Childhood maltreatment and peer victimisation are common sources of early-life interpersonal stress. Childhood maltreatment is associated with atypical frontolimbic emotion processing and regulation, and increased vulnerability for self-harm/suicide. However, few studies have compared the neurofunctional correlates between caregiver- versus peer-inflicted mistreatment.

We compared the alterations of neurofunctional correlates of facial emotion processing in youths exposed to childhood maltreatment or peer victimisation, and explored their associations with self-harm.

Functional magnetic resonance imaging data were collected from 114 age- and gender-matched youths (39 childhood maltreatment, 37 peer victimisation and 38 controls) during an emotion discrimination task. Region-of-interest (amygdala, insula) and whole-brain analyses were conducted.

Groups differed significantly during disgust processing only. Both groups had lower activation in the right amygdala and bilateral posterior insula than controls; left insular underactivation was furthermore related to increased self-harm in maltreated youths. Compared with controls, at the whole-brain level, both groups also had underactivation in a cluster of bilateral limbic-thalamic-striatal, precuneus/posterior cingulate, temporal, fusiform/lingual and cerebellar regions, which was negatively associated with emotional problems in controls, as well as a cluster of somatosensory regions associated with increased self-harm in maltreated youths.

Early-life interpersonal stress from caregivers or peers is associated with common underactivation of limbic-thalamic-striatal, precuneus/posterior cingulate and somatosensory regions during disgust processing. The hypoactivation of key emotion and sensory processing and self-referential brain regions could be a potential suppressive mechanism to cope with the aversive emotion; however, it may also entail increased risk of affective psychopathology in seemingly healthy youths.

Illness and mortality have social origins, and infants and children are especially susceptible to the impacts of adverse social experiences. Early-life stress (ELS) – physiological disruptions suffered by a developing organism – is incorporated into human biology through embodiment. This paper examines whether children who lived and died in New Mexico (2011–2019) embodied social determinants of health. Data were collected from 780 postmortem computed tomography scans in conjunction with data from field notes and autopsy reports for individuals aged 0.5–20.99 years from New Mexico. Variables included in linear/logistic regressions are the per cent of families in poverty by ZIP code and year, housing type (trailer/mobile home, apartment, house), rural/urban residence areas, and race/ethnicity. Health outcome variables are age at death, respiratory conditions, growth stunting and arrest, and porous cranial lesions. Intersections of poverty, housing disparities, and race/ethnicity are examined to understand whether children from New Mexico incorporated ELS into their biology.

Hispanic children have higher odds of growth stunting than non-Hispanic White children. Native American children die younger and have higher odds of respiratory diseases and porous lesions than Hispanic and non-Hispanic Whites. Rural/urban location does not significantly impact age at death, but housing type does. Individuals who lived in trailers/mobile homes had earlier ages at death. When intersections between housing type and housing location are considered, children who were poor and from impoverished areas lived longer than those who were poor from relatively well-off areas.

Children’s health is shaped by factors outside their control. The children included in this study embodied experiences of social and ELS and did not survive to adulthood. They provide the most sobering example of the harm that social factors (structural racism/discrimination, socioeconomic, and political structures) can inflict.

Adverse childhood experiences (ACEs) contribute to elevations in neuropsychiatric and neurocognitive symptoms in HIV+ adults. Emerging data suggest that exposures to threat-related and deprivation-related ACEs may have differential impacts on function, with threat exposure contributing to neuropsychiatric symptoms, and deprivation contributing to executive dysfunction. Yet, it remains unclear how specific types of ACEs impact neuropsychiatric and neurocognitive symptoms in HIV+ adults. Hence, the current study examined whether these two dimensions of adversity contribute differentially to neuropsychiatric symptoms and executive dysfunction in HIV+ adults.

We included a sample of demographically matched HIV+ (N = 72) and HIV-negative (N = 85) adults. Standardized self-report measures assessed threat-related (interpersonal violence) and deprivation-related (poverty/neglect) ACEs, as well as neuropsychiatric symptoms (depression, anxiety, apathy). A brief battery of neuropsychological tests assessed executive functions.

Compared to HIV-negative participants, HIV+ participants reported significantly higher rates of threat exposure (51% vs. 67%, p = .04), while rates of deprivation did not differ significantly (8% vs. 13%, p = .38). In the HIV+ sample, threat exposure was associated with neuropsychiatric symptoms (p < .01) but not executive dysfunction (p = .75). By contrast, deprivation was associated with executive dysfunction, at a trend level (p = .09), but not with neuropsychiatric symptoms (p = .70).

Our data suggest that, relative to HIV-negative samples, HIV+ samples experience higher rates of threat-related ACEs, which contribute to neuropsychiatric symptom elevations. Moreover, our preliminary findings suggest that different types of ACEs could be associated with different profiles of neuropsychiatric and neurocognitive difficulty in HIV+ adults, highlighting the importance of considering dimensions of adversity in future studies.

