It is unclear whether pubertal status or timing of puberty explains the increase in depressive symptoms in girls during adolescence.

This is a longitudinal study based on 2506 girls from the Avon Longitudinal Study of Parents and Children (ALSPAC). Self-reported depressive symptoms at 10.5, 13 and 14 years were assessed using the Short Mood and Feelings Questionnaire (SMFQ). Pubertal status (Tanner breast and pubic hair stage) and timing of menarche were derived from questionnaires administered from age 8 to 14 years. We used multivariable regression models to examine the relative contributions of pubertal status and timing in accounting for increases in level of depressive symptoms at 14 years.

With increasing age, the association between breast development and depressive symptoms strengthened. Pubertal status (breast stage), rather than timing of menarche, was independently associated with depressive symptoms at 14 years. There was strong evidence for a linear relationship between breast stage and depressive symptoms at 14 years [increase in 0.17 s.d. (range 0.10–0.24) of depressive symptoms for advancement of each breast stage].

Depressive symptoms in mid-adolescence were more strongly influenced by breast stage than timing of menarche. This could imply that the female rise in depression during adolescence is due to increasing estrogen levels, and might explain why the gender difference in rates of depression emerges at this stage. Future research should be aimed at identifying the mechanism of action of pubertal change, including direct effects of pubertal hormones and indirect effects mediated by psychosocial factors.

The stress–vulnerability model of psychosis continues to be influential. The aim of this study was to compare emotional and symptomatic responses to stress in individuals at ultra-high risk (UHR) of developing psychosis, in age- and gender-matched healthy controls, and in patients with non-affective psychosis.

A total of 27 UHR, 27 psychotic and 27 healthy individuals completed the experience sampling method, an ambulant diary technique, where they were required to fill in self-assessment questions about their emotions, symptoms and perceived stress at semi-random times of the day for 6 days. Quesionnaire and interview assessments were also completed.

Multilevel regression analyses showed that individuals at UHR of developing psychosis reported greater negative emotions in response to stress than the healthy individuals. Against the initial hypotheses, the UHR individuals also experienced greater emotional reactivity to stress when compared with the patient group. No significant differences were observed between the patients and the non-clinical sample. Stress measures significantly predicted the intensity of psychotic symptoms in UHR individuals and patients, but the extent of this did not significantly differ between the groups.

Individuals at UHR of developing psychosis may be particularly sensitive to everyday stressors. This effect may diminish after transition to psychosis is made and in periods of stability. Subtle increases in psychotic phenomena occur in response to stressful events across the continuum of psychosis.

The Wenchuan earthquake was a catastrophic earthquake in China. The aim of this study is to explore longitudinally the rates of post-traumatic stress disorder (PTSD) and depression in adolescents after the Wenchuan earthquake, and to identify independent predictors of PTSD.

PTSD and depression symptoms among adolescents at 6, 12 and 18 months after the Wenchuan earthquake were investigated using the PTSD Checklist Civilian Version and the Beck Depression Inventory (BDI). Subjects in this study included 548 high school student survivors in a local boarding high school.

The rates of PTSD symptoms were 9.7%, 1.3% and 1.6% at the 6-, 12- and 18-month follow-ups, respectively. BDI scores were found to be the best predictor of severity of PTSD at 6, 12 and 18 months. Gender was another variable contributing significantly to PTSD at 6 and 12 months after the earthquake. In the 12-month follow-up, home damage was found to be a predictor of severity of PTSD symptoms. Being a child with siblings was found to be a predictor of severity of PTSD symptoms at 12 and 18 months after the earthquake.

PTSD symptoms changed gradually at various stages after the earthquake. Depression symptoms were predictive of PTSD symptoms in the 18-month follow-up study. Other predictors of PTSD symptoms included female gender and being a child with siblings. The results of this study may be helpful for further mental health interventions for adolescents after earthquakes.

