Although aggressive (AGG) and non-aggressive rule-breaking (RB) dimensions of antisocial behavior have been shown to be differentially heritable, available studies have disagreed on the extent to which the genetic and environmental factors influencing AGG also influence RB. The current meta-analysis sought to clarify the extent of etiological overlap between AGG and RB.

Thirteen twin/sibling studies examining the covariation between AGG and RB were collected, of which 11 (with 12 independent samples) were ultimately included in the analyses (n=12923 twin/sibling pairs). Genetic and environmental correlations between AGG and RB served as study effect sizes. When squared, these correlations directly index the proportion of genetic and environmental overlap. Data were analyzed using mixed effect models.

Analyses revealed that genetic influences on AGG were largely, but not entirely, distinct from those on RB: only 38.4% of the genetic influences on AGG overlapped with those on RB. Similarly, only 10.2% of the non-shared environmental influences on AGG overlapped with those on RB. Although the conclusion that etiological influences on AGG are partially distinct from those on RB persisted across several potential moderators, the age of the sample and the informant used were found to moderate the extent of overlap.

The findings underscore the presence of meaningful etiological distinctions between AGG and RB, and imply that future conceptualizations of antisocial behavior should be organized (at least in part) around the dimensions of AGG and RB.

Childhood adverse experiences are known to induce persistent changes in the hypothalamic–pituitary–adrenal (HPA) axis reactivity to stress. However, the mechanisms by which these experiences shape the neuroendocrine response to stress remain unclear.

We tested whether bullying victimization influenced serotonin transporter gene (SERT) DNA methylation using a discordant monozygotic (MZ) twin design. A subsample of 28 MZ twin pairs discordant for bullying victimization, with data on cortisol and DNA methylation, were identified in the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative 1994–1995 cohort of families with twins.

Bullied twins had higher SERT DNA methylation at the age of 10 years compared with their non-bullied MZ co-twins. This group difference cannot be attributed to the children's genetic makeup or their shared familial environments because of the study design. Bullied twins also showed increasing methylation levels between the age of 5 years, prior to bullying victimization, and the age of 10 years whereas no such increase was detected in non-bullied twins across time. Moreover, children with higher SERT methylation levels had blunted cortisol responses to stress.

Our study extends findings drawn from animal models, supports the hypothesis that early-life stress modifies DNA methylation at a specific cytosine–phosphate–guanine (CpG) site in the SERT promoter and HPA functioning and suggests that these two systems may be functionally associated.

Childhood emotional maltreatment (CEM) has been associated with disturbances in emotional and behavioral functioning, and with changes in regional brain morphology. However, whether CEM has any effect on the intrinsic organization of the brain is not known. In this study, we investigated the effects of CEM on resting-state functional connectivity (RSFC) using seeds in the limbic network, the default-mode network (DMN) and the salience network, and the left dorsomedial prefrontal cortex (dmPFC).

Using 3-T magnetic resonance imaging (MRI), resting-state functional MRI (RS-fMRI) scans were obtained. We defined seeds in the bilateral amygdala, the dorsal anterior cingulate cortex (dACC), the posterior cingulate cortex (PCC) and the left dmPFC, and used these to examine whether individuals reporting CEM (n=44) differed from individuals reporting no CEM (n=44) in RSFC with other brain regions. The two groups were matched for age, gender, handedness and the presence of psychopathology.

CEM was associated with decreased RSFC between the right amygdala and the bilateral precuneus and a cluster extending from the left insula to the hippocampus and putamen. In addition, CEM was associated with decreased RSFC between the dACC and the precuneus and also frontal regions of the brain.

We found that CEM has a profound effect on RSFC in the limbic network and the salience network. Regions that show aberrant connectivity are related to episodic memory encoding, retrieval and self-processing operations.

Prevalence rates of post-traumatic stress disorder (PTSD) following the experience of war have been shown to be high. However, little is known about the course of the disorder in people who remained in the area of conflict and in refugees.

