Although several aspects of emotion seem to be intact in schizophrenia, there is emerging evidence that patients show an impaired ability to adaptively regulate their emotions. This event-related potential (ERP) study examined whether schizophrenia is associated with impaired neural responses to appraisal frames, that is when negative stimuli are presented in a less negative context.

Thirty-one schizophrenia out-patients and 27 healthy controls completed a validated picture-viewing task with three conditions: (1) neutral pictures preceded by neutral descriptions (‘Neutral’), (2) unpleasant pictures preceded by negative descriptions (‘Preappraised negative’), and (3) unpleasant pictures preceded by more neutral descriptions (‘Preappraised neutral’). Analyses focused on the late positive potential (LPP), an index of facilitated attention to emotional stimuli that is reduced following cognitive emotion regulation strategies, during four time windows from 300 to 2000 ms post-picture onset.

Replicating prior studies, controls showed smaller LPP in Preappraised neutral and Neutral versus Preappraised negative conditions throughout the 300–2000-ms time period. By contrast, patients showed (a) larger LPP in Preappraised neutral and Preappraised negative versus Neutral conditions in the initial period (300–600 ms) and (b) an atypical pattern of larger LPP to Preappraised neutral versus Preappraised negative and Neutral conditions in the 600–1500-ms epochs.

Modulation of neural responses by a cognitive emotion regulation strategy seems to be impaired in schizophrenia during the first 2 s after exposure to unpleasant stimuli.

Prior research has indicated that affiliation with delinquent peers activates genetic influences on delinquency during adolescence. However, because other studies have indicated that the socializing effects of delinquent peers vary dramatically across childhood and adolescence, it is unclear whether delinquent peer affiliation (DPA) also moderates genetic influences on delinquency during childhood.

The current study sought to evaluate whether and how DPA moderated the etiology of delinquency in a sample of 726 child twins from the Michigan State University Twin Registry (MSUTR).

The results robustly supported etiological moderation of childhood delinquency by DPA. However, this effect was observed for shared environmental, rather than genetic, influences. Shared environmental influences on delinquency were found to be several-fold larger in those with higher levels of DPA as compared to those with lower levels. This pattern of results persisted even when controlling for the overlap between delinquency and DPA.

Our findings bolster prior work in suggesting that, during childhood, the association between DPA and delinquency is largely (although not solely) attributable to the effects of socialization as compared to selection. They also suggest that the process of etiological moderation is not specific to genetic influences. Latent environmental influences are also amenable to moderation by measured environmental factors.

Previous studies suggest a link between parental separation or divorce and risk of depression in adolescence. There are, however, few studies that have prospectively examined the effects of timing of biological father absence on risk for depressive symptoms in adolescence while controlling for a range of confounding factors.

We examine the association between father absence occurring in early (the first 5 years) and middle childhood (5–10 years) and adolescent depressive symptoms in a sample comprising 5631 children from the UK-based Avon Longitudinal Study of Parents and Children (ALSPAC). Self-reported depressive symptoms at 14 years were assessed using the Short Mood and Feelings Questionnaire (SMFQ). Father absence was assessed from maternal questionnaires completed at regular intervals from the birth of the study child up to 10 years.

There was evidence for an association between father absence in early childhood and increased odds of depressive symptoms at 14 years. This association was stronger in girls than in boys and remained after adjusting for a range of socio-economic, maternal and familial confounders assessed prior to the father's departure. Conversely, there was no evidence for an association between father absence in middle childhood and depressive symptoms at 14 years.

Father absence in early childhood increases risk for adolescent depressive symptoms, particularly in girls. Future research should be aimed at identifying possible biological and psychosocial mechanisms linking father absence to depressive symptomatology to enable the development of family-based early prevention and intervention programmes targeting young children at risk.

Many patients do not adhere to or benefit from cognitive behaviour therapy (CBT) for post-traumatic stress disorder (PTSD). This randomized controlled trial evaluates the extent to which preparing patients with emotion regulation skills prior to CBT enhances treatment outcome.

A total of 70 adult civilian patients with PTSD were randomized to 12 sessions of either supportive counselling followed by CBT (Support/CBT) or emotion regulation training followed by CBT (Skills/CBT).