Offspring of parents with mental disorder are at risk of a range of adverse outcomes. We sought to establish whether such risks extend to offending by examining rates of criminal conviction, including conviction for violent and sexual offences, among offspring of parents with mental disorder compared to offspring without parental disorder.

From a random sample of the Danish population, a cohort aged ⩽15 years (n=412 117) was followed for the occurrence of conviction between January 1981 and December 2006. Incidence rate ratios (IRRs) and cumulative incidences for offspring conviction by parental mental disorder status were calculated using a Cox regression model. Analyses were repeated for conviction for a serious first offence.

Offspring with history of parental mental disorder had higher rates of conviction than those without parental disorder; rates were highest for those with two affected parents [IRR 3.39, 95% confidence interval (CI) 3.08–3.73]. The association persisted when parental gender, offspring gender and the nature of parental disorder were considered. Absolute rates were lower but relative rates higher for female offspring (IRR 3.26 for males with two affected parents, 4.52 for females). Similar patterns were seen for conviction for serious offences. Associations were attenuated after adjustment was made for family socio-economic position (SEP) and parental criminality.

Offspring of parents with mental disorder represent a group at elevated risk of criminality. This raises the possibility of shared familial vulnerability for mental disorder and criminal behaviour, and highlights the need to consider early identification and intervention in this group.

Despite increased cardiometabolic risk in individuals with mental illness taking antipsychotic medication, metabolic screening practices are often incomplete or inconsistent.

We undertook a systematic search and a PRISMA (Preferred Reporting Items for Systematic reviews and Meta-Analyses) meta-analysis of studies examining routine metabolic screening practices in those taking antipsychotics both for patients in psychiatric care before and following implementation of monitoring guidelines.

We identified 48 studies (n=290 534) conducted between 2000 and 2011 in five countries; 25 studies examined predominantly schizophrenia-spectrum disorder populations; 39 studies (n=218 940) examined routine monitoring prior to explicit guidelines; and nine studies (n=71 594) reported post-guideline monitoring. Across 39 studies, routine baseline screening was generally low and above 50% only for blood pressure [69.8%, 95% confidence interval (CI) 50.9–85.8] and triglycerides (59.9%, 95% CI 36.6–81.1). Cholesterol was measured in 41.5% (95% CI 18.0–67.3), glucose in 44.3% (95% CI 36.3–52.4) and weight in 47.9% (95% CI 32.4–63.7). Lipids and glycosylated haemoglobin (HbA1c) were monitored in less than 25%. Rates were similar for schizophrenia patients, in US and UK studies, for in-patients and out-patients. Monitoring was non-significantly higher in case-record versus database studies and in fasting samples. Following local/national guideline implementation, monitoring improved for weight (75.9%, CI 37.3–98.7), blood pressure (75.2%, 95% CI 45.6–95.5), glucose (56.1%, 95% CI 43.4–68.3) and lipids (28.9%, 95% CI 20.3–38.4). Direct head-to-head pre–post-guideline comparison showed a modest but significant (15.4%) increase in glucose testing (p=0.0045).

In routine clinical practice, metabolic monitoring is concerningly low in people prescribed antipsychotic medication. Although guidelines can increase monitoring, most patients still do not receive adequate testing.

Many studies have linked depression and obesity; few have more than two assessments of depressive symptoms and adiposity to address the potential bidirectional relationship between adiposity and depressive symptoms from young adulthood through old age. We tested whether baseline depressive symptoms are associated with changes in weight, whether baseline adiposity is associated with changes in depressive symptoms, and whether these associations vary by sex.

Participants (n=2251; 47% female) were from the Baltimore Longitudinal Study of Aging (BLSA). Using hierarchical linear modeling (HLM) on 30 years of data, the trajectory of adiposity and depressive symptoms over adulthood was estimated from >10 000 observations (mean=4.5 assessments per participant) of body mass index (BMI; kg/m2), waist circumference and hip circumference and >10 000 observations (mean=4.5 assessments per participant) of the Center for Epidemiological Studies Depression Scale (CES-D). Baseline depressive symptoms and adiposity were then tested as predictors of the trajectory of adiposity and depressive symptoms respectively. Additional analyses tested for sex-specific associations.

