Personal debt is one of many factors associated with anxiety, depression and suicidality. The aim of this study was to examine the relationship between personal debt and suicidal ideation in the context of sociodemographic factors, employment and income, lifestyle behaviours, and recently experienced traumatic events.

Interviews were conducted with a random probability sample comprising 7461 respondents for the third national survey of psychiatric morbidity of adults in England. Fieldwork was carried out throughout 2007. The prevalence of suicidal thoughts in the past week, past year and lifetime was assessed and current sources of debt were recorded.

In 2007, 4.3% of adults in England had thought about taking their own life in the past 12 months, ranging from 1.8% of men aged ⩾55 years to 7.0% of women aged 35–54 years. Those in debt were twice as likely to think about suicide after controlling for sociodemographic, economic, social and lifestyle factors. Difficulty in making hire purchase or mail order repayments and paying off credit card debt, in addition to housing-related debt (rent and mortgage arrears), was strongly associated with suicidal thoughts. Feelings of hopelessness partially mediated the relationship between debt and suicidal ideation.

The number of debts, source of the debt and reasons for debt are key correlates of suicidal ideation. Individuals experiencing difficulties in repaying their debts because they are unemployed or have had a relationship breakdown or have heavy caring responsibilities may require psychiatric evaluation in addition to debt counselling.

The personality disorders (PDs) in the ‘dramatic’ cluster B [antisocial (ASPD), histrionic (HPD), narcissistic (NPD) and borderline (BPD)] demonstrate co-morbidity. However, the degree to which genetic and/or environmental factors influence their co-occurrence is not known and, with the exception of ASPD, the relative impact of genetic and environmental risk factors on liability to the cluster B PDs has not been conclusively established.

PD traits were assessed in 1386 Norwegian twin pairs between the age of 19 and 35 years using the Structured Interview for DSM-IV Personality Disorders (SIDP-IV). Using the statistical package Mx, multivariate twin models were fitted to dimensional representations of the PDs.

The best-fitting model, which did not include sex or shared family environment effects, included common genetic and environmental factors influencing all four dramatic PD traits, and factors influencing only ASPD and BPD. Heritability was estimated at 38% for ASPD traits, 31% for HPD traits, 24% for NPD traits and 35% for BPD traits. BPD traits had the lowest and ASPD traits the highest disorder-specific genetic variance.

The frequently observed co-morbidity between cluster B PDs results from both common genetic and environmental influences. Etiologically, cluster B has a ‘substructure’ in which ASPD and BPD are more closely related to each other than to the other cluster B disorders.

Although there is agreement on the association between delay in treatment of psychosis and outcome, less is known regarding the pathways to care of patients suffering from a first psychotic episode. Pathways are complex, involve a diverse range of contacts, and are likely to influence delay in treatment. We conducted a systematic review on the nature and determinants of the pathway to care of patients experiencing a first psychotic episode.

We searched four databases (Medline, HealthStar, EMBASE, PsycINFO) to identify articles published between 1985 and 2009. We manually searched reference lists and relevant journals and used forward citation searching to identify additional articles. Studies were included if they used an observational design to assess the pathways to care of patients with first-episode psychosis (FEP).

Included studies (n=30) explored the first contact in the pathway and/or the referral source that led to treatment. In 13 of 21 studies, the first contact for the largest proportion of patients was a physician. However, in nine of 22 studies, the referral source for the greatest proportion of patients was emergency services. We did not find consistent results across the studies that explored the sex, socio-economic, and/or ethnic determinants of the pathway, or the impact of the pathway to care on treatment delay.

Additional research is needed to understand the help-seeking behavior of patients experiencing a first-episode of psychosis, service response to such contacts, and the determinants of the pathways to mental health care, to inform the provision of mental health services.

Depression is a complex public health problem with considerable variation in treatment response. The systemic complexity of depression, or the feedback processes among diverse drivers of the disorder, contribute to the persistence of depression. This paper extends prior attempts to understand the complex causal feedback mechanisms that underlie depression by presenting the first broad boundary causal loop diagram of depression dynamics.

We applied qualitative system dynamics methods to map the broad feedback mechanisms of depression. We used a structured approach to identify candidate causal mechanisms of depression in the literature. We assessed the strength of empirical support for each mechanism and prioritized those with support from validation studies. Through an iterative process, we synthesized the empirical literature and created a conceptual model of major depressive disorder.

The literature review and synthesis resulted in the development of the first causal loop diagram of reinforcing feedback processes of depression. It proposes candidate drivers of illness, or inertial factors, and their temporal functioning, as well as the interactions among drivers of depression. The final causal loop diagram defines 13 key reinforcing feedback loops that involve nine candidate drivers of depression.

Future research is needed to expand upon this initial model of depression dynamics. Quantitative extensions may result in a better understanding of the systemic syndrome of depression and contribute to personalized methods of evaluation, prevention and intervention.

In order to reduce the high prevalence of depression, early interventions for people at risk of depression are warranted. This study evaluated the effectiveness of an early guided self-help programme based on acceptance and commitment therapy (ACT) for reducing depressive symptomatology.

Participants with mild to moderate depressive symptomatology were recruited from the general population and randomized to the self-help programme with extensive email support (n=125), the self-help programme with minimal email support (n=125) or to a waiting list control group (n=126). Participants completed measures before and after the intervention to assess depression, anxiety, fatigue, experiential avoidance, positive mental health and mindfulness. Participants in the experimental conditions also completed these measures at a 3-month follow-up.

In the experimental conditions significant reductions in depression, anxiety, fatigue, experiential avoidance and improvements in positive mental health and mindfulness were found, compared with the waiting list condition (effect sizes Cohen's d=0.51–1.00). These effects were sustained at the 3-month follow-up. There were no significant differences between the experimental conditions on the outcome measures.