Skills/CBT resulted in fewer treatment drop-outs, less PTSD and anxiety, and fewer negative appraisals at 6 months follow-up than Support/CBT. Between-condition effect size was moderate for PTSD severity (0.43, 95% confidence interval −0.04 to 0.90). More Skills/CBT (31%) patients achieved high end-state functioning at follow-up than patients in Support/CBT (12%) [χ2(n = 70) = 3.67, p < 0.05].

This evidence suggests that response to CBT may be enhanced in PTSD patients by preparing them with emotion regulation skills. High attrition of participants during the study limits conclusions from this study.

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.

Adolescent marijuana use is associated with increased risk for schizophrenia. We previously reported that marijuana misuse in conjunction with specific cannabinoid receptor 1 (CNR1) genetic variants (rs12720071-G-allele carriers) contributed to white-matter (WM) brain volume deficits in schizophrenia patients. In this study, we assessed the influence of another cannabinoid-related gene, mitogen-activated protein kinase 14 (MAPK14), and potential MAPK14–CNR1 gene–gene interactions in conferring brain volume abnormalities among schizophrenia patients with marijuana abuse/dependence. MAPK14 encodes a member of the MAPK family involved in diverse cellular processes, including CNR1-induced apoptosis.

We genotyped 235 schizophrenia patients on nine MAPK14 tag single nucleotide polymorphisms (tSNPs). Approximately one quarter of the sample had marijuana abuse or dependence. Differential effects of MAPK14 tSNPs on brain volumes across patients with versus without marijuana abuse/dependence were examined using ANCOVA.

Of the MAPK14 tSNPs, only rs12199654 had significant genotype effects and genotype × marijuana misuse interaction effects on WM volumes. rs12199654-A homozygotes with marijuana abuse/dependence had significantly smaller total cerebral and lobar WM volumes. The effects of MAPK14 rs12199654 on WM volume deficits remained significant even after controlling for the CNR1 rs12720071 genotype. There were significant main effects of the MAPK14 CNR1 diplotype and diplotype × marijuana interaction on WM brain volumes, with both genetic variants having additive contributions to WM volume deficits only in patients with marijuana misuse.

Given that CNR1-induced apoptosis is preceded by increased MAPK phosphorylation, our study suggests that potential MAPK14–CNR1 gene–gene interactions may mediate brain morphometric features in schizophrenia patients with heavy marijuana use.

We internally validated previously published rates of remission, continuation and incidence of broadly defined eating disorders during pregnancy in the Norwegian Mother and Child Cohort (MoBa) at the Norwegian Institute of Public Health.

A total of 77 267 pregnant women enrolled at 17 weeks gestation between 2001 and 2009 were split into a training sample (n = 41 243) from the version 2 dataset and a validation sample (n = 36 024) from the version 5 dataset who were not in the original study. Internal validation of original rate models involved fitting a calibration model to compare model parameters between the two samples and bootstrap estimates of bias in the entire version 5 dataset.

Remission, continuation and incidence estimates remained stable. Pre-pregnancy prevalence estimates in the validation sample were: anorexia nervosa (AN; 0.1%), bulimia nervosa (BN; 1.0%), binge eating disorder (BED; 3.3%) and eating disorder not otherwise specified-purging disorder (EDNOS-P; 0.1%). In early pregnancy, estimates were: BN (0.2%), BED (4.8%) and EDNOS-P (<0.01%). Incident BN and EDNOS-P during pregnancy were rare. The highest rates were for full or partial remission for BN and EDNOS-P and continuation for BED.

We validated previously estimated rates of remission, continuation and incidence of eating disorders during pregnancy. Eating disorders, especially BED, during pregnancy were relatively common, occurring in nearly one in every 20 women. Pregnancy was a window of remission from BN but a window of vulnerability for BED. Training to detect eating disorders by obstetricians/gynecologists and interventions to enhance pregnancy and neonatal outcomes warrant attention.

Studies of the relationship between childhood maltreatment and alcohol dependence have not controlled comprehensively for potential confounding by co-occurring maltreatments and other childhood trauma, or determined whether parental history of alcohol disorders operates synergistically with gender and maltreatment to produce alcohol dependence. We addressed these issues using national data.