We studied a representative sample of 522 adults with war-related PTSD in five Balkan countries and 215 compatriot refugees in three Western European countries. They were assessed on average 8 years after the war and reinterviewed 1 year later. We established change in PTSD symptoms, measured on the Impact of Events Scale – Revised (IES-R), and factors associated with more or less favourable outcomes.

During the 1-year period, symptoms decreased substantially in both Balkan residents and in refugees. The differences were significant for IES-R total scores and for the three subscales of intrusions, avoidance and hyperarousal. In multivariable regressions adjusting for the level of baseline symptoms, co-morbidity with depression predicted less favourable symptom change in Balkan residents. More pre-war traumatic events and the use of mental health services within the follow-up period were associated with less improvement in refugees.

Several years after the war, people with PTSD reported significant symptom improvement that might indicate a fluctuating course over time. Co-morbid depression may have to be targeted in the treatment of people who remained in the post-conflict regions whereas the use of mental health services seems to be linked to the persistence of symptoms among refugees.

Although the association between cannabis use and a wide range of psychiatric symptoms is fairly well established, it is not clear whether cannabis use is also a risk factor for general mental health problems at secondary school.

A total of 10 324 secondary school children aged 11–16 years, participating in an ongoing Public Health Service School Survey, gave information on demographics, substance use, school factors and stressful life events and completed the Strengths and Difficulties Questionnaire (SDQ).

Cannabis use in the past month was associated with a clinically relevant score on the SDQ [unadjusted odds ratio (OR) 4.46, 95% confidence interval (CI) 3.46–5.76]. Other risk factors associated with poor psychosocial functioning were: a low level of education, alcohol use, cigarette smoking, hard drug use, frequent truancy, an unfavourable school evaluation, feeling unsafe at school, being victimized, frequent absence due to illness, a mentally ill parent, molestation by a parent, financial problems and feeling distressed by an adverse event. In a full model adjusting for these risk factors, cannabis was not significantly associated with mental health problems, although an association at trend level was apparent. Of these risk factors, regular alcohol use, cigarette smoking, hard drug use, frequent truancy, an unfavourable school evaluation and frequent absence due to illness were also associated with cannabis use.

The association between cannabis use and poor psychosocial functioning in adolescence is due, at least in part, to confounding by other risk factors. Thus, cannabis use can best be viewed as an indicator of risk for mental health problems in adolescence.

Alcohol consumption is influenced by genetic factors. Previous studies have examined the heritability of alcohol consumption, or related phenotypes, from adolescence into adulthood, frequently finding that total heritability changes over time. However, it remains unclear whether the same genes underlie liability to alcohol consumption across development versus whether novel risk genes become important over time.

A population-based study of adult male twins (n=1790) born in Virginia, USA, retrospectively reported on their average monthly alcohol consumption from early adolescence through adulthood. We used twin modeling methods to explore genetic and environmental influences on alcohol consumption over time.

One latent genetic factor accounted for the majority of the heritability in alcohol consumption during mid- to late adolescence, but its influence declined thereafter; from young adulthood forward, heritability was largely attributable to a second genetic factor. The total heritability of alcohol consumption increased from 0 at ages 12–14 years to 0.40 by ages 18–21 years. Shared environmental factors declined in influence over time.

The heritability of alcohol consumption over time is dynamic both quantitatively and qualitatively. These results have important implications for gene identification endeavors. Furthermore, these findings could inform efforts to elucidate developmentally dynamic behaviors, such as antisocial behavior.

Large epidemiological studies are needed to better understand the prevalence and profile of offending by people with mental illness. This study used a whole-of-population design to examine the prevalence, type and pattern of offending across all psychiatric diagnoses, including schizophrenia, compared to the general population.

We used whole-of-population longitudinal record-linked data for a cohort of all Western Australians born 1955–1969 to determine arrest history over the period 1985–1996 and to ascertain recorded history of psychiatric illness. Of the cohort, 116 656 had been arrested and 40 478 were on the psychiatric case register.

