Blunted facial affect is a common negative symptom of schizophrenia. Additionally, assessing the trustworthiness of faces is a social cognitive ability that is impaired in schizophrenia. Currently available pharmacological agents are ineffective at improving either of these symptoms, despite their clinical significance. The hypothalamic neuropeptide oxytocin has multiple prosocial effects when administered intranasally to healthy individuals and shows promise in decreasing negative symptoms and enhancing social cognition in schizophrenia. Although two small studies have investigated oxytocin's effects on ratings of facial trustworthiness in schizophrenia, its effects on facial expressivity have not been investigated in any population.

We investigated the effects of oxytocin on facial emotional expressivity while participants performed a facial trustworthiness rating task in 33 individuals with schizophrenia and 35 age-matched healthy controls using a double-blind, placebo-controlled, cross-over design. Participants rated the trustworthiness of presented faces interspersed with emotionally evocative photographs while being video-recorded. Participants’ facial expressivity in these videos was quantified by blind raters using a well-validated manualized approach (i.e. the Facial Expression Coding System; FACES).

While oxytocin administration did not affect ratings of facial trustworthiness, it significantly increased facial expressivity in individuals with schizophrenia (Z = −2.33, p = 0.02) and at trend level in healthy controls (Z = −1.87, p = 0.06).

These results demonstrate that oxytocin administration can increase facial expressivity in response to emotional stimuli and suggest that oxytocin may have the potential to serve as a treatment for blunted facial affect in schizophrenia.

Somatoform disorders are costly for society in terms of increased healthcare expenditure. Patients' illness perceptions have been found to play a role in somatoform disorders. However, it is unclear whether illness perceptions predict higher health costs in these patients.

A total of 1785 primary care patients presenting a new health complaint completed a questionnaire on their illness perceptions and emotional distress before the consultation. The physicians completed a questionnaire for each patient on diagnostics after the consultation. In a stratified subsample, physician interviewers established diagnoses of DSM-IV somatization and undifferentiated somatoform disorders (n = 144) using the Schedules for Clinical Assessment in Neuropsychiatry. Healthcare expenditure was obtained from Danish health registers for a 2-year follow-up period.

Patients had more negative perceptions of their well-defined physical health problems when they had a co-morbid somatoform disorder. A strong illness identity [β = 0.120, 95% confidence interval (CI) 0.029–0.212, p = 0.012], perceived negative consequences (β = 0.010, 95% CI 0.001–0.019, p = 0.024), a long timeline perspective (β = 0.013, 95% CI 0.005–0.021, p = 0.001), low personal control (β = − 0.009, 95% CI –0.015 to −0.002, p = 0.011) and negative emotional representations (β = 0.009, 95% CI 0.002–0.017, p = 0.020) predicted healthcare expenditure in somatoform disorders.

The results suggest that illness perceptions play a role in the perpetuation of symptoms in somatoform disorders and predict higher future healthcare expenditure among a subgroup of these patients.

Risk for drug abuse (DA) is strongly associated with neighborhood social deprivation (SD). However, the causal nature of this relationship is unclear.

Three Swedish population-based cohorts were followed up over 5 years for incident registration of DA in medical, legal or pharmacy records. In each cohort, we examined the SD–DA association, controlling carefully for individual socio-economic status (SES) with multiple measures, in the entire sample and among pairs of first cousins, paternal and maternal half-siblings, full siblings and monozygotic (MZ) twins discordant for SD exposure. The number of informative relative pairs ranged from 6366 to 166 208.

In all cohorts, SD was prospectively related to risk for incident DA. In relative pairs discordant for SD exposure, the SD–DA association was similar to that seen in the entire population in cousins, half-siblings, full siblings and MZ twins. Eliminating subjects who were residentially unstable or had DA in the first two follow-up years did not alter this pattern. When divided by age, in the youngest groups, the SD–DA association was weaker in siblings than in the entire population.

