Excessive and persistent fear of clusters of holes, also known as trypophobia, has been suggested to reflect cortical hyperexcitability and may be associated with mental health risks. No study, however, has yet examined these associations in representative epidemiological samples.

To examine the prevalence of trypophobia in a population-representative youth sample, its association with mental health and functioning, and its interaction with external stress.

A total of 2065 young people were consecutively recruited from a household-based epidemiological youth mental health study in Hong Kong. Trypophobia, symptoms of anxiety, depression and stress, and exposure to personal stressors were assessed. Logistic regression was used to assess the relationships between trypophobia and mental health. Potential additive and interaction effects of trypophobia and high stress exposure on mental health were also tested.

The prevalence of trypophobia was 17.6%. Trypophobia was significantly associated with severe symptoms of anxiety (odds ratio (OR) = 1.83, 95% CI = 1.32–2.53), depression (OR = 1.78, 95% CI = 1.24–2.56) and stress (OR = 1.68, 95% CI = 1.11–2.53), even when accounting for sociodemographic factors, personal and family psychiatric history, resilience and stress exposure. Dose–response relationships were observed, and trypophobia significantly potentiated the effects of stress exposure on symptom outcomes, particularly for depressive symptoms. Those with trypophobia also showed significantly poorer functioning across domains and poorer health-related quality of life.

Screening for trypophobia in young people may facilitate early risk detection and intervention, particularly among those with recent stress exposure. Nevertheless, the generally small effect sizes suggest that other factors have more prominent roles in determining recent mental health outcomes in population-based samples; these should be explored in future work.

There is insufficient evidence to support the pharmacological treatment of borderline personality disorder. However, previous out-patient cohorts have described high rates of polypharmacy in this group. So far, there have been no national studies that have considered polypharmacy in borderline personality disorder.

To describe psychotropic polypharmacy in people with borderline personality disorder in New Zealand.

New Zealand's national databases have been used to link psychotropic medication dispensing data and diagnostic data for borderline personality disorder. Annual dispensing data for 2014 and 2019 have been compared.

Fifty percent of people with borderline personality disorder who were dispensed medications had three or more psychotropic medications in 2014. This increased to 55.9% in 2019 (P < 0.001). Those on seven or more psychotropics increased from 8.4 to 10.7% (P < 0.023). Quetiapine was the most dispensed psychotropic medication, being given to 53.8% of people dispensed medication with borderline personality disorder in 2019. Lorazepam dispensing showed the largest increase, going from 15.5 to 26.7% between 2014 and 2019 (P < 0.001).

There is a large burden of psychotropic polypharmacy in people with borderline personality disorder. This is concerning because of the lack of evidence regarding the efficacy of these medications in this group.

Hearing loss and tinnitus have been proposed as potential indicators of impaired mental health and brain morphological changes.

To assess the associations of hearing loss and tinnitus with the risk of depression and anxiety and with brain volume.

We conducted a community-based cohort study including 129 610 participants aged 40−69 years at recruitment to the UK Biobank with a follow-up period during 2006–2021 to estimate the risk of depression and anxiety after detection of hearing loss and reported tinnitus. We also assessed the associations of hearing loss and tinnitus with brain volume in a subsample with available brain magnetic resonance imaging data (N = 5222).

We observed an increased risk of depression among individuals with hearing loss (hazard ratio [HR] 1.14, 95% CI 1.03–1.26), tinnitus (HR 1.30, 95% CI 1.21–1.41) or both (HR 1.32, 95% CI 1.15–1.52), compared with individuals with neither hearing loss nor tinnitus. Similar results were noted for anxiety (HR 1.18, 95% CI 1.07–1.30 for hearing loss; HR 1.32, 95% CI 1.22–1.43 for tinnitus; and HR 1.48, 95% CI 1.30–1.68 for both). Hearing loss was associated with decreased overall brain volume as well as decreased volume of different brain regions. The latter associations disappeared after adjustment for whole intracranial volume. Tinnitus was associated with greater left accumbens and right occipital pole volume after adjustment for the whole intracranial volume.

Individuals with tinnitus are at increased risk of depression and anxiety. Hearing loss, on the other hand, is associated with both mood disorders and altered brain morphology.

