Australian & New Zealand Journal of Psychiatry

Elevated prevalence of non-affective psychotic disorders is often found in densely populated areas. This functional magnetic resonance imaging study investigates if reduced trust, a component of impaired social functioning in patients with psychotic disorder, is associated with urban upbringing.

In total, 39 patients (22 first episode and 17 clinical high risk) and 30 healthy controls, aged 16–29, performed two multi-round trust games, with a cooperative and unfair partner during functional magnetic resonance imaging scanning. Baseline trust was operationalized as the first investment made, and changes of trust as changes in investments made over the 20 trials during the games. Urban exposure during upbringing (0–15 years) was defined as higher urban (≥2500 inhabitants/km²) or lower urban (<2500 inhabitants/km²).

Patients displayed lower baseline trust (first investment) than controls, regardless of urbanicity exposure. During cooperative interactions, lower-urban patients showed increasing investments. In addition, during cooperative interactions, group-by-developmental urbanicity interactions were found in the right and left amygdalae, although for the latter only at trend level. Higher urbanicity was associated with decreased activation of the left amygdala in patients and controls during investments and with increased activation of the right and left amygdalae in patients only, during repayments. During unfair interactions, no associations of urbanicity with behavior or brain activation were found.

Urban upbringing was unrelated to baseline trust. Associations with urbanicity were stronger for patients compared to controls, suggesting greater susceptibility to urbanicity effects during the developmental period. Higher-urban patients failed to compensate for the initial distrust specifically during repeated cooperative interactions. This finding highlights potential implications for social functioning. Urban upbringing was linked to differential amygdala activation, suggesting altered mechanisms of feedback learning, but this was not associated with trust game behavior.

Subsyndromal depression is prevalent and associated with poor outcomes in late life, but its epidemiological characteristics have barely been investigated. The aim of this prospective cohort study is to compare the prevalence, incidence and risk factors of subsyndromal depression with those of syndromal depression including major and minor depressive disorders in community-dwelling elderly individuals.

In a nationwide community-based study of randomly sampled Korean elderly population aged 60 years or older (N = 6640), depression was assessed with standardized diagnostic interviews. At baseline and at 2-year and 4-year follow-ups, the authors diagnosed subsyndromal depression by the operational criteria and syndromal depression by the Diagnostic and Statistical Manual of Mental Disorders (4th ed.) diagnostic criteria. Multivariate logistic regression analyses were conducted to identify the risk factors for incident depression.

The age- and gender-adjusted prevalence rate of subsyndromal depression was 9.24% (95% confidence interval = [8.54, 9.93]), which was 2.4-fold higher than that of syndromal depression. The incidence rate of subsyndromal depression was 21.70 per 1000 person-years (95% confidence interval = [19.29, 24.12]), which was fivefold higher than that of syndromal depression. The prevalence to incidence ratio of subsyndromal depression was about half that of syndromal depression. The risk for subsyndromal depression was associated with female gender, low socioeconomic status, poor social support and poor sleep quality, while that of syndromal depression was associated with old age and less exercise.

Subsyndromal depression should be validated as a clinical diagnostic entity, at least in late life, since it has epidemiological characteristics different from those of syndromal depression.

We aimed to explore the relationships between diet quality, dietary inflammatory potential or body mass index and outcomes of a clinical trial of nutraceutical treatment for bipolar depression.

This is a sub-study of a randomised controlled trial of participants with bipolar depression who provided dietary intake data (n = 133). Participants received 16 weeks adjunctive treatment of either placebo or N-acetylcysteine-alone or a combination of mitochondrial-enhancing nutraceuticals including N-acetylcysteine (combination treatment). Participants were followed up 4 weeks post-treatment discontinuation (Week 20). Diet was assessed by the Cancer Council Victoria Dietary Questionnaire for Epidemiological Studies, Version 2, converted into an Australian Recommended Food Score to measure diet quality, and energy-adjusted dietary inflammatory index score to measure inflammatory potential of diet. Body mass index was also measured. Generalised estimating equation models were used to assess whether diet quality, energy-adjusted dietary inflammatory index score and/or body mass index were predictors of response to significant outcomes of the primary trial: depression symptoms, clinician-rated improvement and functioning measures.

In participants taking combination treatment compared to placebo, change in depression scores was not predicted by Australian Recommended Food Score, dietary inflammatory index or body mass index scores. However, participants with better diet quality (Australian Recommended Food Score) reported reduced general depression and bipolar depression symptoms (p = 0.01 and p = 0.03, respectively) and greater clinician-rated improvement (p = 0.02) irrespective of treatment and time. Participants who had a more anti-inflammatory dietary inflammatory index had less impairment in functioning (p = 0.01). Combination treatment may attenuate the adverse effects of pro-inflammatory diet (p = 0.03) on functioning. Participants with lower body mass index who received combination treatment (p = 0.02) or N-acetylcysteine (p = 0.02) showed greater clinician-rated improvement.

