Depressed patients are biased in their response to negative information. They have been found to show a maladaptive behavioral and aberrant electrophysiological response to negative feedback. The aim of this study was to investigate the behavioral and electrophysiological response to feedback validity in drug-free depressed patients.

Fifteen drug-free in-patients with unipolar major depression disorder (MDD) and 30 demographically matched controls performed a time-estimation task in which they received valid and invalid (i.e. related and unrelated to performance) positive and negative feedback. The number of behavioral adjustments to the feedback and the feedback-related negativity (FRN) were measured.

Patients made fewer correct adjustments after valid negative feedback than controls, and their FRNs were larger. Neither patients nor controls adjusted their time estimates following invalid negative feedback.

The FRN results suggest that depressed drug-free in-patients have an atypical rostral anterior cingulate response to feedback that is independent of feedback validity. Their behavioral response to invalid negative feedback, however, is not impaired. This study confirms the notion that the behavioral responses of depressed individuals to negative feedback are context dependent.

To test whether receiving care from a health visitor (HV) trained in identification and psychological intervention methods prevents depression 6–18 months postnatally in women who are not depressed 6 weeks postnatally.

The study was a prospective cluster trial, randomized by GP practice, with follow-up for 18 months in 101 primary care teams in the Trent area of England. The participants were women scoring <12 on the postal Edinburgh Postnatal Depression Scale (EPDS) at 6 weeks postnatally (1474 intervention and 767 control women). Intervention HVs (n=89, 63 clusters) were trained in identifying depressive symptoms using the EPDS and face-to-face clinical assessment and in providing psychologically orientated sessions based on cognitive behavioral or person-centered principles. The control group comprised HVs (n=49, 37 clusters) providing care as usual (CAU). The primary outcome measure was the proportion of women scoring ⩾12 on the EPDS at 6 months postnatally. Secondary outcomes were mean EPDS score, Clinical Outcomes in Routine Evaluation – Outcome Measure (CORE-OM) score, State–Trait Anxiety Inventory (STAI), 12-item Short Form Health Survey (SF-12) and Parenting Stress Index Short Form (PSI-SF) scores at 6, 12 and 18 months.

After adjusting for individual-level covariates, living alone, previous postnatal depression (PND), the presence of one or more adverse life events and the 6-week EPDS score, the odds ratio (OR) for EPDS ⩾12 at 6 months was 0.71 [95% confidence interval (CI) 0.53–0.97, p=0.031] for the intervention group (IG) women compared with the control (CAU) group women. Two subgroups were formed by baseline severity: a ‘subthreshold’ subgroup with a 6-week EPDS score of 6–11 (n=999) and a ‘lowest severity’ subgroup with a 6-week EPDS score of 0–5 (n=1242). There was no difference in psychological effectiveness by subgroup (interaction term: z=−0.28, p=0.782).

This study provides new evidence of a universal, enduring preventive effect for depression in women who screen negative for depression postnatally.

Genetic and environmental influences on child psychopathology have been studied extensively through twin and adoption designs. We offer a novel methodology to examine genetic and environmental influences on the intergenerational transmission of psychopathology using a sample of parents and children conceived through in vitro fertilization (IVF).

The sample included families with children born through IVF methods, who varied as to whether the child was genetically related or unrelated to the rearing mother and father (mother genetically related, n=434; mother genetically unrelated, n=127; father genetically related, n=403; father genetically unrelated, n=156). Using standardized questionnaires, mothers and fathers respectively reported on their own psychopathology (depression, aggression), their parenting behavior toward their child (warmth, hostility) and their child's psychopathology (depression, aggression). A cross-rater approach was used, where opposite parents reported on child symptoms (i.e. fathers reported on symptoms for the mother–child dyad, and vice versa).

For mother–child dyads, a direct association between mother depression and child depression was observed among genetically unrelated dyads, whereas a fully mediated path was observed among genetically related dyads through mother-to-child hostility and warmth. For father–child dyads, direct and mediated pathways were observed for genetically related father–child dyads. For aggression, the direct association between parent aggression and child aggression was fully mediated by parent-to-child hostility for both groups, indicating the role of parent-to-child hostility as a risk mechanism for transmission.