Face-to-face surveys of 27 712 adult participants in a national survey.

Childhood physical, emotional and sexual abuse, and physical neglect were associated with alcohol dependence (p<0.001), controlling for demographics, co-occurring maltreatments and other childhood trauma. Attributable proportions (APs) due to interaction between each maltreatment and parental history revealed significant synergistic relationships for physical abuse in the entire sample, and for sexual abuse and emotional neglect in women (APs, 0.21, 0.31, 0.26 respectively), indicating that the odds of alcohol dependence given both parental history and these maltreatments were significantly higher than the additive effect of each alone (p<0.05).

Childhood maltreatments independently increased the risk of alcohol dependence. Importantly, results suggest a synergistic role of parental alcoholism: the effect of physical abuse on alcohol dependence may depend on parental history, while the effects of sexual abuse and emotional neglect may depend on parental history among women. Findings underscore the importance of early identification and prevention, particularly among those with a family history, and could guide genetic research and intervention development, e.g. programs to reduce the burden of childhood maltreatment may benefit from addressing the negative long-term effects of maltreatments, including potential alcohol problems, across a broad range of childhood environments.

Patients with borderline personality disorder (BPD) show a high prevalence of early adversity, such as childhood trauma. It has also been reported that prenatal adverse conditions, such as prenatal maternal stress, drug taking, tobacco smoking or medical complications, may be associated with an increased risk of mental disorders in the offspring. Prenatal adversity is investigated here for the first time as a potential risk factor in the diagnosis of BPD.

A total of 100 patients with a DSM-IV diagnosis of BPD and 100 matched healthy controls underwent semi-structured interviews about the course of pregnancy, maternal stressors, birth complications and childhood trauma. Further information was obtained from the participants' mothers and from prenatal medical records.

Borderline patients were significantly more often exposed to adverse intrauterine conditions, such as prenatal tobacco exposure (p=0.004), medical complications (p=0.008), prenatal maternal traumatic stress (p=0.015), familial conflicts (p=0.004), low social support (p=0.004) and partnership problems during pregnancy (p=0.014). Logistic regression analyses revealed that the reported prenatal risk factors accounted for 25.7% of the variance in BPD. Prenatal tobacco exposure [odds ratio (OR) 3.37, 95% confidence interval (CI) 1.49–7.65, p=0.004] and medical complications (OR 2.87, 95% CI 1.29–6.38, p=0.010) emerged as important predictors. After controlling for childhood adversity and parental socio-economic status (SES), prenatal risk factors predicted relevant borderline subdomains, such as impulsivity, affective instability, identity disturbance, dissociation and severity of borderline symptoms.

This study provides evidence of an association between prenatal adversity and the diagnosis of BPD. Our findings suggest that prenatal adversity may constitute a potential risk factor in the pathogenesis of BPD.

Animal studies suggest that maternal separation is associated with alterations in the hypothalamic–pituitary–adrenal (HPA) axis through effects that occur in a critical period following birth. Evidence for an association of the diurnal cortisol rhythm with maternal separation in humans is equivocal.

We examined whether maternal separation in childhood is associated with diurnal cortisol pattern in 3712 middle-aged men and women. Two aspects of cortisol release were examined: the cortisol awakening response (CAR) and the diurnal slope in cortisol throughout the day.

Maternal separation in childhood was reported by 12% of participants. Those participants who reported maternal separation had a larger CAR and flatter slopes in cortisol levels compared to those who did not report maternal separation [adjusted mean CAR in those reporting no separation versus separation: 7.1, 95% confidence interval (CI) 6.7–7.5 v. 8.4, 95% CI 7.3–9.5, p = 0.02, corresponding to adjusted mean diurnal slope: −0.129 (95% CI −0.130 to −0.128) v. −0.126 (95% CI −0.128 to −0.124), p = 0.01]. In participants who reported maternal separation, the age of separation was not associated with either cortisol measure (p = 0.11). The association between maternal separation and slope in cortisol secretion was largely explained by smoking behaviour and marital status at the time of sample collection whereas that of the CAR was explained by childhood psychosocial, material factors and adult health behaviours.