People with schizophrenia die almost 20 years earlier than the general population, most commonly from avertable cardiometabolic disease. Existing pharmacological weight-loss agents including metformin have limited efficacy. Recently available glucagon-like peptide (GLP-1) receptor agonists such as semaglutide have shown promise for weight loss but have yet to be trialled in this population.

To examine the efficacy of semaglutide to ameliorate antipsychotic-induced obesity in people with schizophrenia who have been treated with clozapine for more than 18 weeks.

This is a 36-week, double-blinded, randomised placebo-controlled trial. We will recruit 80 clozapine-treated patients with schizophrenia or schizoaffective disorder, aged 18–64 years, with a baseline body mass index ≥26 kg/m2, who will be randomised to subcutaneous semaglutide of 2.0 mg once a week or placebo for 36 weeks. The primary endpoint will be percentage change in body weight from baseline.

This trial will assess the efficacy and side-effects of the GLP-1 receptor agonist semaglutide on body weight and provide evidence on the possible clinical utility of semaglutide in patients with inadequate response to metformin. The study is registered with the Australian New Zealand Clinical Trials Registry (www.anzctr.org.au) with clinical trial registration number ACTRN12621001539820.

This research could benefit individuals with schizophrenia who experience significant health issues, leading to premature mortality, owing to antipsychotic-induced weight gain. Study findings will be disseminated through peer-reviewed publications and conference presentations.

Compulsory Community Treatment Orders (CTOs) enable psychiatric medication without the need for consent. Careful scrutiny of outcomes including mortality is required to ensure compulsory treatment is evidence-based and ethical.

To report mortality for patients placed on CTOs and analyse data according to CTO status, mortality cause and diagnosis.

Data for all patients placed under CTOs between 1 January 2009 and 31 December 2018 was provided by the Ministry of Health, New Zealand. Data included diagnostic and demographic information, dates of CTOs, and any dates and causes of death. Deaths were categorised into suicides, accidents and assaults, and medical causes. Mortality data are reported according to CTO status and diagnosis.

A total of 14 726 patients were placed on CTOs over the study period, during which there were 1328 deaths. The mortality rate was 2.97 on and 2.31 off CTOs (rate ratio 1.29, 95% CI 1.14–1.45; P < 0.01). The mortality rate for accidents and assaults was 0.44 on and 0.25 off CTOs (rate ratio 1.73, 95% CI 1.23–2.42; P < 0.01). The mortality rate for medical causes was 2.33 on and 1.90 off CTOs (rate ratio 1.22, 95% CI 1.07–1.40; P < 0.01). The suicide rate was 0.20 on and 0.15 off of CTOs (rate ratio 1.33, 95% CI 0.81–2.12; P = 0.22).

Increased care and medication provided during compulsory treatment does not the modify the course of illness sufficiently to reduce mortality during CTOs. Higher mortality rates during CTO periods compared with non-CTO periods may reflect greater unwellness during CTOs.

Early-life adverse experiences can elevate the magnitude of the risk of developmental psychopathology, but the potential synergistic effects of multiple factors have not been well studied.

To determine whether prenatal exposures to maternal stress (Superstorm Sandy) and maternal cannabis use synergistically alter the risk of developmental psychopathology.

The study included 163 children (53.4% girls), longitudinally tracked (ages 2–5 years) in relation to the effects of two early-life adverse exposures (Superstorm Sandy and maternal cannabis use). Offspring were grouped by exposure status (neither, only maternal cannabis use, only Superstorm Sandy or both). DSM-IV disorders for offspring were derived from structured clinical interviews; caregiver-reported ratings of family stress and social support were also assessed.

A total of 40.5% had been exposed to Superstorm Sandy and 24.5% to maternal cannabis use. Offspring exposed to both (n = 13, 8.0%), relative to those exposed to neither, had a 31-fold increased risk of disruptive behavioural disorders (DBDs) and a seven-fold increased risk of anxiety disorders. The synergy index demonstrated that offspring with two exposures had synergistic elevation in risk of DBDs (synergy index, 2.06, P = 0.03) and anxiety disorders (synergy index, 2.60, P = 0.004), compared with the sum of single risks. Offspring with two exposures had the highest parenting stress and lowest social support.

