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.

Depression is associated with the metabolic syndrome (MS). We examined whether metabolic dysregulation predicted the 2-year course of clinical depression.

A total of 285 older persons (⩾60 years) suffering from depressive disorder according to DSM-IV-TR criteria was followed up for 2 years. Severity of depression was assessed with the Inventory of Depressive Symptomatology (IDS) at 6-month intervals. Metabolic syndrome was defined according the National Cholesterol Education Programme (NCEP-ATP III). We applied logistic regression and linear mixed models adjusted for age, sex, years of education, smoking, alcohol use, physical activity, somatic co-morbidity, cognitive functioning and drug use (antidepressants, anti-inflammatory drugs) and severity of depression at baseline.

MS predicted non-remission at 2 years (odds ratioper component = 1.26, 95% confidence interval 1.00–1.58), p = 0.047), which was driven by the waist circumference and HDL cholesterol. MS was not associated with IDS sum score. Subsequent analyses on its subscales, however, identified an association with the somatic symptom subscale score over time (interaction time × somatic subscale, p = 0.005), driven by higher waist circumference and elevated fasting glucose level.

Metabolic dysregulation predicts a poor course of late-life depression. This finding supports the concept of ‘metabolic depression’, recently proposed on population-based findings of a protracted course of depressive symptoms in the presence of metabolic dysregulation. Our findings seem to be driven by abdominal obesity (as indicated by the waist circumference) and HDL cholesterol dysregulation.

People with Down's syndrome (DS) are at high risk for developing dementia in middle age. The biological basis for this is unknown. It has been proposed that non-demented adults with DS may undergo accelerated brain ageing.

We used volumetric magnetic resonance imaging (MRI) and manual tracing to compare brain anatomy and ageing in 39 non-demented adults with DS and 42 healthy controls.

Individuals with DS had significant differences in brain anatomy. Furthermore, individuals with DS had a significantly greater age-related reduction in volume of frontal, temporal and parietal lobes, and a significantly greater age-related increase in volume of peripheral cerebrospinal fluid (CSF).

Non-demented adults with DS have differences in brain anatomy and ‘accelerated’ ageing of some brain regions. This may increase their risk for age-related cognitive decline and Alzheimer's disease (AD).

In this study, 30-year longitudinal data from the Christchurch Health and Development Study (CHDS) were used to examine the associations between childhood exposure to sexual abuse and intimate relationship outcomes at age 30. In addition, a broad range of early childhood and family confounding factors were tested, and the role of intervening factors from adolescence was explored.

The investigation analyzed data from a birth cohort of over 900 New Zealand adults studied to the age of 30. At ages 18 and 21 cohort members reported on any exposure to sexual abuse prior to age 16. This information, along with prospective data gathered in childhood and adolescence, was used to predict partnership outcomes at age 30.

After adjustment for early childhood and family factors, exposure to more severe forms of childhood sexual abuse (CSA) was associated with earlier and more frequent cohabitation, higher rates of perpetrated interpartner violence (IPV), and early parenthood, lower relationship satisfaction and investment. Several factors from adolescence partially or fully mediated these associations, notably a history of early consensual sexual intercourse, higher number of sexual partnerships, substance abuse problems, and self-esteem. After adjustment for intervening factors, exposure to CSA remained significantly associated with IPV.

The findings support a causal chain process, whereby early childhood and family factors place some individuals at risk for CSA. The extent of CSA exposure is related to adolescent risk taking, which in turn leads to early and more frequent cohabitation, risk of IPV, and lower relationship satisfaction and investment.

Euthanasia and assisted suicide (EAS) based on a psychiatric disorder (psychiatric EAS) continue to pose ethical and policy challenges, even in countries where the practice has been allowed for years. We conducted a systematic review of reasons, a specific type of review for bioethical questions designed to inform rational policy-making. Our aims were twofold: (1) to systematically identify all published reasons for and against the practice (2) to identify current gaps in the debate and areas for future research.

Following the PRISMA guidelines, we performed a search across seven electronic databases to include publications focusing on psychiatric EAS and providing ethical reasons. Reasons were grouped into domains by qualitative content analysis.

We included 42 articles, most of which were written after 2013. Articles in favor and against were evenly distributed. Articles in favor were mostly full-length pieces written by non-clinicians, with articles against mostly reactive, commentary-type pieces written by clinicians. Reasons were categorized into eight domains: (1) mental and physical illness and suffering (2) decisional capacity (3) irremediability (4) goals of medicine and psychiatry (5) consequences for mental health care (6) psychiatric EAS and suicide (7) self-determination and authenticity (8) psychiatric EAS and refusal of life-sustaining treatment. Parity- (or discrimination-) based reasons were dominant across domains, mostly argued for by non-clinicians, while policy reasons were mostly pointed to by clinicians.

