Overworking is one of the most frequent stressors. The purpose of this study was to determine the effectiveness of behavioural/psycho-educational group training in men who are chronically stressed from overworking.

Of 72 male subjects, 36 were randomly assigned to training for 8 weeks and another 36 formed the control group, which received a placebo intervention. Primary outcome measures were systolic blood pressure, salivary cortisol concentration upon awakening, and self-reported changes on the scales of the Trier Inventory for the Assessment of Chronic Stress (TICS), the State-Trait Anger Expression Inventory (STAXI) and the 36-item Short Form Health Survey (SF-36).

A significant reduction in mean values was observed in daily systolic blood pressure and salivary cortisol concentration on all the TICS and most of the STAXI and SF-36 scales.

Behavioural/psycho-educational group training appears to be effective in the treatment of men suffering from chronic stress due to overworking.

Available research has suggested that affiliation with prosocial peers reduces child and adolescent antisocial behavior. However, the etiologic mechanisms driving this association remain unclear. The current study sought to evaluate whether this association takes the form of a gene–environment interaction (G × E) in which prosocial peer affiliation acts to reduce the consequences of genetic risk for non-aggressive antisocial behavior during childhood.

Our sample consisted of 500 twin pairs aged 6–10 years from the Michigan State University Twin Registry (MSUTR).

The results robustly support moderation by prosocial peer affiliation. Genetic influences on non-aggressive antisocial behavior were observed to be several times larger in those with lower levels of prosocial peer affiliation than in those with higher levels of prosocial peer affiliation. This pattern of results persisted even after controlling for gene–environment correlations and deviant peer affiliation, and when restricting our analyses to those twins who shared all or nearly all of their friends.

Such findings not only suggest that prosocial peer affiliation moderates genetic influences on non-aggressive antisocial behaviors during childhood but also provide support for the theoretical notion that protective environmental experiences may exert their influence by promoting resilience to genetic risk.

Reduced cortical gray-matter volume is commonly observed in patients with psychosis. Cortical volume is a composite measure that includes surface area, thickness and gyrification. These three indices show distinct maturational patterns and may be differentially affected by early adverse events. The study goal was to determine the impact of two distinct obstetrical complications (OCs) on cortical morphology.

A detailed birth history and MRI scans were obtained for 36 patients with first-episode psychosis and 16 healthy volunteers.

Perinatal hypoxia and slow fetal growth were associated with cortical volume (Cohen's d = 0.76 and d = 0.89, respectively) in patients. However, the pattern of associations differed across the three components of cortical volume. Both hypoxia and fetal growth were associated with cortical surface area (d = 0.88 and d = 0.72, respectively), neither of these two OCs was related to cortical thickness, and hypoxia but not fetal growth was associated with gyrification (d = 0.85). No significant associations were found within the control sample.

Cortical dysmorphology was associated with OCs. The use of a global measure of cortical morphology or a global measure of OCs obscured important relationships between these measures. Gyrification is complete before 2 years and its strong relationship with hypoxia suggests an early disruption to brain development. Cortical thickness matures later and, consistent with previous research, we found no association between thickness and OCs. Finally, cortical surface area is largely complete by puberty and the present results suggest that events during childhood do not fully compensate for the effects of early disruptive events.

Electroencephalography and magnetoencephalography (MEG) studies have identified alterations in gamma-band (30–80 Hz) cortical activity in schizophrenia and mood disorders, consistent with neural models of disturbed glutamate (and GABA) neuron influence over cortical pyramidal cells. Genetic evidence suggests specific deficits in GABA-A receptor function in schizoaffective bipolar disorder (SABP), a clinical syndrome with features of both bipolar disorder and schizophrenia. This study investigated gamma oscillations in this under-researched disorder.

MEG was used to measure induced gamma and evoked responses to a visual grating stimulus, known to be a potent inducer of primary visual gamma oscillations, in 15 individuals with remitted SABP, defined using Research Diagnostic Criteria, and 22 age- and sex-matched healthy controls.

Individuals with SABP demonstrated increased sustained visual cortical power in the gamma band (t35 = −2.56, p = 0.015) compared to controls. There were no group differences in baseline gamma power, transient or sustained gamma frequency, alpha band responses or pattern onset visual-evoked responses.

Gamma power is increased in remitted SABP, which reflects an abnormality in the cortical inhibitory-excitatory balance. Although an interaction between gamma power and medication can not be ruled out, there were no group differences in evoked responses or baseline measures. Further work is needed in other clinical populations and at-risk relatives. Pharmaco-magnetoencephalography studies will help to elucidate the specific GABA and glutamate pathways affected.

Genetic variation in the gene encoding ZNF804A, a risk gene for schizophrenia, has been shown to affect brain functional endophenotypes of the disorder, while studies of white matter structure have been inconclusive.

We analysed effects of ZNF804A single nucleotide polymorphism rs1344706 on grey and white matter using voxel-based morphometry (VBM) in high-resolution T1-weighted magnetic resonance imaging scans of 62 schizophrenia patients and 54 matched healthy controls.

We found a significant (p < 0.05, family-wise error corrected for multiple comparisons) interaction effect of diagnostic group x genotype for local grey matter in the left orbitofrontal and right and left lateral temporal cortices, where patients and controls showed diverging effects of genotype. Analysing the groups separately (at p < 0.001, uncorrected), variation in rs1344706 showed effects on brain structure within the schizophrenia patients in several areas including the left and right inferior temporal, right supramarginal/superior temporal, right and left inferior frontal, left frontopolar, right and left dorsolateral/ventrolateral prefrontal cortices, and the right thalamus, as well as effects within the healthy controls in left lateral temporal, right anterior insula and left orbitofrontal cortical areas. We did not find effects of genotype of regional white matter in either of the two cohorts.