Our findings suggest that maternal separation in childhood is associated with alterations in the diurnal cortisol pattern in middle age. These associations are predominantly accounted for by adult circumstances and behaviours.

Cannabis abuse in psychotic patients is associated with rehospitalizations, reduced adherence and increased symptom severity. Previous psychosocial interventions have been ineffective in cannabis use, possibly because of low sample sizes and short interventions. We investigated whether adding CapOpus to treatment as usual (TAU) reduces cannabis use in patients with cannabis use disorder and psychosis.

A total of 103 patients with psychosis and cannabis use disorder were centrally randomized to 6 months of CapOpus plus TAU (n = 52) or TAU (n = 51). CapOpus consisted mainly of motivational interviewing and cognitive behaviour therapy (CBT). TAU was targeted primarily at the psychotic disorder. The primary outcome was self-reported days with cannabis use in the preceding month.

Pre-randomization cannabis use frequency was 14.9 [95% confidence interval (CI) 12.7–17.1] days/month. Post-treatment, the ratio of days/month with cannabis use in CapOpus versus TAU was 0.76 (95% CI 0.38–1.50) (p = 0.42), and 0.80 (95% CI 0.21–3.10) (p = 0.75) at the 4-month follow-up. From 46.4 (95% CI 36.4–56.3) monthly joints pre-randomization, consumption fell to 27.3 (95% CI 12.6–41.9) joints in CapOpus and 48.2 (95% CI 31.8–64.6) in TAU (p = 0.06). Follow-up amounts were 28.4 (95% CI 13.5–43.2) and 41.6 (95% CI 25.2–58.0) joints (p = 0.23). Several subgroup analyses suggested benefits of CapOpus.

CapOpus did not reduce the frequency, but possibly the amount, of cannabis use. This is similar to the findings of previous trials in this population. Implementation of CapOpus-type interventions is thus not warranted at present but subgroup analyses call for further trials.

It is not clear whether the prevalence of dementia and depression among the elderly has changed during the past 30 years.

Population-based samples from Gothenburg, Sweden were examined with identical psychiatric and neuropsychiatric examinations at age 70 years in 1976–1977 (n = 404, response rate 78.8%) and 2000–2001 (n = 579, response rate 66.4%), and at age 75 in 1976–1977 (n = 303, response rate 78%) and 2005–2006 (n = 753, response rate 63.4%). Depression was diagnosed according to DSM-IV and dementia according to Kay's criteria. General linear models (GLMs) were used to test for differences between groups.

Dementia was related to age but not to birth cohort or sex. Major depression was related to sex (higher in women) but not to birth cohort or age. Minor depression was related to birth cohort, sex (higher in women), age (higher at age 75) and the interaction effect of birth cohort × age; that is, the prevalence of minor depression increased with age in the 2000s but not in the 1970s. Thus, the prevalence of minor depression was higher in 2005–2006 than in 1976–1977 among 75-year-olds for both men (12.4% v. 3.7%) and women (19.1% v. 5.6%) whereas there were no birth cohort differences at age 70.

Secular changes were observed only for minor depression, which is considered to be related more to psychosocial factors than major depression. The high prevalence of minor depression in later-born birth cohorts emphasizes the importance of detecting minor depression in the elderly.

Patients with schizophrenia and their first-degree relatives exhibit both abnormally diminished and increased neural activation during cognitive tasks. In particular, excessive task-related activity is often observed when tasks are easy, suggesting that inefficient cerebral recruitment may be a marker of vulnerability for schizophrenia. This hypothesis might best be tested using a very easy task, thus avoiding confounding by individual differences in task difficulty.

Eighteen people with schizophrenia, 18 unaffected full siblings of patients with schizophrenia and 26 healthy controls performed an easy auditory target-detection task in a 3-T magnetic resonance imaging (MRI) scanner. Groups were matched for accuracy on the task. Blood oxygen level-dependent (BOLD) responses to non-target stimuli in participants with vulnerability for schizophrenia (siblings and patients) were compared with those of healthy controls, and those of patients with those of unaffected siblings. BOLD responses to targets were compared with baseline, across groups.

