Previous studies have shown an elevated risk for self-harm in adolescents from ethnic minorities. However, potential contributions to this risk from socio-economic factors have rarely been addressed. The main aim of this article was to investigate any such effects.

A national cohort of 1009 157 children born during 1973–1982 was followed prospectively from 1991 to 2002 in Swedish national registers. Multivariate Cox analyses of proportional hazards were used to estimate the relative risk of hospital admission for self-harm. Parental country/region of birth was used as proxy for ethnicity.

Youth with two parents born outside Sweden (except those from Southern Europe) had higher age- and gender-adjusted hazard ratios (HRs) of self-harm than the majority population (HR 1.6–2.3). The HRs decreased for all immigrant groups when socio-economic factors were accounted for but remained significantly higher for immigrants from Finland and Western countries and for youth with one Swedish-born and one foreign-born parent.

Socio-economic factors explain much of the variation by parental country of birth of hospital admissions for self-harm in youth in Sweden.

No previous study has prospectively investigated incidence and risk factors for suicide attempts among primary care patients with depression.

In the Vantaa Primary Care Depression Study, a stratified random sample of 1119 patients was screened for depression, and Structured Clinical Interviews for DSM-IV used to diagnose Axis I and II disorders. A total of 137 patients were diagnosed with a DSM-IV depressive disorder. Altogether, 82% of patients completed the 5-year follow-up. Information on timing of suicide attempts, plus major depressive episodes (MDEs) and partial or full remission, or periods of substance abuse were examined with life charts. Incidence of suicide attempts and their stable and time-varying risk factors (phases of depression/substance abuse) were investigated using Cox proportional hazard and Poisson regression models.

During the follow-up there were 22 discrete suicide attempts by 14/134 (10.4%) patients. The incidence rates were 0, 5.8 and 107 during full or partial remission or MDEs, or 22.2 and 142 per 1000 patient-years during no or active substance abuse, respectively. In Cox models, current MDE (hazard ratio 33.5, 95% confidence interval 3.6–309.7) was the only significant independent risk factor. Primary care doctors were rarely aware of the suicide attempts.

Of the primary care patients with depressive disorders, one-tenth attempted suicide in 5 years. However, risk of suicidal acts was almost exclusively confined to MDEs, with or without concurrent active substance abuse. Suicide prevention among primary care patients with depression should focus on active treatment of major depressive disorder and co-morbid substance use, and awareness of suicide risk.

Similar to visual hallucinations in visually impaired patients, auditory hallucinations are often suggested to occur in adults with hearing impairment. However, research on this association is limited. This observational, cross-sectional study tested whether auditory hallucinations are associated with hearing impairment, by assessing their prevalence in an adult population with various degrees of objectified hearing impairment.

Hallucination presence was determined in 1007 subjects aged 18–92, who were referred for audiometric testing to the Department of ENT-Audiology, University Medical Center Utrecht, the Netherlands. The presence and severity of hearing impairment were calculated using mean air conduction thresholds from the most recent pure tone audiometry.

Out of 829 participants with hearing impairment, 16.2% (n = 134) had experienced auditory hallucinations in the past 4 weeks; significantly more than the non-impaired group [5.8%; n = 10/173; p < 0.001, odds ratio 3.2 (95% confidence interval 1.6–6.2)]. Prevalence of auditory hallucinations significantly increased with categorized severity of impairment, with rates up to 24% in the most profoundly impaired group (p < 0.001). The corrected odds of hallucination presence increased 1.02 times for each dB of impairment in the best ear. Auditory hallucinations mostly consisted of voices (51%), music (36%), and doorbells or telephones (24%).

Our findings reveal that auditory hallucinations are common among patients with hearing impairment, and increase with impairment severity. Although more research on potential confounding factors is necessary, clinicians should be aware of this phenomenon, by inquiring after hallucinations in hearing-impaired patients and, conversely, assessing hearing impairment in patients with auditory hallucinations, since it may be a treatable factor.

Maternal depression during pregnancy increases the risk for adverse developmental outcomes in children. However, the underpinning biological mechanisms remain unknown. We tested whether depression was associated with levels of and change in the inflammatory state during pregnancy, if early pregnancy overweight/obesity or diabetes/hypertensive pregnancy disorders accounted for/mediated these effects, and if depression added to the inflammation that typically accompanies these conditions.