Our findings demonstrate effects of ZNF804A genetic variation on brain structure, with diverging regional effects in schizophrenia patients and healthy controls in frontal and temporal brain areas. These effects, however, might be dependent on the impact of other (genetic or non-genetic) disease factors.

PredictD is a risk algorithm that was developed to predict risk of onset of major depression over 12 months in general practice attendees in Europe and validated in a similar population in Chile. It was the first risk algorithm to be developed in the field of mental disorders. Our objective was to extend predictD as an algorithm to detect people at risk of major depression over 24 months.

Participants were 4190 adult attendees to general practices in the UK, Spain, Slovenia and Portugal, who were not depressed at baseline and were followed up for 24 months. The original predictD risk algorithm for onset of DSM-IV major depression had already been developed in data arising from the first 12 months of follow-up. In this analysis we fitted predictD to the longer period of follow-up, first by examining only the second year (12–24 months) and then the whole period of follow-up (0–24 months).

The instrument performed well for prediction of major depression from 12 to 24 months [c-index 0.728, 95% confidence interval (CI) 0.675–0.781], or over the whole 24 months (c-index 0.783, 95% CI 0.757–0.809).

The predictD risk algorithm for major depression is accurate over 24 months, extending it current use of prediction over 12 months. This strengthens its use in prevention efforts in general medical settings.

Bipolar disorder (BD) is a highly heritable mood disorder with complex genetic architecture and poorly understood etiology. Previous transcriptomic BD studies have had inconsistent findings due to issues such as small sample sizes and difficulty in adequately accounting for confounders like medication use.

We performed a differential expression analysis in a well-characterized BD case-control sample (Nsubjects = 480) by RNA sequencing of whole blood. We further performed co-expression network analysis, functional enrichment, and cell type decomposition, and integrated differentially expressed genes with genetic risk.

While we observed widespread differential gene expression patterns between affected and unaffected individuals, these effects were largely linked to lithium treatment at the time of blood draw (FDR < 0.05, Ngenes = 976) rather than BD diagnosis itself (FDR < 0.05, Ngenes = 6). These lithium-associated genes were enriched for cell signaling and immune response functional annotations, among others, and were associated with neutrophil cell-type proportions, which were elevated in lithium users. Neither genes with altered expression in cases nor in lithium users were enriched for BD, schizophrenia, and depression genetic risk based on information from genome-wide association studies, nor was gene expression associated with polygenic risk scores for BD.

These findings suggest that BD is associated with minimal changes in whole blood gene expression independent of medication use but emphasize the importance of accounting for medication use and cell type heterogeneity in psychiatric transcriptomic studies. The results of this study add to mounting evidence of lithium's cell signaling and immune-related mechanisms.

There is a paucity of long-term prospective disaster studies of the psychological sequelae among survivors.

At 1½ and 25 years after the Spitak earthquake, 142 early adolescents from two cities were assessed: Gumri (moderate–severe exposure) and Spitak (very severe exposure). The Gumri group included treated and not-treated subjects, while the Spitak group included not-treated subjects. Instruments included: DSM-III-R PTSD-Reaction Index (PTSD-RI); DSM-5 PTSD-Checklist (PCL); Depression Self-Rating Scale (DSRS); and Center for Epidemiological Studies-Depression Scale (CES-D).

(1) Between 1½ and 25 years, PTSD rates and mean scores decreased significantly in the three groups (over 50%). However, at 25 years 9.1–22.4% met DSM-5 PTSD criteria. (2) At 1½ years, the Spitak group had higher PTSD-RI (p < 0.001) and DSRS scores (p < 0.001) compared to the Gumri-not-treated group. At 25 years, the Spitak group that had experienced fewer post-earthquake adversities (p < 0.03), had a greater decrease in PTSD-RI scores (p < 0.02), and lower CES-D scores (p < 0.01). (3) Before treatment, PTSD-RI and DSRS scores did not differ between the Gumri-treated and not-treated groups. At 25-years, the Gumri-treated group showed a greater decrease in PTSD-RI scores (p < 0.03), and lower mean PTSD-RI (p < 0.02), PCL (p < 0.02), and CES-D (p < 0.01) scores. (4) Predictors of PTSD symptom severity at 25-years included: home destruction, treatment, social support, post-earthquake adversities, and chronic medical illnesses.

Post-disaster PTSD and depressive symptoms can persist for decades. Trauma-focused treatment, alleviation of post-disaster adversities, improving the social ecology, and monitoring for chronic medical illnesses are essential components of recovery programs.

Severity is an important characteristic of major depression (MD) and an ‘episode specifier’ in DSM-IV classifying depressive episodes as ‘mild’, ‘moderate’ or ‘severe’. These severity subtypes rely on three different measures of severity: number of criteria symptoms, severity of the symptoms and degree of functional disability. No prior empirical study has evaluated the coherence and validity of the DSM-IV definition of severity of MD.

In a sample of 1015 (518 males, 497 females) Caucasian twins from a population-based registry who met criteria for MD in the year prior to interview, factor analysis and logistic regression were conducted to examine the inter-relationships of the three severity measures and their associations with a wide range of potential validators including demographic factors, risk for future episodes, risk of MD in the co-twin, characteristics of the depressive episode, the pattern of co-morbidity, and personality traits.

Correlations between the three severity measures were significant but moderate. Factor analysis indicated the existence of a general severity factor, but the factor was not highly coherent. The three severity measures showed differential predictive ability for most of the validators.

Severity of MD as defined by the DSM-IV is a multifaceted and heterogeneous construct. The three proposed severity measures reflect partly overlapping but partly independent domains with differential validity as assessed by a wide range of clinical characteristics. Clinicians should probably use a combination of severity measures as proposed in DSM-IV rather than privileging one.