Exposure to multiple forms of victimisation in childhood (often referred to as poly-victimisation) has lifelong adverse effects, including an elevated risk of early-adulthood psychopathology. However, not all poly-victimised children develop mental health difficulties and identifying what protects them could inform preventive interventions. The present study investigated whether individual-, family- and/or community-level factors were associated with lower levels of general psychopathology at age 18, among children exposed to poly-victimisation. Additionally, it examined whether these factors were specific to poly-victimised children or also associated with fewer mental health difficulties in young adults regardless of whether they had been poly-victimised.

We used data from the Environmental Risk (E-Risk) Longitudinal Twin Study, a population-representative cohort of 2,232 children born in 1994–1995 across England and Wales and followed to 18 years of age (with 93% retention, n = 2,066). Poly-victimisation (i.e., exposure to two or more of physical abuse, sexual abuse, emotional abuse and neglect, physical neglect, bullying by peers, and domestic violence) and nine putative protective factors (intelligence quotient, executive functioning, temperament, maternal and sibling warmth, atmosphere at home, maternal monitoring, neighbourhood social cohesion, and presence of a supportive adult) were measured prospectively between ages 5 and 12 years from interviews with mothers and children, surveys of neighbours, child-protection referrals, and researchers’ observations. Early-adulthood psychopathology was assessed in interviews with each twin at age 18 and used to construct a latent factor of general psychopathology.

Approximately a third (n = 720) of participants were prospectively defined as exposed to poly-victimisation (53% male). Poly-victimised children had greater levels of general psychopathology at age 18 than non-poly-victimised children (adjusted [adj.] β = 4.80; 95% confidence interval [95% CI] 3.13, 6.47). Presence of a supportive adult was the only factor robustly associated with lower levels of general psychopathology among poly-victimised children (adj.β = −0.61; 95% CI −0.99, −0.23). However, this association was also evident in the whole sample regardless of poly-victimisation exposure (adj.β = −0.52; 95% CI −0.81, −0.24) and no significant interaction was observed between the presence of a supportive adult and poly-victimisation in relation to age-18 general psychopathology.

Having at least one adult to turn to for support was found to be associated with less psychopathology in early adulthood among both poly-victimised and non-poly-victimised children. This suggests that strategies to promote better availability and utilisation of supportive adults should be implemented universally. However, it may be beneficial to target these interventions at poly-victimised children, given their higher burden of psychopathology in early adulthood.

Fear learning is a core component of conceptual models of how adverse experiences may influence psychopathology. Specifically, existing theories posit that childhood experiences involving childhood trauma are associated with altered fear learning processes, while experiences involving deprivation are not. Several studies have found altered fear acquisition in youth exposed to trauma, but not deprivation, although the specific patterns have varied across studies. The present study utilizes a longitudinal sample of children with variability in adversity experiences to examine associations among childhood trauma, fear learning, and psychopathology in youth.

The sample includes 170 youths aged 10–13 years (M = 11.56, s.d. = 0.47, 48.24% female). Children completed a fear conditioning task while skin conductance responses (SCR) were obtained, which included both acquisition and extinction. Childhood trauma and deprivation severity were measured using both parent and youth report. Symptoms of anxiety, externalizing problems, and post-traumatic stress disorder (PTSD) were assessed at baseline and again two-years later.

Greater trauma-related experiences were associated with greater SCR to the threat cue (CS+) relative to the safety cue (CS−) in early fear acquisition, controlling for deprivation, age, and sex. Deprivation was unrelated to fear learning. Greater SCR to the threat cue during early acquisition was associated with increased PTSD symptoms over time controlling for baseline symptoms and mediated the relationship between trauma and prospective changes in PTSD symptoms.

Childhood trauma is associated with altered fear learning in youth, which may be one mechanism linking exposure to violence with the emergence of PTSD symptoms in adolescence.

Youth adversity is associated with persistence of depression and anxiety symptoms. This association may be greater for disadvantaged societal groups (such as females) compared with advantaged groups (e.g. males). Given that persistent symptoms are observed across a range of disadvantaged, minoritized, and neurodivergent groups (e.g. low compared with high socio-economic status [SES]), the intersection of individual characteristics may be an important moderator of inequality.

Data from HeadStart Cornwall (N = 4441) was used to assess the effect of youth adversity on combined symptoms of depression and anxiety (Strengths and Difficulties Questionnaire emotional problems subscale) measured at three time-points in 11–14-year-olds. Latent trajectories and regressions were estimated for eight intersectionality profiles (based on gender, SES, and hyperactivity/inattention), and moderating effects of the individual characteristics and their intersections were estimated.

Youth adversity was associated with higher average depression/anxiety symptoms at baseline (11–12-years) across all intersectionality profiles. The magnitude of effects differed across profiles, with suggestive evidence for a moderating effect of youth adversity on change over time in depression/anxiety symptoms attributable to the intersection between (i) gender and SES; and (ii) gender, SES, and hyperactivity/inattention.