These data support a possible association between diet (quality and inflammatory potential), body mass index and response to treatment for bipolar depression in the context of a nutraceutical trial. The results should be interpreted cautiously because of limitations, including numerous null findings, modest sample size and being secondary analyses.

Clinical staging is a paradigm in which stages of disease progression are identified; these, in turn, have prognostic value. A staging model that enables the prediction of long-term course in anxiety disorders is currently unavailable but much needed as course trajectories are highly heterogenic. This study therefore tailored a heuristic staging model to anxiety disorders and assessed its validity.

A clinical staging model was tailored to anxiety disorders, distinguishing nine stages of disease progression varying from subclinical stages (0, 1A, 1B) to clinical stages (2A–4B). At-risk subjects and subjects with anxiety disorders (n = 2352) from the longitudinal Netherlands Study of Depression and Anxiety were assigned to these nine stages. The model’s validity was assessed by comparing baseline (construct validity) and 2-year, 4-year and 6-year follow-up (predictive validity) differences in anxiety severity measures across stages. Differences in depression severity and disability were assessed as secondary outcome measures.

Results showed that the anxiety disorder staging model has construct and predictive validity. At baseline, differences in anxiety severity, social avoidance behaviors, agoraphobic avoidance behaviors, worrying, depressive symptoms and levels of disability existed across all stages (all p-values < 0.001). Over time, these differences between stages remained present until the 6-year follow-up. Differences across stages followed a linear trend in all analyses: higher stages were characterized by the worst outcomes. Regarding the stages, subjects with psychiatric comorbidity (stages 2B, 3B, 4B) showed a deteriorated course compared with those without comorbidity (stages 2A, 3A, 4A).

A clinical staging tool would be useful in clinical practice to predict disease course in anxiety disorders.

Given the fundamental emotional, social and physical development that occurs during the early years of life, childhood experiences are formative in shaping a person’s life trajectory. Childhood trauma is a prevalent, multifaceted issue with well-documented long-term adverse health effects in clinical populations however; the impact of childhood trauma in the community is less clear. To address this, this study investigated how childhood trauma may impact physical and psychological health, sleep quality and autonomic function in a non-clinical community sample of adults.

Participants completed questionnaires, an in-laboratory autonomic assessment (including stress reactivity to mental and physical stressors) and overnight autonomic and sleep monitoring. Overall childhood trauma and its subtypes (e.g. physical abuse, emotional neglect) were defined using the Childhood Trauma Questionnaire.

We identified 22 childhood trauma cases (total score > 36) and, of the 89 non-childhood trauma cases, some individuals also experienced significant levels of trauma in one or more of the childhood trauma subtypes. Childhood trauma and some trauma subtypes were significantly correlated with a myriad of negative physiological and physical health outcomes including elevated psychological distress, increased sleep disturbances, reduced emotional wellbeing and lower perceived social support. Autonomic dysregulation was found in those with high levels of childhood trauma, which was reflected in an increased stress response to laboratory tasks. Notably, the experience of physical abuse in childhood was significantly associated with alterations in nocturnal heart rate and heart rate variability.

Together, these results highlight that childhood trauma can have lasting detrimental consequences on an individual’s emotional and physical health, sleep quality and stress reactivity.

To compare the characteristics of clinic attenders in inner city homeless hostels with and without a diagnosed psychotic illness.

A cross-sectional study of homeless people attending psychiatric clinics in three inner city homeless hostels over a period of 8 years. The demographic characteristics, comorbid conditions, pathway to homelessness and pattern of homelessness of clinic attenders with a diagnosis of psychosis were compared with those who were not known to have psychotic illness.

2389 homeless people attended one or more of the clinics in the 8 years of the study, of whom 1222 (51.2%) had a diagnosed psychotic illness, mostly schizophrenia. Those with psychosis were less likely to have been married (23.2% vs 45.5%), were less likely to have worked for more than a year (47.4% vs 74%) and were more likely to have been discharged from hospital to homelessness, to receive the Disability Support Pension (72.2% vs 38.3%), or be under financial management orders (12.0% vs 2.6%). Homeless people with psychosis were also more likely to have been homeless for more than a year, sleep in the open, and were less likely to have a current substance use disorder, problem gambling or a history of early life or recent trauma. A high proportion of those with psychosis (29.5%) had been released from prison to homelessness and a surprising number (22%) reported the loss of public housing tenancy.

The results demonstrate the homeless with psychotic illness are particularly disabled and disadvantaged, often have multiple comorbid conditions, and many have been unable to maintain public housing tenancy. The inability of many of the homeless mentally ill to maintain public housing tenancy suggests the need for more supported housing to help the chronically homeless with psychotic illness maintain tenancy.