A differential pattern of genetic and environmental mediation underlying the intergenerational transmission of psychopathology was observed among genetically related and genetically unrelated father–child and mother–child dyads.

Hypothalamic-pituitary-adrenocortical (HPA) axis abnormalities have been found in patients with a psychotic disorder and first-degree relatives of patients with a psychotic disorder react with subtle increases in non-clinical psychotic experiences and negative emotions in the face of everyday stress. The current study investigated whether HPA axis functioning is altered in individuals at above average genetic risk for psychotic disorder, examining diurnal cortisol profiles, cortisol reactivity to daily stressors and the association between HPA axis activity and subclinical psychotic experiences.

Participants included siblings of patients with a psychotic disorder (n=60) and a healthy comparison group (n=63). The Experience Sampling Method (a structured diary technique) was employed to assess stress, psychotic experiences, negative affect and salivary cortisol repeatedly in the flow of daily life.

Multi-level analyses revealed higher diurnal cortisol levels and heightened cortisol reactivity to negative daily events in siblings compared with controls. Diurnal cortisol slope did not differ between the two groups, but momentary increases in psychotic experiences and negative affect were associated with increased cortisol in the sibling group.

Findings support altered HPA axis activity in individuals at above average genetic risk for psychotic disorder, as evidenced by higher diurnal cortisol levels and increased cortisol reactivity to daily stress. Results also suggest a dynamic association between cortisol secretion and the intensity of psychotic-like experiences and negative emotions in daily life, although the direction of this association remains to be elucidated.

Parental characteristics influence the risk of offspring suicide. In this study we wanted to separate the hereditary from the environmental influence of such factors by comparing their effects in the adopted versus non-adopted.

A register study was conducted in a national cohort of 2 471 496 individuals born between 1946 and 1968, including 27 600 national adoptees, followed-up for suicide during 1987–2001. Cox regression was used to calculate hazard ratios (HR) for suicide of socio-economic indicators of the childhood household and biological parents' suicide, alcohol abuse and psychiatric morbidity separately in the adopted and non-adopted. Differences in effects were tested in interaction analyses.

Suicide and indicators of severe psychiatric disorder in the biological parents had similar effects on offspring suicide in the non-adopted and adopted (HR 1.5–2.3). Biological parents' alcohol abuse was a risk factor for suicide in the non-adopted group only (HR 1.8 v. 0.8, interaction effect: p=0.03). The effects of childhood household socio-economic factors on suicide were similar in adopted and non-adopted individuals, with growing up in a single parent household [HR 1.5 (95% confidence interval 1.4–1.5)] as the most important socio-economic risk factor for the non-adopted.

The main familial effects of parental suicide and psychiatric morbidity on offspring suicide are not mediated by the post-natal environment or imitation, in contrast to effects of parental alcohol abuse that are primarily mediated by the post-natal environment. Social drift over generations because of psychiatric disorders does not seem likely to explain the association of socio-economic living conditions in childhood to suicide.

Psychiatric disorders are common following traumatic brain injury (TBI). However, few studies have examined the course of disorder development and the influence of pre-injury psychiatric history. The present study aimed to examine the frequency of, and association between, psychiatric disorders occurring pre- and post-injury, and to examine the post-injury course of disorders.

Participants were 102 adults (75.5% male) with predominantly moderate-severe TBI. Participants were initially assessed for pre-injury and current disorders, and reassessed at 3, 6 and 12 months post-injury using the Structured Clinical Interview for DSM-IV Disorders (SCID).