The detrimental effects of youth adversity pervade across intersectionality profiles. The extent to which these effects are moderated by intersectionality is discussed in terms of operational factors. The current results provide a platform for further research, which is needed to determine the importance of intersectionality as a moderator of youth adversity on the development of depression and anxiety symptoms in adolescence.

Employing a developmental psychopathology framework, we tested the utility of the hormesis model in examining the strengthening of children and youth through limited levels of adversity in relation to internalizing and externalizing outcomes within a brain-by-development context.

Analyzing data from the Adolescent Brain and Cognitive Development study (N = 11,878), we formed latent factors of threat, deprivation, and unpredictability. We examined linear and nonlinear associations between adversity dimensions and youth psychopathology symptoms and how change of resting-state functional connectivity (rsFC) in the default mode network (DMN) from Time 1 to Time 5 moderates these associations.

A cubic association was found between threat and youth internalizing problems; low-to-moderate family conflict levels reduced these problems. Deprivation also displayed a cubic relation with youth externalizing problems, with moderate deprivation levels associated with fewer problems. Unpredictability linearly increased both problem types. Change in DMN rsFC significantly moderated the cubic link between threat levels and internalizing problems, with declining DMN rsFC levels from Time 1 to Time 5 facilitating hormesis. Hormetic effects peaked earlier, emphasizing the importance of sensitive periods and developmental timing of outcomes related to earlier experiences.

Strengthening through limited environmental adversity is crucial for developing human resilience. Understanding this process requires considering both linear and nonlinear adversity-psychopathology associations. Testing individual differences by brain and developmental context will inform preventive intervention programming.

Shared genetic risk between schizophrenia (SCZ) and bipolar disorder (BD) is well-established, yet the extent to which they share environmental risk factors remains unclear. We compare the associations between environmental exposures during childhood/prior to disorder onset with the risk of developing SCZ and BD.

We conducted a Swedish register-based nested case–control study using 4184 SCZ cases and 18 681 BD cases diagnosed 1988–2013. Cases were matched to five controls by birth year, birth region, and sex. Conditional logistic regression was used to estimate incidence rate ratios (IRR) for SCZ and BD for each exposure (severe childhood infections, adverse childhood experiences (ACEs), substance use disorders (SUDs), urban birth/longest residence).

All SUD types were associated with very high risk (IRR 4.9–25.5), and all forms of ACEs with higher risk (IRR 1.5–4.3) for both disorders. In the mutually adjusted models, ACEs demonstrated slightly higher risk for BD (SCZ IRR 1.30, 1.19-1.42; BD IRR 1.49, 1.44–1.55), while for SUD, risk was higher for SCZ (SCZ IRR 9.43, 8.15–10.92; BD IRR 5.50, 5.15–5.88). Infections were associated with increased risk of BD (IRR 1.21, 1.17–1.26) but not SCZ. Urban birth and urban longest residence were associated with higher risk of SCZ (IRR 1.19, 1.03–1.37), while only the combination of urban birth and rural longest residence showed higher risk for BD (IRR 1.24, 1.13–1.35).

There were both shared and unique environmental risk factors: SUDs and ACEs were risk factors for both disorders, while infections were more strongly associated with BD and urbanicity with SCZ.

Children and adolescents with a history of adverse childhood experiences (ACEs) are more likely than their peers to develop mental health difficulties, but not enough is known about their help-seeking behaviours and preferences. We aimed to determine whether ACEs are associated with access to and perceived unmet need for mental health services and support amongst secondary school students.

We used multi-level logistic regression with data from the 2020 OxWell Student Survey to assess whether ACEs were associated with (1) prior access to mental health support and (2) perceived unmet need for mental health services in a community sample of English secondary school students. We assessed ACEs as a cumulative score from the Center for Youth Wellness Adverse Childhood Experiences Questionnaire: Teen Self-Report version and accounted for current mental health difficulties as measured by the 25-item Revised Children’s Anxiety and Depression Scale (RCADS).

Our analysis included 2018 students across 64 schools, of whom 29.9% (598/2002) reported prior access to mental health support. Of those not reporting prior access, 34.1% (469/1377) reported a perceived unmet need for services. In the unadjusted models, cumulative ACE scores were significantly positively associated with both prior access to mental health support (odds ratio (OR) = 1.36; 95% confidence interval (CI): 1.29–1.43) and perceived unmet need for mental health services (OR = 1.47; 95% CI: 1.37–1.59), meaning that students who had experienced adversity had a greater chance of having previously accessed support as well as perceiving an unmet need for services. After adjusting for mental health difficulties and other sociodemographic variables, cumulative ACE scores were positively associated with prior access (adjusted OR (aOR) = 1.25; 95% CI: 1.17–1.34 with a significant interaction between RCADS and ACE scores, aOR = 0.88; 95% CI: 0.84–0.93) as well as perceived unmet need (aOR = 1.32; 95% CI: 1.21–1.43 with a significant interaction between RCADS and ACE scores, aOR = 0.85; 95% CI: 0.78–0.91).