Our findings are consistent with the double-hit model suggesting that offspring with multiple early-life adverse exposures (Superstorm Sandy and maternal cannabis use) have synergistically increased risks of mental health problems. Given the increasing frequency of major natural disasters and cannabis use, especially among women under stress, these findings have significant public health implications.

Many mental disorders, including depression, bipolar disorder and schizophrenia, are associated with poor dietary quality and nutrient intake. There is, however, a deficit of research looking at the relationship between obsessive–compulsive disorder (OCD) severity, nutrient intake and dietary quality.

This study aims to explore the relationship between OCD severity, nutrient intake and dietary quality.

A post hoc regression analysis was conducted with data combined from two separate clinical trials that included 85 adults with diagnosed OCD, using the Structured Clinical Interview for DSM-5. Nutrient intakes were calculated from the Dietary Questionnaire for Epidemiological Studies version 3.2, and dietary quality was scored with the Healthy Eating Index for Australian Adults – 2013.

Nutrient intake in the sample largely aligned with Australian dietary guidelines. Linear regression models adjusted for gender, age and total energy intake showed no significant associations between OCD severity, nutrient intake and dietary quality (all P > 0.05). However, OCD severity was inversely associated with caffeine (β = −15.50, 95% CI −28.88 to −2.11, P = 0.024) and magnesium (β = −6.63, 95% CI −12.72 to −0.53, P = 0.034) intake after adjusting for OCD treatment resistance.

This study showed OCD severity had little effect on nutrient intake and dietary quality. Dietary quality scores were higher than prior studies with healthy samples, but limitations must be noted regarding comparability. Future studies employing larger sample sizes, control groups and more accurate dietary intake measures will further elucidate the relationship between nutrient intake and dietary quality in patients with OCD.

Psychotic symptoms and elevated fasting blood glucose (FBG) are frequently observed in people with major depressive disorder (MDD), but there is a lack of research into this relationship within this cohort.

This study aimed to preliminarily explore the prevalence of psychotic symptoms and their predictors among patients with MDD and elevated FBG.

This study enrolled 1718 patients with first-episode and drug-naïve (FEDN) MDD. Sociodemographic data and physical and biochemical indicators were collected. Clinical symptoms were assessed with tools such as the Hamilton Rating Scale for Anxiety, Hamilton Rating Scale for Depression (HRSD) and Positive and Negative Syndrome Scale positive subscale.

The odds ratio for psychotic symptoms in those with MDD and elevated FBG (18.7%) was 2.33 times higher than those with MDD without elevated FBG. Presence of psychotic symptoms was significantly correlated with HRSD score, suicide attempts, and total cholesterol and thyroid-stimulating hormone levels. The combination of HRSD score, suicide attempts and thyroid-stimulating hormone levels among patients with MDD and elevated FBG effectively distinguished between individuals with and without psychotic symptoms, achieving an area under the curve of 0.87.

Psychotic symptoms are frequently observed among FEDN MDD patients with elevated FBG, and depressive symptoms, suicide attempts and thyroid-stimulating hormone levels are related to psychotic symptoms in this cohort.

K.R.K. is Editor-in-Chief of BJPsych Open; he took no part in the peer-review of this work.

Poverty in adolescence is associated with later drug use. Few studies have evaluated the role of adolescent psychiatric disorders in this association.

This study aimed to investigate mediation and interaction simultaneously, enabling the disentanglement of the role of adolescent psychiatric disorders in the association between poverty in adolescent and later drug use disorders.

A national cohort study of 634 223 individuals born in 1985–1990, residing in Sweden between the ages of 13 and 18 years, was followed from age 19 years until the first in-patient or out-patient care visit with a diagnosis of drug use disorder. A four-way decomposition method was used to determine the total effect of the association with poverty and possible mediation by and/or interaction with diagnosis of adolescent psychiatric disorders.

The hazard ratios for drug use disorders among those experiencing poverty compared with those ‘never in poverty’ were 1.40 (95% CI, 1.32–1.63) in females and 1.43 (95% CI, 1.37–1.49) in males, after adjusting for domicile, origin and parental psychiatric disorders. Twenty-four per cent of this association in females, and 13% in males, was explained by interaction with and/or mediation by adolescent psychiatric disorders.