Over half of the participants had a pre-injury psychiatric disorder; predominantly substance use, mood, and anxiety disorders. In the first year post-injury, 60.8% of participants had a psychiatric disorder, commonly anxiety and mood disorders. Post-injury disorders were associated with the presence of a pre-injury history (p<0.01), with 74.5% of participants with a pre-injury psychiatric history experiencing a post-injury disorder, which commonly presented at initial assessment or in the first 6 months. However, 45.8% of participants without a pre-injury history developed a novel post-injury disorder, which was less likely to emerge at the initial assessment and generally developed later in the year.

Despite evidence that most post-injury psychiatric disorders represent the continuation of pre-existing disorders, a significant number of participants developed novel psychiatric disorders. This study demonstrates that the timing of onset may differ according to pre-injury history. There seem to be different trajectories for anxiety and depressive disorders. This research has important implications for identifying the time individuals are most at risk of psychiatric disorders post-injury.

There is a lack of specific knowledge about the dose–response effect of multiple parental risk factors for suicide attempts among children and adolescents. The aim of this study was to determine the dose–response effect of multiple parental risk factors on an offspring's risk for suicide attempt.

We designed a population-based two-generation nested case–control study and used Danish register data. A population of 403 431 individuals born between 1983 and 1989 was sampled. Among these, 3465 (0.8%) were registered as having had a suicide attempt. Twenty controls were matched to each case and a link to the offspring's biological parents was established.

There was a dose–response relationship between the number of exposures and the risk of suicide attempts, with the increased risk seeming to be a multiplicative effect. Parental suicide, suicide attempt, psychiatric illness and low level of income were all significant independent risk factors for offspring's suicide attempts.

Knowledge of the effect of multiple risk factors on the likelihood of suicide attempts in children and adolescents is important for risk assessment. Dose–response effects of multiple parental risk factors are multiplicative, but it is rare for children and adolescents to be exposed to multiple parental risk factors simultaneously. Nevertheless, they should be considered along with the offspring's own multiple risk factors in determining the overall risk of a suicide attempt. Further research incorporating both parental and offspring's risk factors is indicated to determine the overall dose–response effect of multiple risk factors.

Research suggests that suicidal behaviour is aggregated in families. However, due to methodological limitations, including small sample sizes, the strength and pattern of this aggregation remains uncertain.

We examined the familial clustering of completed suicide in a Swedish total population sample. We linked the Cause of Death and Multi-Generation Registers and compared suicide rates among relatives of all 83 951 suicide decedents from 1952–2003 with those among relatives of population controls.

Patterns of familial aggregation of suicide among relatives to suicide decedents suggested genetic influences on suicide risk; the risk among full siblings (odds ratio 3.1, 95% confidence interval 2.8–3.5, 50% genetic similarity) was higher than that for maternal half-siblings (1.7, 1.1–2.7, 25% genetic similarity), despite similar environmental exposure. Further, monozygotic twins (100% genetic similarity) had a higher risk than dizygotic twins (50% genetic similarity) and cousins (12.5% genetic similarity) had higher suicide risk than controls. Shared (familial) environmental influences were also indicated; siblings to suicide decedents had a higher risk than offspring (both 50% genetically identical but siblings having a more shared environment, 3.1, 2.8–3.5 v. 2.0, 1.9–2.2), and maternal half-siblings had a higher risk than paternal half-siblings (both 50% genetically identical but the former with a more shared environment). Although comparisons of twins and half-siblings had overlapping confidence intervals, they were supported by sensitivity analyses, also including suicide attempts.

Familial clustering of suicide is primarily influenced by genetic and also shared environmental factors. The family history of suicide should be considered when assessing suicide risk in clinical settings or designing and administering preventive interventions.

Teenage motherhood is relatively common in the UK, but little is known about related health inequalities in this population. We estimated cause-specific mortality risks over three decades in a nationally representative cohort.

We examined premature mortality in a 1.1% sample of all women who were teenagers in England and Wales during the 1970s, 1980s and 1990s using data from the Office for National Statistics Longitudinal Study (ONS LS). Our primary outcome was suicide. Long-term follow-up to 31 December 2006, to a potential maximum age of 49 years, was achieved through near-complete routine linkage to national mortality records. We created a time-dependent exposure variable, with relative risks estimated according to age when women first experienced motherhood versus a reference group of those currently without children.