The ACT-based self-help programme with minimal email support is effective for people with mild to moderate depressive symptomatology.

Against a backdrop of increasing research, clinical and taxonomic attention in non-suicidal self-injury (NSSI), evidence suggests a link between NSSI and eating disorders (ED). The frequency estimates of NSSI in ED vary widely. Little is known about the sources of this variation, and no meta-analysis has quantified the association between ED and NSSI.

Using random-effects meta-analyses, meta-regression analyses, and 1816–6466 unique participants with various ED, we estimated the weighted average percentage of individuals with ED, those with anorexia nervosa (AN) and those with bulimia nervosa (BN) who are reported to have a lifetime history of NSSI across studies. We further examined predictors of NSSI in ED.

The weighted average percentage of patients with a lifetime history of NSSI was 27.3% [95% confidence interval (CI) 23.8–31.0%] for ED, 21.8% (95% CI 18.5–25.6%) for AN, and 32.7% (95% CI 26.9–39.1%) for BN. The difference between BN and AN was statistically significant [odds ratio (OR) 1.77, 95% CI 1.14–2.77, p = 0.013]. The odds of NSSI increased by 24% for every 10% increase in the percentage of participants with histories of suicide attempts (OR 1.24, 95% CI 1.04–1.48, p = 0.020) and decreased by 26% for every 10% increase in the percentage of participants with histories of substance abuse (OR 0.74, 95% CI 0.58–0.95, p = 0.023).

In the specific context of ED, NSSI is highly prevalent and correlates positively with attempted suicide, urging for NSSI-focused treatments. A novel finding is that NSSI is potentially antagonized by substance abuse.

Changes in autonomic nervous system (ANS) function have been observed in a variety of psychological disorders, including posttraumatic stress disorder (PTSD). Analysis of heart rate variability (HRV) provides insight into the functioning of the ANS. Previous research on PTSD found lower HRV in PTSD patients compared to controls, indicating altered sympathetic and parasympathetic activity, but findings are inconsistent. The purpose of this meta-analysis was to examine differences in HRV indices between individuals with PTSD and healthy controls at baseline and during stress.

The included primary studies present an aggregate of studies analyzing different HRV indices. Examined HRV indices were standard deviation of the normalized NN-intervals (SDNN), root mean square of successive differences (RMSSD), low-frequency (LF) and high-frequency (HF) spectral components, LF/HF ratio, and heart rate (HR). Moderating effects of study design, HRV and PTSD assessment, and sample characteristics were examined via subgroup-analyses and meta-regressions.

Random-effects meta-analyses for HRV parameters at rest revealed significant group differences for RMSSD and HF-HRV, suggesting lower parasympathetic activity in PTSD. The aggregated effect size for SDNN was medium, suggesting diminished total variability in PTSD. A small effect was found for LF-HRV. A higher LF/HF ratio was found in the PTSD sample as compared to controls. Individuals with PTSD showed significantly higher HR. During stress, individuals with PTSD showed higher HR and lower HF-HRV, both indicated by small effect sizes.

Findings suggest that PTSD is associated with ANS dysfunction.

Evidence is accumulating that child sexual abuse (CSA) is associated with many psychiatric disorders in adulthood. This paper uses the detailed information available from the 2007 Adult Psychiatric Morbidity Survey of England (APMS 2007) to quantify links between CSA and a range of psychiatric conditions.

The prevalence of psychiatric disorder was established in a random sample of the English household population (n=7403), which also provided sociodemographic and experiential information.

We analyzed six types of common mental disorder, alcohol abuse and drug abuse, and people who screened positively for post-traumatic stress disorder (PTSD) and eating disorders. All were strongly and highly significantly associated with CSA, particularly if non-consensual sexual intercourse was involved, for which odds ratios (ORs) ranged from 3.7 to 12.1. These disorders were also related to adult sexual abuse (ASA), although the likelihood of reverse causality is then increased. Revictimization in adulthood was common, and increased the association of CSA with disorder. For several disorders, the relative odds were higher in females but formal tests for moderation by gender were significant only for common mental disorders and only in relation to non-consensual sexual intercourse. The population attributable fraction (PAF) was higher in females in all cases.

The detailed and high-quality data in APMS 2007 provided important confirmation both of the strength of association of CSA with psychiatric disorder and of its relative non-specificity. Our results have major implications at the public health level and the individual level, in particular the need for better recognition and treatment of the sequelae of CSA.

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.

Approximately 11% of schoolchildren are bullied on a regular basis. It has been argued that continuous exposure to stress is related to the development of psychotic symptoms. The current study sought to investigate whether being bullied in childhood is related to the development of psychotic symptoms.

A search of PubMed, PsycINFO and EMBASE was conducted. The reference lists of included papers were searched to identify other eligible papers. A meta-analysis was performed on a subgroup of studies.

We found four clinical and 10 general population studies that met inclusion criteria. The results of the clinical studies were mixed. However, the results of the non-clinical studies provided more consistent evidence that school bullying is related to the development of non-clinical psychotic symptoms. Stronger associations were found with increased frequency and severity and longer duration of being bullied. We performed a meta-analysis on seven population-based studies, yielding unadjusted and adjusted odds ratios (ORs) of 2.7 [95% confidence interval (CI) 2.1–3.6] and 2.3 (95% CI 1.5–3.4) respectively.

Although there is some evidence of an association between bullying and psychosis in clinical samples, the research is too sparse to draw any firm conclusions. However, population-based non-clinical studies support the role of bullying in the development of psychotic symptoms later in life. These findings are consistent with findings of an increased risk of psychotic symptoms among those exposed to other types of abuse.