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Background No single environmental factor is a necessary or sufficient cause of mental disorder; multifactorial and transdiagnostic approaches are needed to understand the impact of the environment on the development of mental disorders across the life course. Method Using linked multi-agency administrative data for 71 932 children from the New South Wales Child Developmental Study, using logistic regression, we examined associations between 16 environmental risk factors in early life (prenatal period to Results The ERS was associated with all types of mental disorder diagnoses in a dose–response fashion, such that 2.8% of children with no exposure to any of the environmental factors (ERS = 0), compared to 18.3% of children with an ERS of 8 or more indicating exposure to 8 or more environmental factors (ERS ⩾ 8), had been diagnosed with any type of mental disorder up to age 13–14 years. Thirteen of the 16 environmental factors measured (including prenatal factors, neighbourhood characteristics and more proximal experiences of trauma or neglect) were positively associated with at least one category of mental disorder. Conclusion Exposure to cumulative environmental risk factors in early life is associated with an increased likelihood of presenting to health services in childhood for any kind of mental disorder. In many instances, these factors are preventable or capable of mitigation by appropriate public policy settings.

BackgroundParental criminal offending is an established risk factor for offending among offspring, but little evidence is available indicating the impact of offending on early childhood functioning. We used data from a large Australian population cohort to determine associations between exposure to parental offending and a range of developmental outcomes at age 5 years.MethodMulti-generation data in 66 477 children and their parents from the New South Wales Child Development Study were combined using data linkage. Logistic and multinomial regressions tested associations between any and violent offending histories of parents (fathers, mothers, or both parents) obtained from official records, and multiple measures of early childhood developmental functioning (social, emotional–behavioural, cognitive, communication and physical domains) obtained from the teacher-reported 2009 Australian Early Development Census.ResultsParental offending conferred significantly increased risk of vulnerability on all domains, particularly the cognitive domain. Greater risk magnitudes were observed for offending by both parents and by mothers than by fathers, and for violent than for any offending. For all parental offending exposures, vulnerability on multiple domains (where medium to large effects were observed) was more likely than on a single domain (small to medium effects). Relationships remained significant and of comparable magnitude following adjustment for sociodemographic covariates.ConclusionsThe effect of parental offending on early childhood developmental outcomes is pervasive, with the strongest effects on functioning apparent when both parents engage in violent offending. Supporting affected families in early childhood might mitigate both early developmental vulnerability and the propensity for later delinquency among these offspring.

BackgroundPituitary volume enlargements have been observed among individuals with first-episode psychosis. These abnormalities are suggestive of hypothalamic–pituitary–adrenal (HPA) axis hyperactivity, which may contribute to the development of psychosis. However, the extent to which these abnormalities characterize individuals at elevated risk for schizophrenia prior to illness onset is currently unclear, as volume increases, decreases and no volume differences have all been reported relative to controls. The current study aimed to determine whether antipsychotic-naive, putatively at-risk children who present multiple antecedents of schizophrenia (ASz) or a family history of illness (FHx) show pituitary volume abnormalities relative to typically developing (TD) children. An additional aim was to explore the association between pituitary volume and experiences of psychosocial stress.MethodASz (n = 30), FHx (n = 22) and TD (n = 32) children were identified at age 9–12 years using a novel community-screening procedure or as relatives of individuals with schizophrenia. Measures of pituitary volume and psychosocial stress were obtained at age 11–14 years.ResultsNeither ASz nor FHx children showed differences in pituitary volume relative to TD children. Among FHx children only, pituitary volume was negatively associated with current distress relating to negative life events and exposure to physical punishment.ConclusionsThe lack of pituitary volume abnormalities among ASz and FHx children is consistent with our previous work demonstrating that these children are not characterized by elevated diurnal cortisol levels. The findings imply that these biological markers of HPA axis hyperactivity, observed in some older samples of high-risk individuals, may emerge later, more proximally to disease onset.

Background: Over half of children in the general population report unusual or “psychotic-like” experiences (PLEs). The development of a later at-risk mental state is associated with persistent, distressing, PLEs, which are appraised negatively and hard to cope with. We have designed a novel, manualized, cognitive behavioural intervention for children aged 9 to 14 years, which aims to reduce emotional problems, improve coping and resilience, and help children manage PLEs, before an identifiable psychosis risk develops. We report on the feasibility, acceptability and clinical impact of the intervention. Method: Four children who reported PLEs and emotional problems in a community survey completed the intervention, and gave detailed feedback. Clinical outcomes were assessed before, during, and after therapy. Results: Emotional problems, PLE frequency, and PLE impact all decreased during the intervention. Child and therapist satisfaction with the treatment was high. Conclusions: It is feasible, acceptable and helpful to offer psychological interventions to children who report emotional distress and PLEs, prior to the emergence of clear risk factors. Our intervention has the potential to increase resilience to the development of future mental health problems. A larger, randomized controlled evaluation is underway.

BackgroundThe incidence of schizophrenia and the prevalence of psychotic symptoms in the general adult population are elevated in migrant and ethnic minority groups relative to host populations. These increases are particularly prominent among African-Caribbean migrants to the UK. This study examined the associations of ethnicity and migrant status with a triad of putative antecedents of schizophrenia in a UK community sample of children aged 9–12 years. The antecedent triad comprised: (i) psychotic-like experiences; (ii) a speech and/or motor developmental delay or abnormality; and (iii) a social, emotional or behavioural problem.MethodChildren (n=595) and their primary caregivers, recruited via schools and general practitioners in southeast London, completed questionnaires. Four indices of risk were examined for associations with ethnicity and migrant status: (i) certain experience of at least one psychotic-like experience; (ii) severity of psychotic-like experiences (total psychotic-like experience score); (iii) experience of the antecedent triad; and (iv) severity of antecedent triad experiences (triad score).ResultsAfrican-Caribbean children, as compared to white British children, experienced greater risk on all four indices. There were trends for South Asian and Oriental children to present lowered risk on several indices, relative to white British children. Migration status was unrelated to any risk index.ConclusionPrevalence of the putative antecedents of schizophrenia is greater among children of African-Caribbean origin living in the UK than among white British children. This parallels the increased incidence of schizophrenia and elevated prevalence of psychotic symptoms among adults of African-Caribbean origin.