Sex moderated the association between depressive symptoms and weight gain such that women who experienced depressed affect had greater increases in BMI (binteraction=0.12, s.e.=0.04), waist (binteraction=0.22, s.e.=0.10) and hip circumference (binteraction=0.20, s.e.=0.07) across the adult lifespan, controlling for relevant demographic and behavioral covariates. Baseline adiposity was unrelated to the trajectory of depressive symptoms (median b=0.00) for both sexes.

Women who experience symptoms of depression tend to gain more weight across adulthood than men who experience such symptoms. Whether an individual was normal weight or overweight was unrelated to changes in depressive symptoms across adulthood.

Studies conducted in Europe and the USA have shown that co-morbidity between major depressive disorder (MDD) and anxiety disorders is associated with various MDD-related features, including clinical symptoms, degree of familial aggregation and socio-economic status. However, few studies have investigated whether these patterns of association vary across different co-morbid anxiety disorders. Here, using a large cohort of Chinese women with recurrent MDD, we examine the prevalence and associated clinical features of co-morbid anxiety disorders.

A total of 1970 female Chinese MDD patients with or without seven co-morbid anxiety disorders [including generalized anxiety disorder (GAD), panic disorder, and five phobia subtypes] were ascertained in the CONVERGE study. Generalized linear models were used to model association between co-morbid anxiety disorders and various MDD features.

The lifetime prevalence rate for any type of co-morbid anxiety disorder is 60.2%. Panic and social phobia significantly predict an increased family history of MDD. GAD and animal phobia predict an earlier onset of MDD and a higher number of MDD episodes, respectively. Panic and GAD predict a higher number of DSM-IV diagnostic criteria. GAD and blood-injury phobia are both significantly associated with suicidal attempt with opposite effects. All seven co-morbid anxiety disorders predict higher neuroticism.

Patterns of co-morbidity between MDD and anxiety are consistent with findings from the US and European studies; the seven co-morbid anxiety disorders are heterogeneous when tested for association with various MDD features.

Deficits in memory and executive performance are well-established features of bipolar disorder and schizophrenia. By contrast, data on cognitive impairment in schizoaffective disorder are scarce and the findings are conflicting.

We used the Wechsler Memory Scale (WMS-III) and the Behavioural Assessment of the Dysexecutive Syndrome (BADS) to test memory and executive function in 45 schizophrenic patients, 26 schizomanic patients and 51 manic bipolar patients in comparison to 65 healthy controls. The patients were tested when acutely ill.

All three patient groups performed significantly more poorly than the controls on global measures of memory and executive functioning, but there were no differences among the patient groups. There were few differences in memory and executive function subtest scores within the patient groups. There were no differences in any test scores between manic patients with and without psychotic symptoms.

Schizophrenic, schizomanic and manic patients show a broadly similar degree of executive and memory deficits in the acute phase of illness. Our results do not support a categorical differentiation across different psychotic categories with regard to neuropsychological deficits.

Although some evidence suggests that borderline personality disorder (BPD) is primarily a disorder of the emotion regulation system, findings remain inconsistent. One potential explanation for this is the moderating role of dissociation.

In this study, 33 female subjects with BPD and 26 healthy controls (HC; matched by education level and nicotine intake) were presented idiographic aversive, standard unpleasant and neutral scripts. Modulation of startle reflex and electrodermal responses (skin conductance level; SCL) were measured during imagery of emotional and neutral scripts. Additionally, self-reports of emotional experience (valence and arousal) and present-state dissociation were assessed.

Patients with BPD showed elevated levels of dissociative experiences during testing. Present-state dissociation mediated group differences in SCL and startle response between the HC and BPD groups.

