Trials evaluating efficacy of omega-3 highly unsaturated fatty acids (HUFAs) in major depressive disorder report discrepant findings.

To establish the reasons underlying inconsistent findings among randomised controlled trials (RCTs) of omega-3 HUFAs for depression and to assess implications for further trials.

A systematic bibliographic search of double-blind RCTs was conducted between January 1980 and July 2014 and an exploratory hypothesis-testing meta-analysis performed in 35 RCTs including 6665 participants receiving omega-3 HUFAs and 4373 participants receiving placebo.

Among participants with diagnosed depression, eicosapentaenoic acid (EPA)-predominant formulations (>50% EPA) demonstrated clinical benefits compared with placebo (Hedge's G = 0.61, P<0.001) whereas docosahexaenoic acid (DHA)-predominant formulations (>50% DHA) did not. EPA failed to prevent depressive symptoms among populations not diagnosed for depression.

Further RCTs should be conducted on study populations with diagnosed or clinically significant depression of adequate duration using EPA-predominant omega-3 HUFA formulations.

Recent studies point to overlap between neuropsychiatric disorders in symptomatology and genetic aetiology.

To systematically investigate genomics overlap between childhood and adult attention-deficit hyperactivity disorder (ADHD), autism spectrum disorder (ASD) and major depressive disorder (MDD).

Analysis of whole-genome blood gene expression and genetic risk scores of 318 individuals. Participants included individuals affected with adult ADHD (n = 93), childhood ADHD (n = 17), MDD (n = 63), ASD (n = 51), childhood dual diagnosis of ADHD–ASD (n = 16) and healthy controls (n = 78).

Weighted gene co-expression analysis results reveal disorder-specific signatures for childhood ADHD and MDD, and also highlight two immune-related gene co-expression modules correlating inversely with MDD and adult ADHD disease status. We find no significant relationship between polygenic risk scores and gene expression signatures.

Our results reveal disorder overlap and specificity at the genetic and gene expression level. They suggest new pathways contributing to distinct pathophysiology in psychiatric disorders and shed light on potential shared genomic risk factors.

The status and differentiation of comorbid borderline personality disorder and bipolar disorder is worthy of clarification.

To determine whether comorbid borderline personality disorder and bipolar disorder are interdependent or independent conditions.

We interviewed patients diagnosed with either a borderline personality disorder and/or a bipolar condition.

Analyses of participants grouped by DSM diagnoses established that those with comorbid conditions scored similarly to those with a borderline personality disorder alone on all key variables (i.e. gender, severity of borderline personality scores, developmental stressors, illness correlates, self-injurious behaviour rates) and differed from those with a bipolar disorder alone on nearly all non-bipolar item variables. Similar findings were returned for groups defined by clinical diagnoses.

Comorbid bipolar disorder and borderline personality disorder is consistent with the formal definition of comorbidity in that, while coterminous, individuals meeting such criteria have features of two independent conditions.

Anxiety disorders and depression are the most common mental disorders worldwide and have a striking impact on global disease burden. Although depression has consistently been found to increase mortality; the role of anxiety disorders in predicting mortality risk is unclear.

To assess mortality risk in people with anxiety disorders.

We used nationwide Danish register data to conduct a prospective cohort study with over 30 million person-years of follow-up.

In total, 1066 (2.1%) people with anxiety disorders died during an average follow-up of 9.7 years. The risk of death by natural and unnatural causes was significantly higher among individuals with anxiety disorders (natural mortality rate ratio (MRR) = 1.39, 95% CI 1.28–1.51; unnatural MRR= 2.46, 95% CI 2.20–2.73) compared with the general population. Of those who died from unnatural causes, 16.5% had comorbid diagnoses of depression (MRR = 11.72, 95% CI 10.11–13.51).

Anxiety disorders significantly increased mortality risk. Comorbidity of anxiety disorders and depression played an important part in the increased mortality.

Repetitive transcranial magnetic stimulation (rTMS) holds promise for treating generalised anxiety disorder (GAD) but has only been studied in uncontrolled research.

This is the first randomised controlled trial (clinicaltrials.gov: NCT01659736) to investigate the efficacy and neural correlates of rTMS in GAD.

Twenty five participants (active n = 13; sham, n = 12) enrolled. rTMS was targeted at the right dorsolateral prefrontal cortex (DLPFC, 1 Hz, 90% resting motor threshold).

Response and remission rates were higher in the active v. sham groups and there were significant group × time interactions for anxiety, worry and depressive symptoms, favouring active v. sham. In addition, right DLPFC activation during a decision-making gambling task increased at post-treatment for active rTMS only, and changes in neuroactivation correlated significantly with changes in worry symptoms.

Findings provide preliminary evidence that rTMS may improve GAD symptoms in association with modifying neural activity in the stimulation site.

Selective serotonin reuptake inhibitors (SSRIs) and cognitive–behavioural therapy (CBT) are often used concomitantly to treat social anxiety disorder (SAD), but few studies have examined the effect of this combination.