Women who were teenage mothers were around 30% more likely to die prematurely by any cause and almost 60% more likely to die unnaturally, whereas first-time motherhood at mature age conferred lower risk compared to women without children. Teenage motherhood was associated with a more than doubled risk of suicide [mortality rate ratio (MRR) 2.23, 95% confidence interval (CI) 1.30–3.83], and elevated risks of fatal cancer of the cervix and lung were also found. Changing the reference category to first-time mothers at 20 years and above also revealed a significant elevation in risk of accidental death.

The complex psychosocial needs of these women require greater attention from clinicians, public health professionals, social services and policymakers. Their elevated risk of poor health outcomes may persist well beyond the actual teenage motherhood years.

Research suggests that subclinical psychotic experiences during adolescence represent the behavioral expression of liability for psychosis. Little is known, however, about the longitudinal trajectory of liability in general population samples.

Growth mixture modeling was used to examine longitudinal trajectories of self-reported positive psychotic experiences in the Youth Self Report (YSR), completed three times over a period of 6 years by a general population cohort of adolescents aged 10–11 years at baseline (n=2230).

Four groups with distinct developmental trajectories of low, decreasing, increasing and persistent levels of mild positive psychotic experiences were revealed. The persistent trajectory was associated strongly with cannabis use, childhood trauma, developmental problems and ethnic minority status, and consistently displayed strong associations with factors known to predict transition from subclinical psychotic experience to clinical psychotic disorder (severity of and secondary distress due to psychotic experiences, social and attentional problems and affective dysregulation) and also with high levels of parental-reported psychotic experiences and use of mental health care at the end of the follow-up period. Progressively weaker associations were found for the increasing, decreasing and low trajectories respectively.

The results suggest that the outcome of early developmental deviation associated with later expression of psychotic experiences is contingent on the degree of later interaction with environmental risks inducing, first, persistence of psychotic experiences and, second, progression to onset of need for care and service use. Insight into the longitudinal dynamics of risk states in representative samples may contribute to the development of targeted early intervention in psychosis.

The pretreatment neuropsychological profile of drug-resistant patients with major depressive disorder (MDD) referred for electroconvulsive therapy (ECT) may differ from that of their drug-respondent MDD counterparts. Such differences could help in identifying distinct MDD subtypes, thus offering insights into the neuropathology underlying differential treatment responses.

Depressed patients with ECT referral (ECTs), depressed patients with no ECT referral (NECTs) and non-psychiatric Controls (matched groups, n=15) were assessed with memory and executive function tests from the Cambridge Neuropsychological Test Automated Battery (CANTAB).

ECTs scored significantly lower than NECTs in the Mini-Mental State Examination (MMSE; p=0.01). NECTs performed worse than Controls in the Paired Associates Learning (PAL) task (p<0.03; Control/NECT p<0.01) and the Spatial Recognition Memory (SRM) task (p<0.05; Controls/NECTs p<0.05); ECTs performed between Controls and NECTs, not differing from either. In the Intra/Extradimensional (IED) set-shifting task, ECTs performed worse that Controls and NECTS (IED: p<0.01; Controls/ECTs p<0.01), particularly in the shift phases, which suggests reduced attentional flexibility. In Stockings of Cambridge (SOC), ECTs abandoned the test early more often than Controls and NECTs (H=11, p<0.01) but ECTs who completed SOC performed comparably to the other two groups.

A double dissociation emerged from the comparison of cognitive profiles of ECT and NECT patients. ECTs showed executive deficits, particularly in attentional flexibility, but mild deficits in tests of visuospatial memory. NECTs presented the opposite pattern. This suggests predominantly frontostriatal involvement in ECT versus temporal involvement in NECT depressives.