We analyzed plasma high-sensitivity C-reactive protein (hsCRP) and glycoprotein acetyls at three consecutive stages during pregnancy, derived history of depression diagnoses before pregnancy from Care Register for Healthcare (HILMO) (N = 375) and self-reports (N = 347) and depressive symptoms during pregnancy using the Center for Epidemiological Studies Depression Scale completed concurrently to blood samplings (N = 295). Data on early pregnancy body mass index (BMI) and diabetes/hypertensive pregnancy disorders came from medical records.

Higher overall hsCRP levels, but not change, during pregnancy were predicted by history of depression diagnosis before pregnancy [HILMO: mean difference (MD) = 0.69 standard deviation (s.d.) units; 95% confidence interval (CI) 0.26–1.11, self-report: MD = 0.56 s.d.; 95% CI 0.17–0.94] and higher depressive symptoms during pregnancy (0.06 s.d. per s.d. increase; 95% CI 0.00–0.13). History of depression diagnosis before pregnancy also predicted higher overall glycoprotein acetyls (HILMO: MD = 0.52 s.d.; 95% CI 0.12–0.93). These associations were not explained by diabetes/hypertensive disorders, but were accounted for and mediated by early pregnancy BMI. Furthermore, in obese women, overall hsCRP levels increased as depressive symptoms during pregnancy increased (p = 0.006 for interaction).

Depression is associated with a proinflammatory state during pregnancy. These associations are mediated by early pregnancy BMI, and depressive symptoms during pregnancy aggravate the inflammation related to obesity.

Modern personality disorder (PD) theory and research attempt to distinguish transdiagnostic impairments common to all PDs from constructs that explain varied PD expression. Bifactor modeling tests such distinctions; however, the only published PD criteria bifactor analysis focused on only 6 PDs and did not examine the model's construct validity.

We examined the structure and construct validity of competing PD criteria models using confirmatory and exploratory factor analytic methods in 628 patients who completed structured diagnostic interviews and self-reports of personality traits and impairment.

Relative to alternative models, two bifactor models – one confirmatory model with 10 specific factors for each PD (acceptable fit) and one exploratory model with four specific factors resembling broad personality domains (excellent fit) – fit best and were compared via connections with external criteria. General and specific factors related meaningfully and differentially to personality traits, internalizing symptoms, substance use, and multiple indices of psychosocial impairment. As hypothesized, the general factor predicted interpersonal dysfunction above and beyond other psychopathology. The general factor also correlated strongly with many pathological personality traits.

The present study supported the validity of a model with both a general PD impairment dimension and separate individual difference dimensions; however, it also indicated that currently prominent models, which assume general PD impairments and personality traits are non-overlapping, may be misspecified.

Autism spectrum disorder (ASD) and obsessive-compulsive disorder (OCD) share abnormalities in hot executive functions such as reward-based decision-making, as measured in the temporal discounting task (TD). No studies, however, have directly compared these disorders to investigate common/distinct neural profiles underlying such abnormalities. We wanted to test whether reward-based decision-making is a shared transdiagnostic feature of both disorders with similar neurofunctional substrates or whether it is a shared phenotype with disorder-differential neurofunctional underpinnings.

Age and IQ-matched boys with ASD (N = 20), with OCD (N = 20) and 20 healthy controls, performed an individually-adjusted functional magnetic resonance imaging (fMRI) TD task. Brain activation and performance were compared between groups.

Boys with ASD showed greater choice-impulsivity than OCD and control boys. Whole-brain between-group comparison revealed shared reductions in ASD and OCD relative to control boys for delayed-immediate choices in right ventromedial/lateral orbitofrontal cortex extending into medial/inferior prefrontal cortex, and in cerebellum, posterior cingulate and precuneus. For immediate-delayed choices, patients relative to controls showed reduced activation in anterior cingulate/ventromedial prefrontal cortex reaching into left caudate, which, at a trend level, was more decreased in ASD than OCD patients, and in bilateral temporal and inferior parietal regions.

This first fMRI comparison between youth with ASD and with OCD, using a reward-based decision-making task, shows predominantly shared neurofunctional abnormalities during TD in key ventromedial, orbital- and inferior fronto-striatal, temporo-parietal and cerebellar regions of temporal foresight and reward processing, suggesting trans-diagnostic neurofunctional deficits.