Across three cohorts, controlling for individual SES and confounding familial factors, SD prospectively predicted risk for incident DA registration. These results support the hypothesis that the SD–DA association is in part causal and unlikely to result entirely from personal attributes, which both increase risk for DA and cause selection into high SD environments. At least part of the SD–DA association arises because exposure to SD causes an increased risk of DA.

The risk for depression markedly rises during the 5–6 years leading up to the cessation of menstruation, known as the menopause transition. Exposure to extreme estradiol levels may help explain this increase but few studies have examined individual sensitivity to estradiol in predicting perimenopausal depression.

The current study recruited 101 perimenopausal women. During Phase 1, we quantified each woman's sensitivity to changes in estradiol using 12 weekly measures of estrone-3-glucuronide (E1G), a urinary metabolite of estradiol, and concurrent depressive symptoms. The weekly cortisol awakening response was measured to examine the hypothalamic-pituitary-adrenal (HPA) axis in mediating mood sensitivity to estradiol. In Phase 2, depressive symptoms and major depression diagnoses were assessed monthly for 9 months. The relationship between Phase 1 E1G sensitivity and Phase 2 depressive symptoms and major depressive episodes was examined. Several baseline characteristics were examined as potential moderators of this relationship.

The within-person correlation between weekly E1G and mood varied greatly from woman to woman, both in strength and direction. Phase 1 E1G mood sensitivity predicted the occurrence of clinically significant depressive symptoms in Phase 2 among certain subsets of women: those without a prior history of depression, reporting a low number of baseline stressful life events, and reporting fewer months since their last menstrual period. HPA axis sensitivity to estradiol fluctuation did not predict Phase 2 outcomes.

Mood sensitivity to estradiol predicts risk for perimenopausal depression, particularly among women who are otherwise at low risk and among those who are early in the transition.

It is unknown whether patient disengagement from early intervention services for psychosis is as prevalent in low- and middle-income countries (LMICs) like India, as it is in high-income countries (HICs). Addressing this gap, we studied two first-episode psychosis programs in Montreal, Canada and Chennai, India. We hypothesized lower service disengagement among patients and higher engagement among families in Chennai, and that family engagement would mediate cross-site differences in patient disengagement.

Sites were compared on their 2-year patient disengagement and family engagement rates conducting time-to-event analyses and independent samples t tests on monthly contact data. Along with site and family involvement, Cox proportional hazards regression included known predictors of patient disengagement (e.g. gender).

The study included data about 333 patients (165 in Montreal, 168 in Chennai) and their family members (156 in Montreal, 168 in Chennai). More Montreal patients (19%) disengaged before 24 months than Chennai patients (1%), χ2(1, N = 333) = 28.87, p < 0.001. Chennai families had more contact with clinicians throughout treatment (Cohen's d = −1.28). Family contact significantly predicted patient disengagement in Montreal (HR = 0.87, 95% CI 0.81–0.93). Unlike in Chennai, family contact declined over time in Montreal, with clinicians perceiving such contact as not necessary (Cohen's d = 1.73).

This is the first investigation of early psychosis service engagement across a HIC and an LMIC. Patient and family engagement was strikingly higher in Chennai. Maintaining family contact may benefit patient engagement, irrespective of context. Findings also suggest that differential service utilization may underpin cross-cultural variations in psychosis outcomes.

Maternal smoking during pregnancy (SDP) has been studied extensively as a risk factor for adverse offspring outcomes and is known to co-occur with other familial risk factors. Accounting for general familial risk factors has attenuated associations between SDP and adverse offspring outcomes, and identifying these confounds will be crucial to elucidating the relationship between SDP and its psychological correlates.

The current study aimed to disentangle the relationship between maternal SDP and co-occurring risk factors (maternal criminal activity, drug problems, teen pregnancy, educational attainment, and cohabitation at childbirth) using a population-based sample of full- (n=206 313) and half-sister pairs (n=19 363) from Sweden. Logistic regression models estimated the strength of association between SDP and co-occurring risk factors. Bivariate behavioral genetic models estimated the degree to which associations between SDP and co-occurring risk factors are attributable to genetic and environmental factors.