An association between childhood maltreatment and subsequent alcohol abuse and/or dependence (AAD) has been found in multiple studies of females. Less is known about the association between childhood maltreatment and AAD among males, and the mechanisms that underlie this association in either gender. One explanation is that childhood maltreatment increases risk for AAD. An alternative explanation is that the same genetic or environmental factors that increase a child's risk for being maltreated also contribute to risk for AAD in adulthood.

Lifetime diagnosis of AAD was assessed using structured clinical interviews in a sample of 3527 male participants aged 19–56 years from the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders. The sources of childhood maltreatment–AAD association were estimated using both a matched case–control analysis of twin pairs discordant for childhood maltreatment and bivariate twin modeling.

Approximately 9% of participants reported childhood maltreatment, defined as serious neglect, molestation, or physical abuse occurring before the age of 15 years. Those who experienced childhood maltreatment were 1.74 times as likely to meet AAD criteria compared with males who did not experience childhood maltreatment. The childhood maltreatment–AAD association largely reflected environmental factors in common to members of twin pairs. Additional exploratory analyses provided evidence that AAD risk associated with childhood maltreatment was significantly attenuated after adjusting for measured family-level risk factors.

Males who experienced childhood maltreatment had an increased risk for AAD. Our results suggest that the childhood maltreatment–AAD association is attributable to broader environmental adversity shared between twins.

Although several studies have reported that repetitive transcranial magnetic stimulation (rTMS) treatment has demonstrable efficacy in patients with depression, the parameters needed to optimize therapeutic efficacy remain unclear. To this end we determined the efficacy of low-frequency right rTMS to the dorsolateral prefrontal cortex (DLPFC) compared to two forms of bilateral rTMS to the DLPFC: (1) sequential low-frequency right-sided followed by high-frequency left-sided rTMS and (2) sequential low-frequency rTMS to both hemispheres.

A total of 219 patients with treatment-resistant depression (TRD) were randomized to a 4-week course of rTMS applied with one of the three treatment conditions. Outcomes were assessed with standard rating scales.

Overall, slightly more than 50% of the patients achieved clinical response criteria. There was no substantial difference in response between the unilateral and bilateral treatment groups. Successful response to rTMS was predicted by a greater degree of baseline depression severity.

There is no substantial difference in efficacy between unilateral right-sided rTMS and the two forms of bilateral rTMS assessed in the study. Furthermore, our results call into question the specificity between frequency and laterality and rTMS response.

Visual and verbal episodic memory deficits are putative endophenotypes for schizophrenia; however, the extent of any genetic overlap of these with schizophrenia is unclear. In this study, we set out to quantify the genetic and environmental contributions to variance in visual and verbal memory performance, and to quantify their genetic relationship with schizophrenia.

We applied bivariate genetic modelling to 280 twins in a classic twin study design, including monozygotic (MZ) and dizygotic (DZ) pairs concordant and discordant for schizophrenia, and healthy control twins. We assessed episodic memory using subtests of the Wechsler Memory Scale – Revised (WMS-R).

Genetic influences (i.e. heritability) contributed significantly to variance in immediate recall of both verbal memory and visual learning, and the delayed recall of verbal and visual memory. Liability to schizophrenia was associated with memory impairment, with evidence of significant phenotypic correlations between all episodic memory measures and schizophrenia. Genetic factors were the main source of the phenotypic correlations for immediate recall of visual learning material; both immediate and delayed recall of verbal memory; and delayed recall of visual memory that, for example, shared genetic variance with schizophrenia, which accounted for 88% of the phenotypic correlation (rph=0.41) between the two.

Verbal memory and visual learning and memory are moderately heritable, share a genetic overlap with schizophrenia and are valid endophenotypes for the condition. The inclusion of these endophenotypes in genetic association studies may improve the power to detect susceptibility genes for schizophrenia.

Previous neuroimaging studies have demonstrated abnormalities in visual body image processing in anorexia and bulimia nervosa, possibly underlying body image disturbance in these disorders. Although cognitive behavioural interventions have been shown to be successful in improving body image disturbance in eating disorders, no randomized controlled study has yet analysed treatment-induced changes in neuronal correlates of visual body image processing.