The period prevalence of arrest for people with any psychiatric illness was 32.1%. The highest arrest prevalence, by diagnostic category, was for substance use disorders (59.4%); the prevalence for schizophrenia was 38.7%. Co-morbid substance use disorders significantly increased risk of arrest in people with schizophrenia. The prevalence of mental illness among offenders was 11.1%: 6.5% of offenders had substance use disorders and 1.7% had schizophrenia. For the majority of offenders with a psychiatric illness, first arrest preceded first contact with mental health services; for schizophrenia only, this proportion was increasing over time. The mean percentage annual change in the number of arrests during 1985–1996 rose significantly for offenders with a psychiatric illness other than schizophrenia and dropped significantly for those with no mental illness. Compared to non-psychiatric offenders, offenders with schizophrenia were more likely to offend alone, to offend in open places and to target strangers.

Our findings open the way to an informed approach to the management of offenders with mental illness.

Cognitive impairment is a core feature of schizophrenia. Its relationship with duration of untreated psychosis (DUP), a potentially malleable prognostic factor, has been less studied, with inconsistent findings being observed in the literature. Previous research investigating such a relationship was mostly cross-sectional and none of those prospective studies had a follow-up duration beyond 2 years.

A total of 93 Hong Kong Chinese aged 18 to 55 years presenting with first-episode schizophrenia-spectrum disorder were studied. DUP and pre-morbid adjustment were measured using a structured interview incorporating multiple sources of information. Psychopathological evaluation was administered at intake, after clinical stabilization of the first psychotic episode, and at 12, 24 and 36 months. Cognitive functions were measured at clinical stabilization, and at 12, 24 and 36 months.

DUP exerted differential effects on various cognitive domains, with memory deficits being the most related to DUP even when potential confounders including pre-morbid adjustment and sex were adjusted. Prolonged DUP was associated with more severe impairment in visual memory at clinical stabilization and verbal memory at 24 and 36 months. Further, patients with a long DUP were found to have worse outcomes on negative symptoms at 36 months. The effects of DUP on verbal memory remained significant even when negative symptoms were taken into consideration.

Our findings provided further supportive evidence that delayed treatment to first-episode psychosis is associated with poorer cognitive and clinical outcomes. In addition, DUP may specifically affect memory function and its adverse impact on verbal memory may only become evident at a later stage of the recovery process.

Although depression and mania are often assumed to be polar opposites, studies have shown that, in patients with bipolar disorder, they are weakly positively correlated and vary somewhat independently over time. Thus, when investigating relationships between specific psychological processes and specific symptoms (mania and depression), co-morbidity between the symptoms and changes over time must be taken into account.

A total of 253 bipolar disorder patients were assessed every 24 weeks for 18 months using the Hamilton Rating Scale for Depression (HAMD), the Bech–Rafaelsen Mania Assessment Scale (MAS), the Rosenberg Self-Esteem Questionnaire (RSEQ), the Dysfunctional Attitudes Scale (DAS), the Internal, Personal and Situational Attributions Questionnaire (IPSAQ) and the Personal Qualities Questionnaire (PQQ). We calculated multilevel models using the xtreg module of Stata 9.1, with psychological and clinical measures nested within each participant.

Mania and depression were weakly, yet significantly, associated; each was related to distinct psychological processes. Cross-sectionally, self-esteem showed the most robust associations with depression and mania: depression was associated with low positive and high negative self-esteem, and mania with high positive self-esteem. Depression was significantly associated with most of the other self-referential measures, whereas mania was weakly associated only with the externalizing bias of the IPSAQ and the achievement scale of the DAS. Prospectively, low self-esteem predicted future depression.

The associations between different self-referential thinking processes and different phases of bipolar disorder, and the presence of the negative self-concept in both depression and mania, have implications for therapeutic management, and also for future directions of research.

Previous research has implicated the behavioral activation system (BAS) in depression. The relationship of BAS functioning to aspects of cognitive vulnerability to depression, however, is not known.

The present study investigated associations among level of BAS functioning and the encoding and recall of positive and negative self-referent information in currently non-depressed participants with a history of recurrent major depression (recovered; RMD) and in never-depressed control participants (CTL). Participants completed self-report measures of levels of BAS and behavioral inhibition system (BIS) functioning. Following a negative mood induction, participants were presented with a series of positive and negative adjectives; they indicated which words described them and later recalled as many of the words as they were able.