Inflammation is a possible biological mechanism underlying the association between childhood maltreatment and psychosis. Previous investigations on this regard were mainly conducted on chronic schizophrenia and lacked control for confounders. We aim to investigate the role of familial liability, childhood maltreatment and recent stress in determining cytokine abnormalities at the onset of psychosis.

We recruited 114 first-episode psychosis (FEP) patients, 57 unaffected biological siblings of FEP patients, and 251 community-based controls. Plasma cytokines (IL-1β, IL-6, TNF-α, IFN-γ, IL-4, IL-10 and TGF-β) were measured and differences across the groups analysed after adjusting for potential confounders.

FEP had a higher pro- and anti-inflammatory cytokine profile (IL-1β, IL-6, TNF-α, IL-10 and TGF-β), which was not observed in unaffected siblings. Siblings presented decreased IL-1β when compared with patients and controls. Childhood maltreatment was associated with higher levels of TGF-β in both patients and siblings when compared with controls. Physical childhood abuse was associated with increased levels of TGF-β in FEP patients but with decreased levels in controls. Other childhood maltreatment subtypes or recent stressors did not affect cytokine levels in any of the groups.

Normal or reduced cytokines in siblings represent possibly a protective factor and suggest that the identified inflammatory profile in FEP can be a real pathophysiological component of psychosis. Experience of childhood maltreatment may contribute as long-term immune priming for the TGF-β pathway, and increased levels of this cytokine in both patients and siblings exposed to childhood maltreatment point to a possible biological candidate of familial risk for psychosis.

Although early life adversity (ELA) increases risk for psychopathology, mechanisms linking ELA with the onset of psychopathology remain poorly understood. Conceptual models have argued that ELA accelerates development. It is unknown whether all forms of ELA are associated with accelerated development or whether early maturation is a potential mechanism linking ELA with psychopathology. We examine whether two distinct dimensions of ELA – threat and deprivation – have differential associations with pubertal timing in girls, and evaluate whether accelerated pubertal timing is a mechanism linking ELA with the onset of adolescent psychopathology.

Data were drawn from a large, nationally representative sample of 4937 adolescent girls. Multiple forms of ELA characterized by threat and deprivation were assessed along with age at menarche (AAM) and the onset of DSM-IV fear, distress, externalizing, and eating disorders.

Greater exposure to threat was associated with earlier AAM (B = −0.1, p = 0.001). Each 1-year increase in AAM was associated with reduced odds of fear, distress, and externalizing disorders post-menarche (ORs = 0.74–0.85). Earlier AAM significantly mediated the association between exposure to threat and post-menarche onset of distress (proportion mediated = 6.2%), fear (proportion mediated = 16.3%), and externalizing disorders (proportion mediated = 2.9%).

Accelerated pubertal development in girls may be one transdiagnostic pathway through which threat-related experiences confer risk for the adolescent onset of mental disorders. Early pubertal maturation is a marker that could be used in both medical and mental health settings to identify trauma-exposed youth that are at risk for developing a mental disorder during adolescence in order to better target early interventions.

Childhood abuse is associated with abnormalities in brain structure and function. Few studies have investigated abuse-related brain abnormalities in medication-naïve, drug-free youth that also controlled for psychiatric comorbidities by inclusion of a psychiatric control group, which is crucial to disentangle the effects of abuse from those associated with the psychiatric conditions.

Cortical volume (CV), cortical thickness (CT) and surface area (SA) were measured in 22 age- and gender-matched medication-naïve youth (aged 13–20) exposed to childhood abuse, 19 psychiatric controls matched for psychiatric diagnoses and 27 healthy controls. Both region-of-interest (ROI) and whole-brain analyses were conducted.

For the ROI analysis, the childhood abuse group compared with healthy controls only, had significantly reduced CV in bilateral cerebellum and reduced CT in left insula and right lateral orbitofrontal cortex (OFC). At the whole-brain level, relative to healthy controls, the childhood abuse group showed significantly reduced CV in left lingual, pericalcarine, precuneus and superior parietal gyri, and reduced CT in left pre-/postcentral and paracentral regions, which furthermore correlated with greater abuse severity. They also had increased CV in left inferior and middle temporal gyri relative to healthy controls. Abnormalities in the precuneus, temporal and precentral regions were abuse-specific relative to psychiatric controls, albeit at a more lenient level. Groups did not differ in SA.

Childhood abuse is associated with widespread structural abnormalities in OFC–insular, cerebellar, occipital, parietal and temporal regions, which likely underlie the abnormal affective, motivational and cognitive functions typically observed in this population.