The ethical debate about psychiatric EAS is relatively young, with prominent reasons of parity. More direct engagement is needed to address ethical and policy considerations.

Alexithymia (difficulties in identifying and describing emotion) is a transdiagnostic trait implicated in social–emotional and mental health problems in the general population. Many autistic individuals experience significant social-communication difficulties and elevated anxiety/depression and alexithymia. Nevertheless, the role of alexithymia in explaining individual variability in the quality/severity of social-communication difficulties and/or anxiety and depression symptoms in autism remains poorly understood.

In total, 337 adolescents and adults (autism N = 179) were assessed for alexithymia on the Toronto Alexithymia Scale and for social-communication difficulties, anxiety and depression symptoms. A total of 135 individuals (autism N = 76) were followed up 12–24 months later. We used regression models to establish cross-sectional and longitudinal associations between alexithymia, social-communication difficulties, anxiety and depression symptoms.

Autistic individuals reported significantly higher alexithymia than comparison individuals (p < 0.001, r effect size = 0.48), with 47.3% of autistic females and 21.0% of autistic males meeting cut-off for clinically relevant alexithymia (score ⩾61). Difficulties in describing feelings were particularly associated with current self-reported social-communication difficulties [p < 0.001, β = 0.57, 95% confidence interval (CI) 0.44–0.67] and predicted later social-communication difficulties (p = 0.02, β = 0.43, 95% CI 0.07–0.82). Difficulties in identifying feelings were particularly associated with current anxiety symptom severity (p < 0.001, β = 0.54, 95% CI 0.41–0.77) and predicted later anxiety (p = 0.01; β = 0.31, 95% CI 0.08–0.62).

Our findings suggest that difficulties in identifying v. describing emotion are associated with differential clinical outcomes in autism. Psychological therapies targeting emotional awareness may improve social-communication and anxiety symptoms in autism, potentially conferring long-term benefits.

Research on the long-term course of major depressive disorder (MDD) is hindered by the absence of established course criteria and by idiosyncratic definitions of chronicity. The aims of this study were to derive an empirical index of MDD course, to examine its predictive validity, and to identify the adulthood outcomes associated with a chronic course.

Indicators for a MDD course factor were rationally selected and subjected to principal components (PCA) and confirmatory factor analyses (CFA) among 426 subjects with a lifetime history of MDD by age 30. Scores on the index prior to age 19 were examined as predictors of course from age 19 to 30. Associations between the index and outcomes of interest at age 30 were examined.

Three indicators loaded highly on a chronic course index and displayed adequate internal consistency: early onset age, number of episodes, and duration of ill time. Predictive validity of the index was supported. A more chronic course was associated with greater symptom severity, greater likelihood of treatment utilization, and greater psychosocial impairment in multiple domains. Treatment utilization interacted with chronicity to predict relatively few outcomes and did not reduce the negative impact of a chronic course.

The course of MDD through early adulthood is best represented by a composite of early onset age, number of episodes, and duration of ill time. A chronic course through early adulthood is associated with numerous indicators of psychosocial impairment. Mental health treatment utilization in a naturalistic setting does not appear to reduce the negative impact of chronic MDD.

Cannabis use appears to be a risk factor for schizophrenia. Moreover, cannabis abusers show impaired decision-making capacities, linked to the orbitofrontal cortex (OFC). Although there is substantial evidence that first-episode schizophrenia patients show impairments in cognitive tasks associated with the dorsolateral prefrontal cortex (DLPFC), it is not clear whether decision making is impaired at schizophrenia onset. In this study, we examined the association between antecedents of cannabis abuse and cognitive impairment in cognitive tasks associated with the DLPFC and the OFC in a sample of first-episode patients with schizophrenia-spectrum disorders.

One hundred and thirty-two patients experiencing their first episode of a schizophrenia-spectrum psychosis were assessed with a cognitive battery including DLPFC-related tasks [backward digits, verbal fluency (FAS) and the Trail Making Test (TMT)] and an OFC-related task [the Iowa Gambling Task (GT)]. Performance on these tasks was compared between patients who had and had not abused cannabis before their psychosis onset.

No differences were observed between the two groups on the performance of any of the DLPFC-related tasks. However, patients who had abused cannabis before their psychosis onset showed a poorer total performance on the gambling task and a lower improvement on the performance of the task compared to no-abusers.

Pre-psychotic cannabis abuse is associated with decision-making impairment, but not working memory and executive function impairment, among first-episode patients with a schizophrenia-spectrum psychosis. Further studies are needed to examine the direction of causality of this impairment; that is, does the impairment make the patients abuse cannabis, or does cannabis abuse cause the impairment?