Although usually thought of as external environmental stressors, a significant heritable component has been reported for measures of stressful life events (SLEs) in twin studies.

We examined the variance in SLEs captured by common genetic variants from a genome-wide association study (GWAS) of 2578 individuals. Genome-wide complex trait analysis (GCTA) was used to estimate the phenotypic variance tagged by single nucleotide polymorphisms (SNPs). We also performed a GWAS on the number of SLEs, and looked at correlations between siblings.

A significant proportion of variance in SLEs was captured by SNPs (30%, p = 0.04). When events were divided into those considered to be dependent or independent, an equal amount of variance was explained for both. This ‘heritability’ was in part confounded by personality measures of neuroticism and psychoticism. A GWAS for the total number of SLEs revealed one SNP that reached genome-wide significance (p = 4 × 10−8), although this association was not replicated in separate samples. Using available sibling data for 744 individuals, we also found a significant positive correlation of R2 = 0.08 in SLEs (p = 0.03).

These results provide independent validation from molecular data for the heritability of reporting environmental measures, and show that this heritability is in part due to both common variants and the confounding effect of personality.

Anorexia nervosa (AN) is a psychiatric disorder with high mortality.

A retrospective register study of 609 males who received hospitalized care for AN in Sweden between 1973 and 2010 was performed. The standardized mortality ratios (SMRs) and Cox regression-derived hazard ratios (HRs) were calculated as measures of mortality. The incidence rate ratios (IRRs) were calculated to compare the mortality rates in patients with AN and controls both with and without psychiatric diagnoses.

The SMR for all causes of death was 4.1 [95% confidence interval (CI) 3.1–5.3]. For those patients with psychiatric co-morbidities, the SMR for all causes of death was 9.1 (95% CI 6.6–12.2), and for those without psychiatric co-morbidity, the SMR was 1.6 (95% CI 0.9–2.7). For the group of patients with alcohol use disorder, the SMR for natural causes of death was 11.5 (95% CI 5.0–22.7), and that for unnatural causes was 35.5 (95% CI 17.7–63.5). The HRs confirmed the increased mortality for AN patients with psychiatric co-morbidities, even after adjusting for confounders. The IRRs revealed no significant difference in mortality patterns between the AN patients with psychiatric co-morbidity and the controls with psychiatric diagnoses, with the exceptions of alcohol use disorder and neurotic, stress-related and somatoform disorders, which seemed to confer a negative synergistic effect on mortality.

Mortality in male AN patients was significantly elevated compared with the general population among only the patients with psychiatric co-morbidities. Specifically, the presence of alcohol and other substance use disorders was associated with more profound excess mortality.

What determines inter-individual variability to impairments in behavioural control that may underlie road-traffic accidents, and impulsive and violent behaviours occurring under the influence of cannabis, the most widely used illicit drug worldwide?

Employing a double-blind, repeated-measures design, we investigated the genetic and neural basis of variable sensitivity to cannabis-induced behavioural dyscontrol in healthy occasional cannabis users. Acute oral challenge with placebo or Δ9-tetrahydrocannabinol (THC), the main psychoactive ingredient in cannabis, was combined with functional magnetic resonance imaging, while participants performed a response inhibition task that involved inhibiting a pre-potent motor response. They were genotyped for rs1130233 single nucleotide polymorphisms (SNPs) of the protein kinase B (AKT1) gene.

Errors of inhibition were significantly (p = 0.008) increased following administration of THC in carriers of the A allele, but not in G allele homozygotes of the AKT1 rs1130233 SNP. The A allele carriers also displayed attenuation of left inferior frontal response with THC evident in the sample as a whole, while there was a modest enhancement of inferior frontal activation in the G homozygotes. There was a direct relationship (r = − 0.327, p = 0.045) between the behavioural effect of THC and its physiological effect in the inferior frontal gyrus, where AKT1 genotype modulated the effect of THC.

These results require independent replication and show that differing vulnerability to acute psychomotor impairments induced by cannabis depends on variation in a gene that influences dopamine function, and is mediated through modulation of the effect of cannabis on the inferior frontal cortex, that is rich in dopaminergic innervation and critical for psychomotor control.