Although it is encouraging that adolescents with experience of adversity are more likely than their peers with similar levels of depression and anxiety symptoms to have accessed mental health support, there remains a concern that those who have not accessed support are more likely to perceive an as-yet unmet need for it. Mental health support must be available, accessible and acceptable to all who need it, especially for those groups that traditionally have not accessed services, including the more marginalised and vulnerable populations.

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.

Despite growing concerns about mental health during the COVID-19 pandemic, particularly in people with pre-existing mental health disorders, research has shown that symptoms of depression and anxiety were generally quite stable, with modest changes in certain subgroups. However, individual differences in cumulative exposure to COVID-19 stressors have not been yet considered.

We aimed to quantify and investigate the impact of individual-level cumulative exposure to COVID-19-pandemic-related adversity on changes in depressive and anxiety symptoms and loneliness. In addition, we examined whether the impact differed among individuals with various levels of pre-pandemic chronicity of mental health disorders.

Between April 2020 and July 2021, 15 successive online questionnaires were distributed among three psychiatric case–control cohorts that started in the 2000s (N = 1377). Outcomes included depressive and anxiety symptoms and loneliness. We developed a COVID-19 Adversity Index (CAI) summarising up to 15 repeated measures of COVID-19-pandemic-related exposures (e.g. exposure to COVID-19 infection, negative economic impact and quarantine). We used linear mixed linear models to estimate the effects of COVID-19-related adversity on mental health and its interaction with pre-pandemic chronicity of mental health disorders and CAI.

Higher CAI scores were positively associated with higher increases in depressive symptoms, anxiety symptoms and loneliness. Associations were not statistically significantly different between groups with and without (chronic) pre-pandemic mental health disorders.

Individual differences in cumulative exposure to COVID-19-pandemic-related adversity are important predictors of mental health, but we found no evidence for higher vulnerability among people with (chronic) pre-pandemic mental health disorders.

Childhood trauma and adversity are common across societies and have strong associations with physical and psychiatric morbidity throughout the life-course. One possible mechanism through which childhood trauma may predispose individuals to poor psychiatric outcomes is via associations with brain structure. This study aimed to elucidate the associations between childhood trauma and brain structure across two large, independent community cohorts.

The two samples comprised (i) a subsample of Generation Scotland (n=1,024); and (ii) individuals from UK Biobank (n=27,202). This comprised n=28,226 for mega-analysis. MRI scans were processed using Free Surfer, providing cortical, subcortical, and global brain metrics. Regression models were used to determine associations between childhood trauma measures and brain metrics and psychiatric phenotypes.

Childhood trauma associated with lifetime depression across cohorts (OR 1.06 GS, 1.23 UKB), and related to early onset and recurrent course within both samples. There was evidence for associations between childhood trauma and structural brain metrics. This included reduced global brain volume, and reduced cortical surface area with highest effects in the frontal (β=−0.0385, SE=0.0048, p(FDR)=5.43x10−15) and parietal lobes (β=−0.0387, SE=0.005, p(FDR)=1.56x10−14). At a regional level the ventral diencephalon (VDc) displayed significant associations with childhood trauma measures across both cohorts and at mega-analysis (β=−0.0232, SE=0.0039, p(FDR)=2.91x10−8). There were also associations with reduced hippocampus, thalamus, and nucleus accumbens volumes.

Associations between childhood trauma and reduced global and regional brain volumes were found, across two independent UK cohorts, and at mega-analysis. This provides robust evidence for a lasting effect of childhood adversity on brain structure.

Childhood adversities have been associated with long-lasting brain morphological differences and poor psychological outcomes over the lifespan. Evidence with regard to protective factors counteracting the detrimental effect of childhood adversity on neurobiology is scarce.

Therefore, we examined the interplay of childhood adversity with multiple protective factors in relation to brain morphology in a child and an adult cohort.

We analyzed data from two epidemiological longitudinal birth cohorts, the Generation R Study (N=3,008) and the Mannheim Study of Children at Risk (MARS) (N=179). Cumulative exposure to 12 adverse events (such as physical and sexual abuse), and the presence of protective factors, including child temperament, cognition, self-esteem, friendship quality and maternal sensitivity were assessed at different time points during childhood. Anatomical scans were acquired at the ages of 9-11 years in Generation R and at 25 years in MARS.

Childhood adversity was related to smaller global brain volumes in Generation R, with similar effect sizes observed for the cerebellar volume in MARS. While small interaction effects between adversity and protective factors were found on the medial orbitofrontal cortex, the cerebellum and the amygdala in either cohort study, no interactions were consistent across cohorts or survived correction for multiple comparisons.

We found no consistent or strong evidence for interaction effects between multiple protective factors and childhood adversities on brain structure in a child and an adult cohort study. Instead, small interaction effects were found in either children or adults warranting further investigation and more fine-grained analyses.

TB:consultancy for Actelion, Hexal Pharma, Lilly, Lundbeck, Medice, Novartis, Shire; conference support by Lilly, Medice, Novartis, Shire; clinical trials by Shire and Viforpharma; royalties by Hogrefe, Kohlhammer, CIP Medien, Oxford University Press