These results suggest that careful attention must be paid to the moderating effect of dissociative symptoms on the psychophysiological responses of BPD patients. Furthermore, the findings have important implications for the assessment and treatment of BPD, including the need to carefully assess BPD patients for dissociative symptoms and to incorporate the treatment of dissociation.

Examining predictors of the outcomes of major depressive disorder (MDD) is important for clinical practice and population health. There are few population-based longitudinal studies on this topic. The objectives of this study were to (1) estimate the proportions of persistent and recurrent MDD among those with MDD over 1 year, and (2) identify demographic, socio-economic, workplace psychosocial and clinical factors associated with the outcomes.

From a population-based longitudinal study of the working population, participants with a lifetime diagnosis of MDD were selected (n=834). They were classified into two groups: those with and those without current MDD. The proportions of 1-year persistence and recurrence of MDD were estimated. MDD was assessed by the World Health Organization (WHO) Composite International Diagnostic Interview, CIDI-Auto 2.1, by telephone.

The proportions of persistent and recurrent MDD in 1 year were 38.5% [95% confidence interval (CI) 31.1–46.5] and 13.3% (95% CI 10.2–17.1) respectively. Long working hours, negative thinking and having co-morbid social phobia were predictive of persistence of MDD. Perceived work–family conflict, the severity of a major depressive episode and symptoms of depressed mood were significantly associated with the recurrence of MDD.

Clinical and psychosocial factors are important in the prognosis of MDD. The factors associated with persistence and recurrence of MDD may be different. More large longitudinal studies on this topic are needed so that clinicians may predict potential outcomes based on the clinical profile and provide interventions accordingly. They may also take clinical action to change relevant psychosocial factors to minimize the chance of persistence and/or recurrence of MDD.

This study aimed to identify the course of unmet needs by patients with a first episode of schizophrenia and to determine associated variables.

We investigated baseline assessments in the European First Episode Schizophrenia Trial (EUFEST) and also follow-up interviews at 6 and 12 months. Latent class growth analysis was used to identify patient groups based on individual differences in the development of unmet needs. Multinomial logistic regression determined the predictors of group membership.

Four classes were identified. Three differed in their baseline levels of unmet needs whereas the fourth had a marked decrease in such needs. Main predictors of class membership were prognosis and depression at baseline, and the quality of life and psychosocial intervention at follow-up. Depression at follow-up did not vary among classes.

We identified subtypes of patients with different courses of unmet needs. Prognosis of clinical improvement was a better predictor for the decline in unmet needs than was psychopathology. Needs concerning social relationships were particularly persistent in patients who remained high in their unmet needs and who lacked additional psychosocial treatment.

Genetic studies in adults indicate that genes influencing the personality trait of neuroticism account for substantial genetic variance in anxiety and depression and in somatic health. Here, we examine for the first time the factors underlying the relationship between neuroticism and anxiety/depressive and somatic symptoms during adolescence.

The Somatic and Psychological Health Report (SPHERE) assessed symptoms of anxiety/depression (PSYCH-14) and somatic distress (SOMA-10) in 2459 adolescent and young adult twins [1168 complete pairs (35.4% monozygotic, 53% female)] aged 12–25 years (mean=15.5±2.9). Differences between boys and girls across adolescence were explored for neuroticism, SPHERE-34, and the subscales PSYCH-14 and SOMA-10. Trivariate analyses partitioned sources of covariance in neuroticism, PSYCH-14 and SOMA-10.

Girls scored higher than boys on both neuroticism and SPHERE, with SPHERE scores for girls increasing slightly over time, whereas scores for boys decreased or were unchanged. Neuroticism and SPHERE scores were strongly influenced by genetic factors [heritability (h2)=40–52%]. A common genetic source influenced neuroticism, PSYCH-14 and SOMA-10 (impacting PSYCH-14 more than SOMA-10). A further genetic source, independent of neuroticism, accounted for covariation specific to PSYCH-14 and SOMA-10. Environmental influences were largely specific to each measure.