To evaluate whether adding escitalopram to internet-delivered CBT (ICBT) improves clinical outcome and alters brain reactivity and connectivity in SAD.

Double-blind, randomised, placebo-controlled neuroimaging trial of ICBT combined either with escitalopram (n = 24) or placebo (n = 24), including a 15-month clinical follow-up (trial registration: ISRCTN24929928).

Escitalopram+ICBT, relative to placebo+ICBT, resulted in significantly more clinical responders, larger reductions in anticipatory speech state anxiety at post-treatment and larger reductions in social anxiety symptom severity at 15-month follow-up and at a trend-level (P = 0.09) at post-treatment. Right amygdala reactivity to emotional faces also decreased more in the escitalopram+ICBT combination relative to placebo+ICBT, and in treatment responders relative to non-responders.

Adding escitalopram improves the outcome of ICBT for SAD and decreased amygdala reactivity is important for anxiolytic treatment response.

Anxiety disorders are common, and cognitive–behavioural therapy (CBT) is a first-line treatment. Candidate gene studies have suggested a genetic basis to treatment response, but findings have been inconsistent.

To perform the first genome-wide association study (GWAS) of psychological treatment response in children with anxiety disorders (n = 980).

Presence and severity of anxiety was assessed using semi-structured interview at baseline, on completion of treatment (post-treatment), and 3 to 12 months after treatment completion (follow-up). DNA was genotyped using the Illumina Human Core Exome-12v1.0 array. Linear mixed models were used to test associations between genetic variants and response (change in symptom severity) immediately post-treatment and at 6-month follow-up.

No variants passed a genome-wide significance threshold (P=5×10–8) in either analysis. Four variants met criteria for suggestive significance (P<5×10–6) in association with response post-treatment, and three variants in the 6-month follow-up analysis.

This is the first genome-wide therapygenetic study. It suggests no common variants of very high effect underlie response to CBT. Future investigations should maximise power to detect single-variant and polygenic effects by using larger, more homogeneous cohorts.

Health anxiety, hypochondriasis and personality disturbance commonly coexist. The impact of personality status was assessed in a secondary analysis of a randomised controlled trial (RCT).

To test the impact of personality status using ICD-11 criteria on the clinical and cost outcomes of treatment with cognitive–behavioural therapy for health anxiety (CBT-HA) and standard care over 2 years.

Personality dysfunction was assessed at baseline in 444 patients before randomisation and independent assessment of costs and outcomes made on four occasions over 2 years.

In total, 381 patients (86%) had some personality dysfunction with 184 (41%) satisfying the ICD criteria for personality disorder. Those with no personality dysfunction showed no treatment differences (P = 0.90) and worse social function with CBT-HA compared with standard care (P<0.03) whereas all other personality groups showed greater improvement with CBT-HA maintained over 2 years (P<0.001). Less benefit was shown in those with more severe personality disorder (P<0.05). Costs were less with CBT-HA except for non-significant greater differences in those with moderate or severe personality disorder.

The results contradict the hypothesis that personality disorder impairs response to CBT in health anxiety in both the short and medium term.

Cognitive–behavioural therapy (CBT) is one of the most promising treatments for chronic fatigue syndrome (CFS). It is unclear whether CBT is effective for Black and minority ethnic (BME) groups.

To assess the effectiveness of CBT in BME patients compared with White British patients presenting to a specialist CFS service.

Data from 67 (19.0%) BME participants and 285 (81.0%) White British participants referred to a specialist CFS service in the UK were collected at baseline and after CBT treatment.

Pairwise comparisons revealed that both BME participants and White British participants significantly improved on measures of fatigue severity (P<0.001), physical functioning (P<0.001) and work/social adjustment (P<0.001). Independent samples t-tests showed that BME participants improved despite exhibiting significantly higher baseline damage beliefs (P = 0.009), catastrophising (P = 0.024), all-or-nothing behaviour (P = 0.036) and avoidance/resting behaviour (P = 0.001), compared with White British participants.

To our knowledge, this study is the first to indicate that CBT is effective for treating CFS in a group of patients from diverse BME backgrounds.

There is an established disparity between physical and mental healthcare. Parity of research outputs has not been assessed internationally across influential medical journals.

To assess parity of publication between physical and mental health, and within psychiatry.

Four major medical disciplines were identified and their relative burden estimated. All publications from the highest-impact general medical journals in 2001, 2006 and 2011 were categorised accordingly. The frequency of psychiatry, cardiology, oncology and respiratory medicine articles were compared with the expected proportion (given illness burdens). Six subspecialties within psychiatry were also compared.

Psychiatry was consistently and substantially underrepresented; other specialties were overrepresented. Dementia and psychosis demonstrated overrepresentation, with addiction and anxiety disorders represented proportionately and other disorders underrepresented. The underrepresentation of mood disorders increased more recently.

There appears to be an important element of disparity of esteem; further action is required to achieve equivalence between mental and physical health research publications.