The relationship of BAS functioning to self-referent processing was dependent on participant group. Although lower BAS reward responsivity was associated with the endorsement and recall of fewer positive words across groups, the magnitude of these associations was stronger, and was only significant, within the RMD group. Furthermore, only for RMD participants was lower BAS reward responsivity associated with the endorsement of more negative words. These effects were not accounted for by depressive or anxiety symptoms, current mood, or level of BIS functioning.

These results indicate that BAS functioning may be distinctively linked to negatively biased self-referent processing, one facet of cognitive vulnerability to depression, in individuals with a history of major depressive disorder. Enhancing BAS functioning may be important in buffering cognitive vulnerability to depression.

Convergent studies provide support for abnormalities in the structure and functioning of the prefrontal cortex (PFC) and the amygdala, the key components of the neural system that subserves emotional processing in major depressive disorder (MDD). We used resting-state functional magnetic resonance imaging (fMRI) to examine potential amygdala–PFC functional connectivity abnormalities in treatment-naive subjects with MDD.

Resting-state fMRI data were acquired from 28 individuals with MDD and 30 healthy control (HC) subjects. Amygdala–PFC functional connectivity was compared between the MDD and HC groups.

Decreased functional connectivity to the left ventral PFC (VPFC) from the left and right amygdala was observed in the MDD group, compared with the HC group (p < 0.05, corrected).

The treatment-naive subjects with MDD showed decreased functional connectivity from the amygdala to the VPFC, especially to the left VPFC. This suggests that these connections may play an important role in the neuropathophysiology of MDD at its onset.

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.

Controversy exists regarding whether people in the community who meet criteria for a non-psychotic mental disorder diagnosis are necessarily in need of treatment. Some have argued that these individuals require treatment and that policy makers need to develop outreach programs for them, whereas others have argued that the current epidemiologic studies may be diagnosing symptoms of distress that in many cases are self-limiting and likely to remit without treatment. All prior studies that have addressed this issue have been cross-sectional. We examined the longitudinal outcomes of individuals with depressive, anxiety and substance use (DAS) disorder(s) who had not previously received any treatment.

Data came from a nationally representative US sample. A total of 34 653 non-institutionalized adults (age ≥20 years) were interviewed at two time points, 3 years apart. DAS disorders, mental health service use and quality of life (QoL) were assessed at both time points.

Individuals with a DAS disorder who had not previously received any treatment were significantly more likely than those who had been previously treated to have remission of their index disorder(s) without subsequent treatment, to be free of co-morbid disorder(s) and not to have attempted suicide during the 3-year follow-up period (50.7% v. 33.0% respectively, p < 0.05). At wave 2, multiple linear regression demonstrated that people with a remission of their baseline DAS disorder(s) had levels of functioning similar to those without a DAS disorder.

Individuals with an untreated DAS disorder at baseline have a substantial likelihood of remission without any subsequent intervention.

Emotion dysregulation represents a core symptom of borderline personality disorder (BPD). Deficits in emotion perception are thought to underlie this clinical feature, although studies examining emotion recognition abilities in BPD have yielded inconsistent findings.

The results of 10 studies contrasting facial emotion recognition in patients with BPD (n = 266) and non-psychiatric controls (n = 255) were quantitatively synthesized using meta-analytic techniques.

Patients with BPD were less accurate than controls in recognizing facial displays of anger and disgust, although their most pronounced deficit was in correctly identifying neutral (no emotion) facial expressions. These results could not be accounted for by speed/accuracy in the test-taking approach of BPD patients.

Patients with BPD have difficulties recognizing specific negative emotions in faces and may misattribute emotions to faces depicting neutral expressions. The contribution of state-related emotion perception biases to these findings requires further clarification.

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.

Parent and teacher ratings of attention deficit hyperactivity disorder (ADHD) symptoms yield high estimates of heritability whereas self-ratings typically yield lower estimates. To understand why, the present study examined the etiological overlap between parent, teacher and self-ratings of ADHD symptoms in a population-based sample of 11–12-year-old twins.