Subjects with vulnerability for schizophrenia showed significant hyperactivation to non-targets in brain areas activated by targets in all groups, in addition to reduced deactivation to non-targets in areas suppressed by targets in all groups. Siblings showed greater activation than patients to non-targets in the medial frontal cortex. Patients exhibited significantly longer reaction times (RTs) than unaffected siblings and healthy controls.

Inefficient cerebral recruitment is a vulnerability marker for schizophrenia, marked by reduced suppression of brain areas normally deactivated in response to task stimuli, and increased activation of areas normally activated in response to task stimuli. Moreover, siblings show additional activation in the medial frontal cortex that may be protective.

Obsessive-compulsive disorder (OCD) has been associated with response inhibition deficits under motivationally neutral contingencies. We examined response inhibition performance in the presence of reward and punishment. We further investigated whether the hypothesized difficulties in flexibly updating behaviour based on external feedback in OCD would also lead to a reduced ability to adjust to changes in the reward and punishment contingencies.

Participants completed a go/no-go task that used punishments or rewards to promote response activation or suppression. The task was administered to OCD patients free of current Axis-I co-morbidities including major depression (n = 20) and a group of healthy controls (n = 32).

Compared with controls, patients with OCD had increased commission errors in punishment conditions, and failed to slow down immediately after receiving punishment. The punishment-induced increase in commission errors correlated with self-report measures of OCD symptom severity. Additionally, patients did not differ from controls in adapting their overall response style to the changes in task contingencies.

Individuals with OCD showed reduced response control selectively under punishment conditions, manifesting in an impulsive response style that was related to their current symptom severity. This stresses failures of cognitive control in OCD, particularly under negative motivational contingencies.

Pathological gambling (PG) is an impulse control disorder characterized by excessive monetary risk seeking in the face of negative consequences. We used tools from the field of behavioral economics to refine our description of risk-taking behavior in pathological gamblers. This theoretical framework allowed us to confront two hypotheses: (1) pathological gamblers distort winning probabilities more than controls; and (2) pathological gamblers merely overweight the whole probability range.

Eighteen pathological gamblers and 20 matched healthy participants performed a decision-making task involving choices between safe amounts of money and risky gambles. The online adjustment of safe amounts, depending on participants' decisions, allowed us to compute ‘certainty equivalents’ reflecting the subjective probability weight associated with each gamble. The behavioral data were then fitted with a mathematical function known as the ‘probability weighting function’, allowing us to disentangle our two hypotheses.

The results favored the second hypothesis, suggesting that pathological gamblers' behavior reflects economic preferences globally shifted towards risk, rather than excessively distorted probability weighting. A mathematical parameter (elevation parameter) estimated by our fitting procedure was found to correlate with gambling severity among pathological gamblers, and with gambling affinity among controls.

PG is associated with a specific pattern of economic preferences, characterized by a global (i.e. probability independent) shift towards risky options. The observed correlation with gambling severity suggests that the present ‘certainty equivalent’ task may be relevant for clinical use.

Externalizing traits or behaviors are typically assessed by self-report scales or criminal records. Few genetically informative studies have used both methods to determine whether they assess the same genetic or environmental risk factors.

We examined 442 male Swedish twin pairs with self-reported externalizing behaviors at age 16–17 years [externalizing traits (EXT), self-reported delinquency (SRD), impulsivity (IMP), grandiosity (GRD) and callousness (CLS)] and criminal behavior (CB) from the National Suspect Registry from age 13 to 25 years. Multivariate structural equation modeling was conducted with Mx.

The best-fit model contained one genetic, one shared environmental and two non-shared environmental common factors, and variable specific genetic and non-shared environmental factors. The risk for CB was influenced substantially by both genetic (a2 = 0.48) and familial–environmental factors (c2 = 0.22). About one-third of the genetic risk for CB but all of the shared environmental risk was indexed by the self-report measures. The degree to which the individual measures reflected genetic versus familial–environmental risks for CB varied widely. GRD and CLS were correlated with CB mainly through common genetic risk factors. SRD and CB covaried largely because of shared familial–environmental factors. For EXT and IMP, observed correlations with CB resulted in about equal parts from shared genetic and shared familial–environmental factors.