It is well known that the hypothalamic–pituitary–adrenal (HPA) axis is compromised in major depression and bipolar disorder. There is increasing evidence that subtle HPA abnormalities, such as elevated cortisol levels, precede the development of an affective disorder. Interpersonal stress is also associated with the development of affective disorders. The present study sought to determine whether interpersonal chronic and episodic stress moderated the relationship between cortisol levels in the natural environment and risk status, defined as having a parent with bipolar disorder.

Sixty-two offspring of parents with bipolar disorder (OBD) and 60 offspring with no family history of affective disorders (OFH−), aged 19.48 years (s.d.=3.38, range 14–28), completed interviews assessing mental disorders and chronic and episodic stress, and provided saliva samples over 3 days.

Regression analyses revealed that the OBD who experienced high interpersonal chronic stress displayed a larger cortisol rise following awakening than the OBD reporting low interpersonal chronic stress. The same relationship was also found for levels of non-interpersonal chronic stress. The OBD who reported experiencing severe interpersonal episodic stress exhibited higher levels of daytime cortisol than the OBD reporting interpersonal episodic stress of mild severity. Importantly, none of the above relationships were detected in the OFH−. Each of the interactions between family history of affective disorders and stress remained after controlling for age, gender and offspring lifetime affective disorders and current non-affective disorders.

A biological sensitivity to stress may underlie the susceptibility to affective disorders among the OBD.

Herpes virus infections can cause cognitive impairment during and after acute encephalitis. Although chronic, latent/persistent infection is considered to be relatively benign, some studies have documented cognitive impairment in exposed persons that is untraceable to encephalitis. These studies were conducted among schizophrenia (SZ) patients or older community dwellers, among whom it is difficult to control for the effects of co-morbid illness and medications. To determine whether the associations can be generalized to other groups, we examined a large sample of younger control individuals, SZ patients and their non-psychotic relatives (n=1852).

Using multivariate models, cognitive performance was evaluated in relation to exposures to herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2) and cytomegalovirus (CMV), controlling for familial and diagnostic status and sociodemographic variables, including occupation and educational status. Composite cognitive measures were derived from nine cognitive domains using principal components of heritability (PCH). Exposure was indexed by antibodies to viral antigens.

PCH1, the most heritable component of cognitive performance, declines with exposure to CMV or HSV-1 regardless of case/relative/control group status (p = 1.09 × 10−5 and 0.01 respectively), with stronger association with exposure to multiple herpes viruses (β = −0.25, p = 7.28 × 10−10). There were no significant interactions between exposure and group status.

Latent/persistent herpes virus infections can be associated with cognitive impairments regardless of other health status.

There is growing evidence on the importance of experiences of stressful events in the development of psychopathology. This study aimed to investigate the role of stressful events in the continuity of internalizing and externalizing problems, as well as the cross-influence of these problems from early childhood to late adolescence.

Data came from a general population sample of 396 children followed from the ages of 3 to 18 years. Parent-ratings of internalizing and externalizing problems at ages 3, 5, 10 and 18 years were used. Parents also reported on the presence of stressful events between the ages of 3 and 5 years, and 5 and 10 years. Adolescent reports on stressful events over the ages of 10–18 years were used. Structural equation models were used to disentangle/analyse the role of stressful events in the development of internalizing and externalizing problems.

From the age of 3 years onwards externalizing symptoms predicted experiences of stressful events. In turn, these experiences predicted later externalizing problems. Stressful events also explained part of the continuity of internalizing problems from the age of 10 years onwards, but not during childhood. From childhood onwards, cross-influences from externalizing problems to subsequent internalizing problems were found to run through stressful events. Only in adolescence cross-influences from internalizing problems to externalizing problems were found, again via stressful events.

From childhood onwards to late adolescence, stressful events play a significant role in both the continuity and the co-occurrence of externalizing and internalizing problems. Theoretical and methodological implications of these findings are discussed.

Transition across eating disorder diagnoses is common, reflecting instability of specific eating disorder presentations. Previous studies have examined temporal stability of diagnoses in adult treatment-seeking samples but have not uniformly captured initial presentation for treatment. The current study examines transitions across eating disorder diagnostic categories in a large, treatment-seeking sample of individuals born in Sweden and compares these transitions across two birth cohorts and from initial diagnosis.

Data from Swedish eating disorders quality registers were extracted in 2013, including 9622 individuals who were seen at least twice from 1999 to 2013. Patterns of remission were examined in the entire sample and subsequently compared across initial diagnoses. An older (born prior to 1990) and younger birth cohort were also identified, and analyses compared these cohorts on patterns of diagnostic transition.

Although diagnostic instability was common, transition between threshold eating disorder diagnoses was infrequent. For all diagnoses, transition to remission was likely to occur following a diagnosis state that matched initial diagnosis, or through a subthreshold diagnostic state. Individuals in the younger cohort were more likely to transition to a state of remission than those in the older cohort.

Results indicate more temporal continuity in eating disorder presentations than suggested by previous research and highlight the importance of early detection and intervention in achieving remission.