days (7–12 months post-discharge). Caregivers in the ECHO group had reduced burden (Eating Disorder Symptom Impact Scale, EDSIS), expressed emotion (Family Questionnaire, FQ) and time spent caregiving at 6 months but these effects were diminished at 12 months.

Small but sustained improvements in symptoms and bed use are seen in the intervention group. Moreover, caregivers were less burdened and spent less time providing care. Caregivers had most benefit at 6 months suggesting that booster sessions, perhaps jointly with the patients, may be needed to maintain the effect. Sharing skills and information with caregivers may be an effective way to improve outcomes. This randomised controlled trial (RCT) was registered with Current Controlled Trials ISRCTN06149665.

Hyperprolactinaemia is a troublesome side-effect of treatment with antipsychotics.

This double-blind, placebo-controlled study aimed at examining the effect of adjunctive treatment with 10 mg aripiprazole on prolactin levels and sexual side-effects in patients with schizophrenia symptomatically maintained on risperidone.

Thirty patients taking risperidone were enrolled into the trial (CTRI/2012/11/003114). Aripiprazole was administered at a fixed daily dose of 10 mg/day for 8 weeks. Serum prolactin was measured at baseline and at 8 weeks. Hyperprolactinaemia-related problems, psychopathology and side-effects were evaluated every 2 weeks.

Prolactin levels decreased by 58% in the aripiprazole group compared with an increase by 22% in the placebo group. Prolactin levels normalised in 46% of patients in the aripiprazole group (number needed to treat, NNT=2). Aripiprazole improved erectile dysfunction in five out of six patients. There were no significant differences in change in psychopathology or side-effects between groups.

Adjunctive aripiprazole reduced prolactin levels in those treated with risperidone, with no effect on psychopathology and extrapyramidal symptoms. This is a potential treatment for hyperprolactinaemia observed during treatment with second-generation antipsychotics.

Clozapine causes significant metabolic disturbances including obesity and type 2 diabetes. Recent evidence that reduced glucagon-like-peptide-1 (GLP-1) may contribute to aetiology of clozapine-associated metabolic dysregulation suggests a potential therapeutic role for GLP-1 agonists.

This open-label, pilot randomised controlled trial evaluates the effect of exenatide in clozapine-treated obese adults who have schizophrenia, with or without poorly controlled diabetes. Sixty out-patients will be randomised to once weekly extended release exenatide or treatment as usual for 24 weeks.

To evaluate the feasibility of larger studies regarding methodology, acceptability, tolerability and estimate efficacy for glycaemic control or weight loss. Secondary outcomes are psychosis severity and metabolic parameters.

This is the first trial investigating GLP-1 agonists for glycaemic control and weight loss in clozapine-treated patients with either diabetes or obesity. Clozapine-associated obesity and diabetes with exenatide (CODEX) will provide proof-of-concept empirical evidence addressing whether this novel treatment is practical and worthy of further investigation.

Intellectual ability may be an endophenotypic marker for bipolar disorder.

Within a large birth cohort, we aimed to assess whether childhood IQ (including both verbal IQ (VIQ) and performance IQ (PIQ) subscales) was predictive of lifetime features of bipolar disorder assessed in young adulthood.

We used data from the Avon Longitudinal Study of Parents and Children (ALSPAC), a large UK birth cohort, to test for an association between measures of childhood IQ at age 8 years and lifetime manic features assessed at age 22–23 years using the Hypomania Checklist-32 (HCL-32; n=1881 individuals). An ordinary least squares linear regression model was used, with normal childhood IQ (range 90–109) as the referent group. We adjusted analyses for confounding factors, including gender, ethnicity, handedness, maternal social class at recruitment, maternal age, maternal history of depression and maternal education.

There was a positive association between IQ at age 8 years and lifetime manic features at age 22–23 years (Pearson's correlation coefficient 0.159 (95% CI 0.120–0.198), P>0.001). Individuals in the lowest decile of manic features had a mean full-scale IQ (FSIQ) which was almost 10 points lower than those in the highest decile of manic features: mean FSIQ 100.71 (95% CI 98.74–102.6) v. 110.14 (95% CI 107.79–112.50), P>0.001. The association between IQ and manic features was present for FSIQ, VIQ and for PIQ but was strongest for VIQ.