In adolescence, genetic risk factors indexed by neuroticism contribute substantially to anxiety/depression and, to a lesser extent, perceived somatic health. Additional genetic covariation between anxiety/depressive and somatic symptoms, independent of neuroticism, had greatest influence on somatic distress, where it was equal in influence to the factor shared with neuroticism.

Depression in fathers in the postnatal period is associated with an increased risk of child behaviour problems. A key potential pathway of risk transmission is exposure of the child to negative cognitions and affect in the context of early parenting. This study examines paternal speech during face-to-face father–infant interactions at 3 months.

Currently depressed (n=19) and non-depressed (n=19) fathers were individually matched on age and education. Speech was coded for cognitive biases and mentalizing statements using a modified version of previous measures of maternal speech. Paternal depression was diagnosed using a structured psychiatric interview.

Depression in fathers was associated with more speech focused on the paternal experience and less on the infants' experience. Depressed fathers' speech comprised more negative and critical utterances, compared with non-depressed fathers.

Important differences emerge in the speech of fathers who experience depression. Examining negative cognitions in the speech of these fathers as early as 3 months may help in understanding children's risk in relation to paternal psychopathology.

Brain structure appears to alter after antipsychotic administration, but it is unknown whether these alterations are associated with improvement of psychopathology in patients with schizophrenia. In this study, the authors explore this relationship.

Altogether, 66 first-episode, drug-naive patients with schizophrenia and 23 well-matched healthy controls underwent brain magnetic resonance imaging scans at baseline. All 23 healthy controls and 42 of the patients were rescanned after 6 weeks follow-up. The patients received regular antipsychotic treatment during the 6-week period and their psychopathology was assessed using the Positive and Negative Syndrome Scale (PANSS) at baseline and 6 weeks. The difference in PANSS scores between baseline and 6 weeks was expressed as a ratio of the scores at baseline – ‘PANSS reduction ratio’. A modified tensor-based morphometry procedure was applied to analyse longitudinal images. Correlations between regional volume changes, PANSS reduction ratio and antipsychotic drug dosages were explored.

Compared with healthy controls, there was a significant increase in grey-matter volume of the right putamen in patients after 6 weeks treatment. This volume change was positively correlated with a positive PANSS reduction score but not related to drug dosages.

Putaminal volume increased after 6 weeks antipsychotic treatment in first-episode schizophrenia. The increased volume was closely correlated with improved psychopathology, suggesting the putamen might be a biomarker to predict the treatment response in schizophrenia.

The high incidence of the metabolic syndrome in patients with psychosis is mainly attributed to antipsychotic treatment. However, it is also possible that psychological stress plays a role, inducing a chronic inflammatory process that may predispose to the development of metabolic abnormalities. We investigated the association between childhood maltreatment and inflammatory and metabolic biomarkers in subjects with first-episode psychosis and healthy controls.

Body mass index (BMI), weight and waist circumference were measured in 95 first-episode psychosis patients and 97 healthy controls. Inflammatory and metabolic markers were measured in a subsample of 28 patients and 45 controls. In all the subjects we collected information on childhood maltreatment and recent stressors.

Patients with childhood maltreatment had higher BMI [25.0 (s.e.=0.6) kg/m2] and C-reactive protein (CRP) levels [1.1 (s.e.=0.6) mg/dl] when compared with healthy controls [23.4 (s.e.=0.4) kg/m2, p=0.030 and 0.2 (s.e.=0.1) mg/dl, p=0.009, respectively]. In contrast, patients without childhood maltreatment were not significantly different from healthy controls for either BMI [24.7 (s.e.=0.6) kg/m2, p=0.07] or CRP levels [0.5 (s.e.=0.2) mg/dl, p=0.25]. After controlling for the effect of BMI, the difference in CRP levels across the three groups remained significant (F2,58=3.6, p=0.035), suggesting that the increase in inflammation was not driven by an increase in adipose tissue.