Maternal SDP was associated with an increase in all co-occurring risk factors. Of the variance associated with SDP, 45% was attributed to genetic factors and 53% was attributed to unshared environmental factors. In bivariate models, genetic factors accounted for 21% (non-drug-, non-violence-related crimes) to 35% (drug-related crimes) of the covariance between SDP and co-occurring risk factors. Unshared environmental factors accounted for the remaining covariance.

The genetic factors that influence a woman's criminal behavior, substance abuse and her offspring's rearing environment all influence SDP. Therefore, the intergenerational transmission of genes conferring risk for antisocial behavior and substance misuse may influence the associations between maternal SDP and adverse offspring outcomes.

Childhood sexual abuse (CSA) has been shown to be a risk factor for personality disorder (PD). However, no previous studies have examined whether associations exist between sexual abuse and abnormal personality as measured both categorically and dimensionally. Such enquiry would more fully illuminate the impact of CSA on adult personality.

Using a large nationally representative sample, we set out to examine associations between CSA and categorically defined PD. We also examined associations between CSA and the five dimensions of personality (openness to experience, conscientiousness, extraversion, agreeableness and neuroticism). A total of 1520 young adults were interviewed to determine the prevalence of sexual abuse occurring before age 16 years. A dimensional measure of personality was completed by 1469 participants, and 1145 had an informant-based PD assessment.

PD was independently associated with repeated CSA [fully adjusted odds ratio (OR) 1.9, 95% confidence interval (CI) 1.1–3.4]. Repeated sexual abuse was also associated with higher neuroticism and lower agreeableness (p values for both <0.001). Adjusting for the effects of potential confounders and mediators, including earlier symptoms of anxiety and depression, had little impact on the strength of associations.

We conclude that repeated CSA is independently associated with categorically defined PD, and also with higher neuroticism and lower agreeableness. Our findings suggest that if a dimensional classification of PDs is adopted in future classification systems, there might be meaningful continuity with previous aetiological research conducted using the current categorical system.

To effectively shape mental healthcare policy in modern-day China, up-to-date epidemiological data on mental disorders is needed. The objective was to estimate the prevalence, age-of-onset (AOO) and sociodemographic correlates of mental disorders in a representative household sample of the general population (age ⩾ 18) in the Tianjin Municipality in China.

Data came from the Tianjin Mental health Survey (TJMHS), which was conducted between July 2011 and March 2012 using a two-phase design. 11 748 individuals were screened with an expanded version of the General Health Questionnaire and 4438 subjects were selected for a diagnostic interview by a psychiatrist, using the Structured Clinical Interview for the Diagnostic and Statistical Manual – fourth edition (SCID).

The lifetime and 1-month prevalence of any mental disorder were 23.6% and 12.8%, respectively. Mood disorders (lifetime: 9.3%; 1-month: 3.9%), anxiety disorders (lifetime: 4.5% 1-month: 3.1%) and substance-use disorders (lifetime: 8.8%; 1-month: 3.5%) were most prevalent. The median AOO ranged from 25 years [interquartile range (IQR): 23–32] for substance-use disorders to 36 years (IQR: 24–50) for mood disorders. Not being married, non-immigrant status (i.e. local ‘Hukou’), being a farmer, having <6 years of education and male gender were associated with a higher lifetime prevalence of any mental disorder.

Results from the current survey indicate that mental disorders are steadily reported more commonly in rapidly-developing urban China. Several interesting sociodemographic correlates were observed (e.g. male gender and non-immigrant status) that warrant further investigation and could be used to profile persons in need of preventive intervention.

Referral for brief intervention among people who misuse alcohol is reported to be effective but its impact among those who present to services following deliberate self-harm (DSH) has not been examined.