Altogether, 32 females with eating disorders were randomly assigned either to a manualized cognitive behavioural body image therapy consisting of 10 group sessions, or to a waiting list control condition. Using functional magnetic resonance imaging, brain responses to viewing photographs of one's own and another female's body taken from 16 standardized perspectives while participants were wearing a uniform bikini were acquired before and after the intervention and the waiting time, respectively.

Data indicate a general blood oxygen level dependent signal enhancement in response to looking at photographs of one's own body from pre- to post-treatment, whereas exclusively in the control group activation decreases from pre- to post-waiting time were observed. Focused activation increases from pre- to post-treatment were found in the left middle temporal gyrus covering the coordinates of the extrastriate body area and in bilateral frontal structures including the middle frontal gyrus.

Results point to a more intense neuronal processing of one's own body after the cognitive behavioural body image therapy in cortical regions that are responsible for the visual processing of the human body and for self-awareness.

Pre-adult onset of major depressive disorder (MDD) may predict a more severe phenotype of depression. As data from naturalistic psychiatric specialty care settings are scarce, we examined phenotypic differences between pre-adult and adult onset MDD in a large sample of consecutive out-patients.

Altogether, 1552 out-patients, mean age 39.2±11.6 years, were diagnosed with current MDD on the Mini-International Neuropsychiatric Interview Plus diagnostic interview as part of the usual diagnostic procedure. A total of 1105 patients (71.2%) had complete data on all variables of interest. Pre-adult onset of MDD was defined as having experienced the signs and symptoms of a first major depressive episode before the age of 18 years. Patients were stratified according to the age at interview (20–40/40–65 years). Correlates of pre-adult onset were analysed using logistic regression models adjusted for age, age squared and gender.

Univariate analyses showed that pre-adult onset of MDD had a distinct set of demographic (e.g. less frequently living alone) and clinical correlates (more co-morbid DSM-IV – Text Revision diagnoses, more social phobia, more suicidality). In the multivariate model, we found an independent association only for a history of suicide attempts [odds ratio (OR) 3.15, 95% confidence intervals (CI) 1.97–5.05] and current suicidal thoughts (OR 1.81, 95% CI 1.26–2.60) in patients with pre-adult versus adult onset MDD.

Pre-adult onset of MDD is associated with more suicidality than adult onset MDD. Age of onset of depression is an easy to ascertain characteristic that may help clinicians in weighing suicide risk.

Recent work suggests that epigenetic differences may be associated with psychiatric disorders. Here we investigate, in a community-based sample, whether methylation profiles distinguish between individuals with and without lifetime depression. We also investigate the physiologic consequences that may be associated with these profiles.

Using whole blood-derived genomic DNA from a subset of participants in the Detroit Neighborhood Health Study (DNHS), we applied methylation microarrays to assess genome-wide methylation profiles for over 14 000 genes in 33 persons who reported a lifetime history of depression and 67 non-depressed adults. Bioinformatic functional analyses were performed on the genes uniquely methylated and unmethylated in each group, and inflammatory biomarkers [interleukin (IL)-6 and C-reactive protein (CRP)] were measured to investigate the possible functional significance of the methylation profiles observed.

Uniquely unmethylated gene sets distinguished between those with versus without lifetime depression. In particular, some processes (e.g. brain development, tryptophan metabolism) showed patterns suggestive of increased methylation among individuals with depression whereas others (e.g. lipoprotein) showed patterns suggestive of decreased methylation among individuals with depression. IL-6 and CRP levels were elevated among those with lifetime depression and, among those with depression only, IL-6 methylation showed an inverse correlation with circulating IL-6 and CRP.

Genome-wide methylation profiles distinguish individuals with versus without lifetime depression in a community-based setting, and show coordinated signals with pathophysiological mechanisms previously implicated in the etiology of this disorder. Examining epigenetic mechanisms in concert with other dynamic markers of physiologic functioning should improve our understanding of the neurobiology of depression.