A higher childhood IQ score, and high VIQ in particular, may represent a marker of risk for the later development of bipolar disorder. This finding has implications for understanding of how liability to bipolar disorder may have been selected through generations. It will also inform future genetic studies at the interface of intelligence, creativity and bipolar disorder and is relevant to the developmental trajectory of bipolar disorder. It may also improve approaches to earlier detection and treatment of bipolar disorder in adolescents and young adults.

Few studies have examined the contribution of specific disaster-related experiences to post-traumatic stress disorder (PTSD) symptoms.

To examine the roles of peri-traumatic stress and distress due to lingering disaster-related disruption in explaining linkages between disaster exposure and PTSD symptoms among a cohort exposed to the 2010–2011 Canterbury (New Zealand) earthquakes.

Structural equation models were fitted to data obtained from the Christchurch Health and Development Study at age 35 (n=495), 20–24 months following the onset of the disaster. Measures included: earthquake exposure, peri-traumatic stress, disruption distress and PTSD symptoms.

The associations between earthquake exposure and PTSD symptoms were explained largely by the experience of peri-traumatic stress during the earthquakes (β=0.189, P<0.0001) and disruption distress following the earthquakes (β=0.105, P<0.0001).

The results suggest the importance of minimising post-event disruption distress following exposure to a natural disaster.

The 2011 Great Japan tsunami and nuclear leaks displaced 300 000 people, but there are no large studies of psychological distress suffered by these refugees.

To provide a first assessment of major factors associated with distress and dysfunctional behaviour following the disasters.

All refugee families living in Miyagi were sent a questionnaire 10–12 months after the disasters. 21 981 participants (73%) returned questionnaires. Questions assessed psychological distress (Kessler Psychological Distress Scale, K6), dysfunctional behaviours, demographics, event exposure, change in physical activity, household visitors and emotional support.

Nine percent scored 13+ on the K6 indicating risk of severe mental illness. Psychological distress was greater among Fukushima refugees. Demographic variables, family loss, illness history and change in physical activity were associated with psychological distress and dysfunctional behaviours. Associations between psychological distress and dysfunction and visitors/supporters depended on relation to supporter.

Practitioners need to recognise existing disease burden, community histories and family roles when intervening following disasters.

Empirical studies of rationality (syllogisms) in patients with schizophrenia have obtained different results. One study found that patients reason more logically if the syllogism is presented through an unusual content.

To explore syllogism-based rationality in schizophrenia.

Thirty-eight first-admitted patients with schizophrenia and 38 healthy controls solved 29 syllogisms that varied in presentation content (ordinary v. unusual) and validity (valid v. invalid). Statistical tests were made of unadjusted and adjusted group differences in models adjusting for intelligence and neuropsychological test performance.

Controls outperformed patients on all syllogism types, but the difference between the two groups was only significant for valid syllogisms presented with unusual content. However, when adjusting for intelligence and neuropsychological test performance, all group differences became non-significant.

When taking intelligence and neuropsychological performance into account, patients with schizophrenia and controls perform similarly on syllogism tests of rationality.

Cross-sectional studies suggest that the serotonin transporter promoter region polymorphism (5-HTT gene-linked polymorphic region, 5HTTLPR) moderates the relationship between childhood abuse and major depressive disorder.

To examine whether the 5HTTLPR polymorphism moderates the effect childhood abuse has on 5-year depressive symptom severity trajectories in adulthood.

At 5-year follow-up, DNA from 333 adult primary care attendees was obtained and genotyped for the 5HTTLPR polymorphism. Linear mixed models were used to test for a genotype × childhood abuse interaction effect on 5-year depressive symptom severity trajectories.

After covariate adjustment, homozygous s allele carriers with a history of severe childhood abuse had significantly greater depressive symptom severity at baseline compared with those without a history of severe childhood abuse and this effect persisted throughout the 5-year period of observation.

The 5HTTLPR s/s genotype robustly moderates the effects of severe childhood abuse on depressive symptom severity trajectories in adulthood.