In adolescence, measures of grandiose and callous temperament best tap the genetic liability to CB. Measures of antisocial behaviors better index familial–environmental risks for CB. A substantial proportion of the genetic risk to CB was not well reflected in any of the self-report measures.

Cannabis use is associated with increased risk for psychotic-like experiences (PLEs) and psychotic disorders. It remains unclear whether this relationship is causal or due to confounding.

A total of 1929 young adults aged 18–30 years participated in a nationwide internet-based survey in The Netherlands and gave information on demographics, substance use and parental psychiatric illness and completed the Community Assessment of Psychic Experiences (CAPE).

Cigarette smoking and cannabis use were equally strongly associated with the frequency of PLEs in a fully adjusted model (β = 0.098 and 0.079 respectively, p < 0.05). Cannabis use was associated with distress from PLEs in a model adjusted for an elaborate set of confounders excluding smoking (β = 0.082, p < 0.05). However, when cigarette smoking was included in the model, cannabis use was not a significant predictor of distress from PLEs. Cigarette smoking remained associated with distress from PLEs in a fully adjusted model (β = 0.107, p < 0.001).

Smoking is an equally strong independent predictor of frequency of PLEs as monthly cannabis use. Our results suggest that the association between moderate cannabis use and PLEs is confounded by cigarette smoking.

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.

Autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD), and associated subclinical traits, regularly co-occur with one another. However, the aetiology of their co-occurrence remains poorly understood. This paper provides the first genetically informative, longitudinal analysis of the interaction between traits of ASD and ADHD, and explores their genetic and environmental overlap.

Parents of approximately 5000 twin pairs completed questionnaires assessing traits of ASD and ADHD when twins were aged 8 and 12 years. Cross-lagged longitudinal modelling explored their developmental association, enabling a consideration of phenotypic-driven processes. Overlapping aetiological influences on traits at age 12 years were explored using bivariate twin modelling.

Traits of ADHD at age 8 years were more strongly predictive of traits of ASD at 12 years than traits of ASD at 8 years were of traits of ADHD at 12 years. Analysis of traits by subscales assessing specific symptom domains suggested that communication difficulties were most strongly associated with traits of ADHD. Bivariate modelling suggested moderate genetic overlap on traits in males (genetic correlation = 0.41), and a modest degree of overlap in females (genetic correlation = 0.23) at age 12 years.

Traits of ADHD at age 8 years significantly influence traits of ASD at age 12 years, after controlling for their initial relationship at age 8 years. In particular, early ADHD traits influenced later communication difficulties. These findings demonstrate the dynamic nature of co-occurring traits across development. In addition, these findings add to a growing body of literature suggesting that traits of ASD and ADHD may arise via similar aetiological processes.

A new diagnostic category, hoarding disorder (HD), has been proposed for inclusion in DSM-5. This study field-tested the validity, reliability and perceived acceptability of the proposed diagnostic criteria for HD.

Fifty unselected individuals with prominent hoarding behavior and 20 unselected, self-defined ‘collectors’ participated in thorough psychiatric assessments, involving home visits whenever possible. A semi-structured interview based on the proposed diagnostic criteria for HD was administered and scored by two independent raters. ‘True’ diagnoses were made by consensus according to the best-estimate diagnosis procedure. The percentage of true positive HD cases (sensitivity) and true negative HD cases (specificity) was calculated, along with inter-rater reliability for the diagnosis and each criterion. Participants were asked about their perceptions of the acceptability, utility and stigma associated with the new diagnosis.

Twenty-nine (58%) of the hoarding individuals and none of the collectors fulfilled diagnostic criteria for HD. The sensitivity, specificity and inter-rater reliability of the diagnosis, and of each individual criterion and the specifiers, were excellent. Most participants with HD (96%) felt that creating a new disorder would be very or somewhat acceptable, useful (96%) and not too stigmatizing (59%).

The proposed HD criteria are valid, reliable and perceived as acceptable and useful by the sufferers. Crucially, they seem to be sufficiently conservative and unlikely to overpathologize normative behavior. Minor changes in the wording of the criteria are suggested.