The objective of this study was to investigate long-term cognitive and emotional sequelae of mild traumatic brain injury (mTBI), as previous research has remained inconclusive with respect to their prevalence and extent.

Thirty-three individuals who had sustained mTBI on average 6 years prior to the study and 33 healthy control subjects were matched according to age, gender and education. Structural brain damage at time of testing was excluded by magnetic resonance imaging (MRI). A comprehensive neuropsychological test battery was conducted to assess learning, recall, working memory, attention and executive function. Psychiatric symptoms were assessed by the Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-I) and the Beck Depression Inventory (BDI). Possible negative response bias was ruled out by implementing the Word Memory Test (WMT).

The mTBI individuals had significant impairments in all cognitive domains compared to the healthy control subjects. Effect sizes of cognitive deficits were medium to large, and could not be accounted for by self-perceived deficits, depression, compensation claims or negative response bias. BDI scores were significantly higher in the patient group, and three patients fulfilled DSM-IV criteria for a mild episode of major depression.

Primarily, well-recovered individuals who had sustained a minor trauma more than half a decade ago continue to have long-term cognitive and emotional sequelae relevant for everyday social and professional life. mTBI may lead to a lasting disruption of neurofunctional circuits not detectable by standard structural MRI and needs to be taken seriously in clinical and forensic evaluations.

Subclinical psychotic experiences during adolescence may represent liability for developing psychotic disorder. Both coping style and the degree of persistence of psychotic experiences may play a role in the progression to clinical psychotic disorder, but little is known about the causal relationship between the two.

Path modelling was used to examine longitudinal relationships between subclinical positive psychotic experiences and three styles of coping (task-, emotion- and avoidance-oriented) in an adolescent general population sample (n=813) assessed three times in 3 years. Distinct developmental trajectories of psychotic experiences, identified with growth mixture modelling, were compared on the use of these coping styles.

Over time, emotion-oriented coping in general was bi-directionally related to psychotic experiences. No meaningful results were found for task- or avoidance-oriented coping. Females reported using a wider range of coping styles than males, but the paths between coping and psychotic experiences did not differ by gender. Persistence of psychotic experiences was associated with a greater use of emotion-oriented coping, whereas a decrease in experiences over time was associated with an increased use of task-orientated coping.

Emotion-oriented coping is the most important coping style in relation to psychotic experiences, as it may contribute to a ‘vicious cycle’ and is associated with persistence of experiences. In addition, more task-oriented coping may result in a decrease in psychotic experiences. Results suggest that opportunities for intervention may already be present at the level of subclinical psychosis.

To identify sources of race/ethnic differences related to post-traumatic stress disorder (PTSD), we compared trauma exposure, risk for PTSD among those exposed to trauma, and treatment-seeking among Whites, Blacks, Hispanics and Asians in the US general population.

Data from structured diagnostic interviews with 34 653 adult respondents to the 2004–2005 wave of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) were analysed.

The lifetime prevalence of PTSD was highest among Blacks (8.7%), intermediate among Hispanics and Whites (7.0% and 7.4%) and lowest among Asians (4.0%). Differences in risk for trauma varied by type of event. Whites were more likely than the other groups to have any trauma, to learn of a trauma to someone close, and to learn of an unexpected death, but Blacks and Hispanics had higher risk of child maltreatment, chiefly witnessing domestic violence, and Asians, Black men, and Hispanic women had higher risk of war-related events than Whites. Among those exposed to trauma, PTSD risk was slightly higher among Blacks [adjusted odds ratio (aOR) 1.22] and lower among Asians (aOR 0.67) compared with Whites, after adjustment for characteristics of trauma exposure. All minority groups were less likely to seek treatment for PTSD than Whites (aOR range: 0.39–0.61), and fewer than half of minorities with PTSD sought treatment (range: 32.7–42.0%).

When PTSD affects US race/ethnic minorities, it is usually untreated. Large disparities in treatment indicate a need for investment in accessible and culturally sensitive treatment options.