Consecutive patients who presented to an Emergency Department (ED) following an episode of DSH were screened for alcohol misuse. Those found to be misusing alcohol were randomly assigned to brief intervention plus a health information leaflet or to a health information leaflet alone. The primary outcome was whether the patient reattended an ED following a further episode of DSH during the subsequent 6 months. Secondary outcomes were alcohol consumption, mental health and satisfaction with care measured 3 and 6 months after randomization.

One hundred and three people took part in the study. Follow-up data on our primary outcome were obtained for all subjects and on 63% for secondary outcomes. Half those referred for brief intervention received it. Repetition of DSH was strongly associated with baseline alcohol consumption, but not influenced by treatment allocation. There was a non-significant trend towards the number of units of alcohol consumed per drinking day being lower among those randomized to brief intervention.

Referral for brief intervention for alcohol misuse following an episode of DSH may not influence the likelihood of repetition of self-harm. Longer-term interventions may be needed to help people who deliberately harm themselves and have evidence of concurrent alcohol misuse.

It has been proposed that non-steroidal anti-inflammatory drugs (NSAIDs) may interfere with the efficacy of antidepressants and contribute to treatment resistance in major depressive disorder (MDD). This effect requires replication and a test of whether it is specific to serotonin-reuptake inhibiting (SRI) antidepressants.

We tested the effect of concomitant medication with NSAIDs on the efficacy of escitalopram, a SRI antidepressant, and nortriptyline, a tricyclic antidepressant, among 811 subjects with MDD treated for up to 12 weeks in the GENDEP study. Effects of NSAIDs on improvement of depressive symptoms were tested in mixed-effect linear models. Effects on remission were tested in logistic regression. Age, sex, baseline severity and centre of recruitment were considered as potential confounding factors.

Ten percent (n=78) of subjects were taking NSAIDs during the antidepressant treatment. Older subjects were significantly more likely to take NSAIDs. After controlling for age, sex, centre of recruitment and baseline severity, concomitant medication with NSAIDs did not significantly influence the efficacy of escitalopram [β=0.035, 95% confidence interval (CI) −0.145 to 0.215, p=0.704] or nortriptyline (β=0.075, 95% CI −0.131 to 0.281, p=0.476). Although slightly fewer subjects who took NSAIDs reached remission [odds ratio (OR) 0.80, 95% CI 0.49–1.31, p=0.383], this non-significant effect was reversed after controlling for age, sex, baseline severity and recruitment centre effects (OR 1.04, 95% CI 0.61–1.77, p=0.882).

NSAIDs are unlikely to affect the efficacy of SRI or other antidepressants. Concurrent use of NSAIDs and antidepressants does not need to be avoided.

Twin studies have suggested that additive genetic factors significantly contribute to liability to bulimia nervosa (BN). However, the diagnostic criteria for BN remain controversial. In this study, an item-factor model was used to examine the BN diagnostic criteria and the genetic and environmental contributions to BN in a population-based twin sample. The validity of the equal environment assumption (EEA) for BN was also tested.

Participants were 1024 female twins (MZ n=614, DZ n=410) from the population-based Mid-Atlantic Twin Registry. BN was assessed using symptom-level (self-report) items consistent with DSM-IV and ICD-10 diagnostic criteria. Items assessing BN were included in an item-factor model. The EEA was measured by items assessing similarity of childhood and adolescent environment, which have demonstrated construct validity. Scores on the EEA factor were used to specify the degree to which twins shared environmental experiences in this model.

The EEA was not violated for BN. Modeling results indicated that the majority of the variance in BN was due to additive genetic factors. There was substantial variability in additive genetic and environmental contributions to specific BN symptoms. Most notably, vomiting was very strongly influenced by additive genetic factors, while other symptoms were much less heritable, including the influence of weight on self-evaluation. These results highlight the importance of assessing eating disorders at the symptom level.

Refinement of eating disorder phenotypes could ultimately lead to improvements in treatment and targeted prevention, by clarifying sources of variation for specific components of symptomatology.