Schizotypy represents an index of psychosis-proneness in the general population, often associated with childhood trauma exposure. Both schizotypy and childhood trauma are linked to structural brain alterations, and it is possible that trauma exposure moderates the extent of brain morphological differences associated with schizotypy.

We addressed this question using data from a total of 1182 healthy adults (age range: 18–65 years old, 647 females/535 males), pooled from nine sites worldwide, contributing to the Enhancing NeuroImaging Genetics through Meta-Analysis (ENIGMA) Schizotypy working group. All participants completed both the Schizotypal Personality Questionnaire Brief version (SPQ-B), and the Childhood Trauma Questionnaire (CTQ), and underwent a 3D T1-weighted brain MRI scan from which regional indices of subcortical gray matter volume and cortical thickness were determined.

A series of multiple linear regressions revealed that differences in cortical thickness in four regions-of-interest were significantly associated with interactions between schizotypy and trauma; subsequent moderation analyses indicated that increasing levels of schizotypy were associated with thicker left caudal anterior cingulate gyrus, right middle temporal gyrus and insula, and thinner left caudal middle frontal gyrus, in people exposed to higher (but not low or average) levels of childhood trauma. This was found in the context of morphological changes directly associated with increasing levels of schizotypy or increasing levels of childhood trauma exposure.

These results suggest that alterations in brain regions critical for higher cognitive and integrative processes that are associated with schizotypy may be enhanced in individuals exposed to high levels of trauma.

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.

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 <6 years of age) and later diagnoses of mental disorder recorded in health service data (from age 6 to 13 years), both individually and summed as an environmental risk score (ERS).

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.

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.

Elevated levels of pro-inflammatory cytokines are consistently reported in schizophrenia (SZ) and bipolar-I disorder (BD), as well as among individuals who have been exposed to childhood trauma. However, higher levels of inflammatory markers in these disorders are yet to be investigated with respect to levels of exposure to different types of childhood trauma.

Participants were 68 cases with a diagnosis of schizophrenia/schizoaffective disorder (SZ), 69 cases with a diagnosis of psychotic BD and 72 healthy controls (HC). Serum levels of interleukin 6 (IL-6), tumour necrosis factor-α (TNF-α) and C-reactive protein (CRP) were quantified, and childhood trauma exposure was assessed with the Childhood Trauma Questionnaire.

The SZ group had significantly higher levels of IL-6, TNF-α and CRP when compared with the HC group (all p < 0.05, d = 0.41–0.63), as well as higher levels of TNF-α when compared with the BD group (p = 0.014, d = 0.50); there were no differences between the BD and HC groups for any markers. Exposure to sexual abuse was positively associated (standardised β = 0.326, t = 2.459, p = 0.018) with levels of CRP in the SZ group, but there were no significant associations between any form of trauma exposure and cytokine levels in the HC or BD groups.

These results contribute to the evidence for a chronic state of inflammation in SZ but not BD cases. Differential associations between trauma exposure and levels of pro-inflammatory cytokines across the diagnostic categories suggest that trauma may impact biological (stress and immune) systems differently in these patient groups.

The intergenerational risk for mental illness is well established within diagnostic categories, but the risk is unlikely to respect diagnostic boundaries and may be reflected more broadly in early life vulnerabilities. We aimed to establish patterns of association between externalising and internalising vulnerabilities in early childhood and parental mental disorder across the full spectrum of diagnoses.

A cohort of Australian children (n = 69 116) entering the first year of school in 2009 were assessed using the Australian Early Development Census, providing measures of externalising and internalising vulnerability. Parental psychiatric diagnostic status was determined utilising record-linkage to administrative health datasets.

Parental mental illness, across diagnostic categories, was associated with all child externalising and internalising domains of vulnerability. There was little evidence to support interaction by parental or offspring sex.

These findings have important implications for informing early identification and intervention strategies in high-risk offspring and for research into the causes of mental illness. There may be benefits to focusing less on diagnostic categories in both cases.

Emotion regulation involves the initiation of new emotional responses and continual alteration of current emotions in response to rapidly changing environmental and social stimuli. The capacity to effectively implement emotion regulation strategies is essential for psychological health; impairments in the ability to regulate emotions may be critical to the development of clinical levels of depression, anxiety and mania.

This review provides a summary of findings from current research examining the neural mechanisms of emotion regulation by means of conscious cognitive strategies of reappraisal. These findings are considered in the context of related concepts of emotion perception and emotion generation, with discussion of the likely cognitive neuropsychological contributions to emotion regulation and the implications for psychiatric disorders.

Convergent evidence implicates an inhibitory role of prefrontal cortex and cingulate regions upon subcortical and cortical emotion generation systems in the cognitive control of emotional experience. Concurrent modulation of cortical activity by the peripheral nervous system is highlighted by recent studies using simultaneous physiological and neuroimaging techniques. Individual differences in emotion perception, generation of affect and neuropsychological skills are likely to have direct consequences for emotion regulation.

Emotion regulation relies on synergy within brain stem, limbic and cortical processes that promote the adaptive perception, generation and regulation of affect. Aberrant emotion processing in any of these stages may disrupt this self-sustaining regulatory system, with the potential to manifest in distinct forms of emotion dysregulation as seen in major psychiatric disorders such as depression, bipolar disorder and schizophrenia.