Participants were from the Twins Early Development Study (TEDS). ADHD symptoms were assessed using the Strengths and Difficulties Questionnaire (SDQ) hyperactivity scale completed by parents, teachers and children. Structural equation modeling was used to examine genetic and environmental contributions to phenotypic variance/covariance.

The broad-sense heritability of ADHD symptoms was 82% for parent ratings, 60% for teacher ratings and 48% for self-ratings. Post-hoc analyses revealed significantly higher heritability for same-teacher than different-teacher ratings of ADHD (76% v. 49%). A common pathway model best explained the relationship between different informant ratings, with common genetic influences accounting for 84% of the covariance between parent, teacher and self-rated ADHD symptoms. The remaining variance was explained by rater-specific genetic and non-shared environmental influences.

Despite different heritabilities, there were shared genetic influences for parent, teacher and self-ratings of ADHD symptoms, indicating that different informants rated some of the same aspects of behavior. The low heritability estimated for self-ratings and different-teacher ratings may reflect increased measurement error when different informants rate each twin from a pair, and/or greater non-shared environmental influences. Future studies into the genetic influences on ADHD should incorporate informant data in addition to self-ratings to capture a pervasive, heritable component of ADHD symptomatology.

Attention deficit hyperactivity disorder (ADHD) symptoms and autistic traits often occur together. The pattern and etiology of co-occurrence are largely unknown, particularly in adults. This study investigated the co-occurrence between both traits in detail, and subsequently examined the etiology of the co-occurrence, using two independent adult population samples.

Data on ADHD traits (Inattention and Hyperactivity/Impulsivity) were collected in a population sample (S1, n = 559) of unrelated individuals. Data on Attention Problems (AP) were collected in a population-based family sample of twins and siblings (S2, n = 560). In both samples five dimensions of autistic traits were assessed (social skills, routine, attentional switching, imagination, patterns).

Hyperactive traits (S1) did not correlate substantially with the autistic trait dimensions. For Inattention (S1) and AP (S2), the correlations with the autistic trait dimensions were low, apart from a prominent correlation with the attentional switching scale (0.47 and 0.32 respectively). Analyses in the genetically informative S2 revealed that this association could be explained by a shared genetic factor.

Our findings suggest that the co-occurrence of ADHD traits and autistic traits in adults is not determined by problems with hyperactivity, social skills, imagination or routine preferences. Instead, the association between those traits is due primarily to shared attention-related problems (inattention and attentional switching capacity). As the etiology of this association is purely genetic, biological pathways involving attentional control could be a promising focus of future studies aimed at unraveling the genetic causes of these disorders.

Patients with attention deficit-hyperactivity disorder (ADHD) exhibit difficulties in multiple attentional functions. Although high heritability rates suggest a strong genetic impact, aetiological pathways from genes and environmental factors to the ADHD phenotype are not well understood. Tracking the time course of deviant task processing using event-related electrophysiological brain activity should characterize the impact of familiality on the sequence of cognitive functions from preparation to response control in ADHD.

Preparation and response control were assessed using behavioural and electrophysiological parameters of two versions of a cued continuous performance test with varying attentional load in boys with ADHD combined type (n = 97), their non-affected siblings (n = 27) and control children without a family history of ADHD (n = 43).

Children with ADHD and non-affected siblings showed more variable performance and made more omission errors than controls. The preparatory Cue-P3 and contingent negative variation (CNV) following cues were reduced in both ADHD children and their non-affected siblings compared with controls. The NoGo-P3 was diminished in ADHD compared with controls whilst non-affected siblings were located intermediate but did not differ from both other groups. No clear familiality effects were found for the Go-P3. Better task performance was further associated with higher CNV and P3 amplitudes.

Impairments in performance and electrophysiological parameters reflecting preparatory processes and to some extend also for inhibitory response control, especially under high attentional load, appeared to be familially driven in ADHD and may thus constitute functionally relevant endophenotypes for the disorder.