Childhood maltreatment is associated with higher BMI, and increased CRP levels, in patients with a first-episode psychosis. Further studies need to confirm the mechanisms underlying the putative causal relationship between childhood maltreatment and higher BMI, and whether this is indeed mediated by increased inflammation.

Previous work suggests that exposure to childhood adversity is associated with the combination of delusions and hallucinations. In the present study, associations between (severity of) auditory vocal hallucinations (AVH) and (i) social adversity [traumatic experiences (TE) and stressful events (SE)] and (ii) delusional ideation were examined.

A baseline case-control sample of children with and without AVH were re-assessed on AVH after 5 years and interviewed about the experience of social adversity and delusions.

A total of 337 children (mean age 13.1 years, s.d.=0.5) were assessed: 40 children continued to hear voices that were present at baseline (24%, persistent group), 15 heard voices only at follow-up (9%, incident group), 130 children no longer reported AVH that were present at baseline (remitted group) and 152 never heard voices (referent group). Both TE and SE were associated with both incident and persistent AVH, as well as with greater AVH severity and delusional ideation at follow-up. In addition, the combination of AVH and delusions displayed a stronger association with TE and SE compared with either AVH or delusions alone.

Early childhood AVH are mostly benign and transitory. However, experience of social adversity is associated with persistence, severity and onset of new AVH closer to puberty, and with delusional ideation.

Negative memory bias is thought to be one of the main cognitive risk and maintenance factors for depression, but its neural substrates are largely unknown. Here, we studied whether memory bias is related to amygdala and hippocampal volume, two structures that are critical for emotional memory processes and that show consistent volume alterations in depression.

Structural magnetic resonance imaging (MRI) was carried out in 272 healthy participants (62% female, 18–50 years old). All images were acquired on 1.5 T Siemens MRI scanners. Automatic segmentation of amygdala and hippocampus was performed using the FIRST module of FSL. Negative memory bias was assessed by the self-referent encoding/evaluation test.

Negative memory bias was associated with larger amygdala (p=0.042) and smaller hippocampal (p=0.029) volumes. In additional analyses, we found that, compared with the associations found with hippocampus and amygdala volume separately, a stronger association was found between negative memory bias and the ratio of amygdala:hippocampus volume (p=0.021).

In non-depressed subjects we found that larger amygdala and smaller hippocampal volumes are associated with negative memory bias. This suggests that an increased amygdala:hippocampus volume ratio plays a role in cognitive vulnerability often seen in individuals with high risk for depression and that these structural brain differences may pre-date the onset of depression.

This study examines the structure of the Personality Belief Questionnaire (PBQ), a self-report instrument designed to assess dysfunctional beliefs associated with personality pathology, as proposed by the cognitive theory of personality dysfunction.

The PBQ was examined using exploratory factor analysis (EFA) with responses from 438 depressed out-patients, and confirmatory factor analysis (CFA) with responses from 683 treatment-seeking psychiatric out-patients. All participants were assessed for personality disorder (PD) using a standard clinical interview. The validity of the resulting factor structure was assessed in the combined sample (n=1121) by examining PBQ scores for patients with and without PD diagnoses.

Exploratory and confirmatory analyses converged to indicate that the PBQ is best described by seven empirically identified factors: six assess dysfunctional beliefs associated with forms of personality pathology recognized in DSM-IV. Validity analyses revealed that those diagnosed with a PD evidenced a higher average score on all factors, relative to those without these disorders. Subsets of patients diagnosed with specific DSM-IV PDs scored higher, on average, on the factor associated with their respective diagnosis, relative to all other factors.

The pattern of results has implications for the conceptualization of personality pathology. To our knowledge, no formal diagnostic or assessment system has yet systematically incorporated the role of dysfunctional beliefs into its description of personality pathology. The identification of dysfunctional beliefs may not only aid in case conceptualization but also may provide unique targets for psychological treatment. Recommendations for future personality pathology assessment systems are provided.