Part of the association between poverty in adolescence and later drug use disorders was due to mediation by and/or interaction with psychiatric disorders. Narrowing socioeconomic inequalities in adolescence might help to reduce the risks of later drug use disorders. Interventions aimed at adolescents with psychiatric disorders might be especially important.

The prevalence of non-suicidal self-injury (NSSI) among adolescents underscores the importance of understanding the complex factors that drive this behaviour. Framed within broader constructs of emotional regulation theories, alexithymia and peer victimisation are thought to interact to influence NSSI behaviours.

This research addresses whether alexithymia and peer victimisation serve as risk factors for NSSI and, if so, how these factors interact with each other.

This quantitative study analysed data from 605 adolescents, using a range of validated self-report measures including the Toronto Alexithymia Scale. Statistical analyses including one-way analysis of variance, multiple regression and structural equation modelling were employed to scrutinise the relationships among the variables.

Alexithymia and peer victimisation significantly predicted NSSI behaviours. Specifically, the ‘difficulty in identifying feelings’ subscale of alexithymia emerged as a noteworthy predictor of NSSI (P < 0.001). Peer victimisation mediated the relationship between alexithymia and NSSI, explaining approximately 24.50% of alexithymia's total effect on NSSI. In addition, age was a significant predictor of NSSI, but gender and education years were not (P > 0.05). These relationships were found to be invariant across genders.

This study enriches our understanding of the interplay between alexithymia, peer victimisation and NSSI, particularly within the Chinese context. Its findings have significant implications for a rethinking of alexithymia's theoretical construct and interventions targeting emotional literacy and peer dynamics among adolescents. Future research could benefit from a longitudinal design to establish causality.

Current assessment and management models often do not adequately address the many aspects of managing complex brain disorders involving disordered affect, behaviour and cognition (ABC). A more collaborative model of care, where several specialties can jointly assess and manage patients with complex brain disorders, is gaining attention.

In this case report, we present two cases that highlight the benefits of the ‘brain medicine’ clinical model.

The Brain Medicine Clinic employs an integrated clinical model in which psychiatrists and neurologists provide integrated interdisciplinary assessments of patients with complex brain disorders, leading to comprehensive assessment. We describe the clinical model and the trajectories of two patients with complex brain disorders seen in this clinic. In these case descriptions, we explain how the brain medicine clinical approach leads to an improved patient experience.

The Brain Medicine Clinic assessments resulted in a neurobiopsychosocial formulation of symptoms and, consequently, holistic individualised treatment plans for two patients with complex brain disorders. This approach to patients’ conditions emerges from the understanding that there are multifactorial causes of brain disorders at the social, cultural, psychological and biological level.

Integrated interdisciplinary assessments allow for tailored treatment plans for individuals experiencing complex brain disorders, while creating efficiencies for the patient and the healthcare system.

Prenatal selective serotonin reuptake inhibitor (SSRI) antidepressant exposure is associated with increased internalising and anxious behaviours in young children; whether this continues into early adolescence is unknown. Also, it is not well established whether it is the in utero exposure to SSRIs or the underlying maternal mood that contributes more to these associations.

To examine associations between maternal depressive symptoms, prenatal SSRI antidepressant treatment and internalising and anxiety behaviours from childhood into pre-adolescence.

From a prospective longitudinal cohort, measures of maternal depressive symptoms and SSRI use and child outcomes (n = 191 births) were obtained from the second trimester to 12 years. Maternal reports of internalising and anxiety behaviours in children were obtained at 3, 6 and 12 years.

Multilevel mixed-effects models revealed that maternal depressed mood at the third trimester assessment, not prenatal SSRI exposure, was associated with longitudinal patterns of higher levels of internalising and anxiety behaviours across childhood from 3 to 12 years of age. At each age, hierarchical regressions showed that maternal mood at the third trimester, compared with current maternal depression or prenatal SSRI exposure, explained a greater proportion of the variance in internalising and anxiety behaviours.

Even with prenatal SSRI treatment, maternal depressed mood during the third trimester still had an enduring effect as it was associated with increased levels of internalising and anxiety behaviours across childhood and into early adolescence. Importantly, we found no evidence of a ‘main effect’ association between prenatal SSRI exposure and internalising and anxiety behaviours in children.